العنوان البديل: Hypoxic postconditioning protects myocardium by regulating autophagy in aging cardiomyocytes through piRNA-005854. (English)

المؤلفون: 迟宏扬, 杨慧霞, 郝银菊, 杨安宁, 白志刚, 焦 运, 熊建团, 马胜超, 姜怡邓

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 5/8/2024, Vol. 28 Issue 13, p2054-2060, 7p

مصطلحات موضوعية: LACTATE dehydrogenase, ISCHEMIC postconditioning, REPERFUSION injury, MYOCARDIAL injury, WESTERN immunoblotting, GALACTOSE, CREATINE kinase

الملخص (بالإنجليزية): BACKGROUND: Ischemic postconditioning is one of the effective ways to reduce ischemia-reperfusion injury and has been more and more widely used in clinical practice in recent years, but its specific molecular mechanism has yet to be studied. OBJECTIVE: To investigate the role and mechanism of piRNA-005854 in the aging cardiomyocytes caused by hypoxic postconditioning. METHODS: In vitro, cardiomyocytes were administered 8 mg/mL D-galactose for 9 days to induce their aging. β-Galactosidase staining was used to observe the aging of cardiomyocytes. Senescent cells were treated with hypoxia/reoxygenation and hypoxic postconditioning. ELISA was utilized to detect changes in myocardial injury markers creatine kinase isoenzyme MB and lactate dehydrogenase levels. Western blot assay was applied to detect the expression changes of autophagy-related proteins LC3II, p62, ULK1 and phosphorylated ULK1 in aging cardiomyocytes. qRT-PCR was employed to determine the expression level of piRNA-005854. piRNA-005854 inhibitor and piRNA-005854 mimics were transferred into aging cardiomyocytes and followed with hypoxic postconditioning. Western blot assay was used to examine the expression of LC3II, p62, ULK1 and phosphorylated ULK1. RESULTS AND CONCLUSION: (1) D-galactose induced obvious senescence of cardiomyocytes 9 days later. (2) Compared with the normoxia group, creatine kinase isoenzyme MB and lactate dehydrogenase levels increased in the hypoxia/reoxygenation group (P < 0.01); LC3 II/I expression was increased; p62 expression was decreased; ULK1 phosphorylation level was increased, and piRNA-005854 expression was increased (P < 0.01). (3) Compared with the hypoxia/ reoxygenation group, creatine kinase isoenzyme MB and lactate dehydrogenase levels significantly reduced in the hypoxic postconditioning group (P < 0.01); LC3 II/I expression significantly decreased (P < 0.05); p62 expression increased (P < 0.01); ULK1 phosphorylation level decreased (P < 0.05), and piRNA-005854 expression decreased (P < 0.01). (4) After transfection of piRNA-005854 inhibitor, LC3II/I expression was decreased (P < 0.01); the expression of p62 was increased significantly (P < 0.05); the phosphorylation level of ULK1 was decreased significantly (P < 0.01). After transfection of piRNA-005854 mimics, LC3II/ I expression was increased significantly; the expression of p62 was decreased, and the phosphorylation level of ULK1 was increased significantly (P < 0.01). (5) The results show that piRNA-005854-mediated reduction of ULK1-dependent autophagy level is a possible mechanism that hypoxic postconditioning exerts its protective effect on aging cardiomyocytes. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：缺血后处理是减轻缺血再灌注损伤的有效方式之一, 近年来被越来越广泛地应用于临床实践, 但其具体分子机制还有待研究。 目的：探讨piRNA-005854在衰老心肌细胞缺氧后处理中的作用及机制。 方法：体外给予心肌细胞8 mg/mL D-半乳糖9 d诱导其衰老, β-半乳糖苷酶染色观察心肌细胞的衰老情况；衰老后细胞给予缺氧/复氧处 理和缺氧后处理, ELISA检测心肌损伤标志物肌酸激酶同工酶MB以及乳酸脱氢酶水平；Western blot检测衰老心肌细胞中自噬相关蛋白 LC3Ⅱ、p62和ULK1及其磷酸化ULK1的表达；qRT-PCR检测piRNA-005854的表达水平；进一步用piRNA-005854 inhibitor及piRNA-005854 mimics 转染衰老心肌细胞并进行缺氧后处理, Western blot检测LC3Ⅱ、p62和ULK1及其磷酸化ULK1的表达。 结果与结论：①D-半乳糖诱导9 d后心肌细胞出现明显衰老；②与正常氧组比较, 缺氧/复氧组肌酸激酶同工酶MB以及乳酸脱氢酶水平增 加(P < 0.01)；LC3Ⅱ/Ⅰ表达升高、p62表达降低、ULK1磷酸化水平升高、piRNA-005854表达升高(P < 0.01)；③与缺氧/复氧组比较, 缺氧后 处理组肌酸激酶同工酶MB以及乳酸脱氢酶水平明显减少(P < 0.01)；LC3Ⅱ/Ⅰ表达明显降低(P < 0.05)、p62表达升高(P < 0.01)、ULK1磷酸化 水平降低(P < 0.05)、piRNA-005854表达降低(P < 0.01)；④转染piRNA-005854 inhibitor后, LC3Ⅱ/Ⅰ表达降低(P < 0.01), p62表达明显升高(P < 0.05), ULK1磷酸化水平明显降低(P < 0.01)；转染piRNA-005854 mimics后, LC3Ⅱ/Ⅰ表达显著升高, p62表达降低, ULK1磷酸化水平明显增 加(P < 0.01)；⑤结果表明, piRNA-005854介导的ULK1依赖性自噬水平降低是衰老心肌细胞缺氧后处理发挥保护作用的可能机制。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Role of METTL3 in homocysteine-induced autophagy in mouse islet beta cells. (English)

المؤلفون: 马凌桔, 汪乐新, 迟宏扬, 张竞文, 彭红建, 高春兰, 姜怡邓, 黄 晖, 杨 力, 马胜超 2，

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 9/18/2024, Vol. 28 Issue 26, p4221-4225, 5p

الملخص (بالإنجليزية): BACKGROUND: Hyperhomocysteinemia is closely related to the function of islet β cells, but its specific molecular mechanism is not fully understood. OBJECTIVE: To investigate the role of N6 methyltransferase-like 3 (METTL3) in homocysteine (Hcy)-induced autophagy of mouse islet β cells. METHODS: The 3rd and 4th generation mouse islet β cells were taken for the experiment. (1) Cell modeling and grouping: cells in control group were not treated with Hcy, while those in homocysteine group were treated with 100 µmol/L Hcy for 48 hours. (2) The mouse islet β-cells were transfected with the plasmids overexpressing Ad-METTL3 and si-METTL3 according to the instructions of LipofectamineTM 2000. Three different interfering fragments were designed, and the one with the best interfering efficiency was verified and screened by PCR. (3) After transfection, the cells were divided into control group, Hcy group, Ad-NC (negative control)+Hcy group, Ad-METTL3+Hcy group, si-NC (negative control)+Hcy group and si-METTL3+Hcy group. (4) qRT-PCR and western blot were used to detect the expression levels of METTL3 and autophagy-related proteins LC3II/I and p62 in cells. Insulin level was determined by ELISA to evaluate insulin secretion capacity of islet cells. Autophagy-related proteins and insulin level were detected after overexpression and interference with METTL3. RESULTS AND CONCLUSION: Compared with the control group, the expression level of LC3II/I was increased (P < 0.05), the expression of p62 was significantly reduced (P < 0.05), and the insulin secretion capacity was significantly decreased (P < 0.05) in the Hcy group. Compared with the control group, the protein and mRNA levels of METTL3 were reduced in the Hcy group (P < 0.05). After METTL3 silencing in islet β cells, Hcy further upregulated the expression of LC3II/I (P < 0.05), significantly dowregulated the expression of p62 (P < 0.05), and increased the insulin level (P < 0.05). After overexpression of METTL3, Hcy significantly decreased the LC3II/I expression and increased the p62 expression in islet β cells (P < 0.05). To conclude, METTL3 is involved in the Hcy-induced autophagy regulation of islet β cells and plays a role in the regulation of insulin secretion. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：高同型半胱氨酸(homocysteine，Hcy)血症与胰岛β细胞功能密切相关，但其具体分子机制尚不完全明确。 目的：探讨METTL3在Hcy诱导小鼠胰岛β细胞自噬中的作用。 方法：取第3，4代小鼠胰岛β细胞进行实验。①细胞模型建立和分组：对照组细胞不加入Hcy，Hcy组细胞加入浓度为100 µmol/L Hcy干预 48 h；②按LipofectamineTM 2000说明书将过表达质粒Ad-METTL3及si-METTL3转染小鼠胰岛β细胞，设计3种不同干扰片段，PCR验证、筛选出 干扰效率最好的干扰片段；③转染后实验分组：对照组、Hcy组、Ad-NC(阴性对照)+Hcy组、Ad-METTL3+Hcy组、si-NC(阴性对照)+Hcy组和 si-METTL3+Hcy组；④采用qRT-PCR及Western blot检测细胞中METTL3及细胞自噬相关蛋白LC3Ⅱ/Ⅰ、p62的表达；ELISA法测定胰岛素水平来 评价胰岛β细胞胰岛素分泌能力；分别过表达和干扰METTL3后检测细胞自噬相关蛋白及胰岛素水平。 结果与结论：①与对照组相比，Hcy组自噬相关蛋白LC3Ⅱ/Ⅰ的表达水平升高(P < 0.05)，而p62表达明显降低( P < 0.05)，胰岛素分泌能力 明显下降(P < 0.05)；②与对照组相比，Hcy组中METTL3蛋白及mRNA水平表达均降低(P < 0.05)；③胰岛β细胞中沉默METTL3后，Hcy进一 步上调了细胞中LC3Ⅱ/Ⅰ的表达(P < 0.05)，而p62表达显著下降(P < 0.05)，细胞中胰岛素水平增加(P < 0.05)；过表达METTL3后，Hcy则使 LC3Ⅱ/Ⅰ表达显著降低且p62 表达则增高( P < 0.05)；④结论：METTL3参与了Hcy诱导的胰岛β细胞自噬调控，对胰岛素的分泌发挥着调控作用。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Effect of cyclic RNA hsa-circ-0001360 on homocysteine-induced apoptosis of human umbilical vein endothelial cells. (English)

المؤلفون: 况园军, 于素美, 钟颖怡, 章旭红, 马胜超, 杨安宁, 郝银菊, 熊建团, 焦 运, 姜怡邓

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 9/8/2024, Vol. 28 Issue 25, p4060-4064, 5p

الملخص (بالإنجليزية): BACKGROUND: Increased homocysteine level induces apoptosis of human umbilical vein endothelial cells, but the mechanism remains unclear. OBJECTIVE: To investigate the role of hsa-circ-0001360 in human umbilical vein endothelial cell apoptosis induced by homocysteine. METHODS: In vitro cultured human umbilical vein endothelial cells were divided into control group, homocysteine group, interference control group, interference control + homocysteine group, hsa-circ-0001360 interference group, hsa-circ-0001360 + homocysteine interference group, overexpression control group, overexpression control + homocysteine group, hsa-circ-0001360 overexpression group and hsa-circ-0001360 + homocysteine overexpression group. All groups were treated with 100 μmol/L homocysteine. After 72 hours of intervention, the expressions of apoptosis-related proteins Bax, Bcl-2, and Caspase-3 were detected by western blot assay. The apoptotic rate was detected by flow cytometry. Quantitative real-time PCR was used to detect the expression of hsacirc-0001360. RESULTS AND CONCLUSION: (1) Compared with the control group, the expression of Caspase-3 and Bax was significantly increased (P < 0.01), and the expression of Bcl-2 was significantly decreased (P < 0.01), and the apoptotic rate was significantly increased (P < 0.01) in the homocysteine group. (2) Compared with control group, the expression of hsa-circ-0001360 was significantly increased in the homocysteine group (P < 0.01). (3) The expression of hsa-circ-0001360 was significantly higher in the cytoplasm than that in the nucleus (P < 0.01). (4) Compared with the interference control C group and interference control + homocysteine group, the expressions of Caspase-3 and Bax were significantly decreased (P < 0.01), while the expression of Bcl-2 was significantly increased (P < 0.01); the apoptotic rate was significantly decreased (P < 0.01) in sh-hsa-circ-0001360 interference group and sh-hsa-circ-0001360 + homocysteine interference group. (5) Compared with overexpression control group and overexpression control + homocysteine group, the expressions of Caspase-3 and Bax were significantly increased (P < 0.01), while the expression of Bcl-2 was significantly decreased (P < 0.01); the apoptotic rate was significantly increased (P < 0.01) in the hsa-circ-0001360 overexpression group and the hsa-circ-0001360 + homocysteine overexpression group. (6) In conclusion, hsa-circ-0001360 can promote the apoptosis of human umbilical vein endothelial cells induced by homocysteine. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：同型半胱氨酸水平上升会诱导人脐静脉内皮细胞发生凋亡，但机制尚不清楚。 目的：探讨hsa-circ-0001360在同型半胱氨酸诱导人脐静脉内皮细胞发生凋亡中的作用。 方法：体外培养人脐静脉内皮细胞，将其分为对照组、同型半胱氨酸组、干扰对照组、干扰对照+同型半胱氨酸组、干扰hsa-circ-0001360 组、干扰hsa-circ-0001360+同型半胱氨酸组、过表达对照组、过表达对照+同型半胱氨酸组、过表达hsa-circ-0001360组和过表达 hsa-circ-0001360+同型半胱氨酸组，同型半胱氨酸的干预浓度均为100 μmol/L。干预细胞72 h后，应用Western blot检测凋亡相关蛋白Bax、 Bcl-2和Caspase-3的表达；流式细胞仪检测细胞的凋亡率；实时荧光定量PCR(qRT-PCR)检测hsa-circ-0001360的表达水平。 结果与结论：①与对照组相比，同型半胱氨酸组人脐静脉内皮细胞中Caspase-3和Bax的表达明显升高(P < 0.01)，Bcl-2的表达明显降低( P < 0.01)，细胞凋亡率明显增高(P < 0.01)；②与对照组相比，同型半胱氨酸组人脐静脉内皮细胞中hsa-circ-0001360的表达明显升高(P < 0.01)； ③hsa-circ-0001360在人脐静脉内皮细胞的细胞质中表达显著高于细胞核(P < 0.01)；④与干扰对照组或干扰对照+同型半胱氨酸组相比，干 扰hsa-circ-0001360组和干扰hsa-circ-0001360+同型半胱氨酸组人脐静脉内皮细胞中Caspase-3、Bax的表达明显降低(P < 0.01)，Bcl-2的表达明 显升高(P < 0.01)，细胞凋亡率明显降低(P < 0.01)；⑤与过表达对照组或过表达对照+同型半胱氨酸组相比，过表达hsa-circ-0001360组和过 表达hsa-circ-0001360+同型半胱氨酸组人脐静脉内皮细胞中Caspase-3、Bax的表达明显升高(P < 0.01)，Bcl-2的表达明显降低(P < 0.01)，细胞 凋亡率明显升高(P < 0.01)；⑥以上结果表明，hsa-circ-0001360可以促进同型半胱氨酸诱导人脐静脉内皮细胞发生凋亡。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Effects of long non-coding RNA H19 on apoptosis of osteoblasts induced by dexamethasone. (English)

المؤلفون: 杨慧霞, 白志刚, 迟宏扬, 马天龙, 马胜超, 姜怡邓

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 10/8/2023, Vol. 27 Issue 28, p4513-4518, 6p

مصطلحات موضوعية: LINCRNA, FEMUR head, PROTEIN expression, CELLULAR signal transduction, FLOW cytometry, IDIOPATHIC femoral necrosis

الملخص (بالإنجليزية): BACKGROUND: The pathogenesis of steroid-induced osteonecrosis of femoral head is still unclear, which is closely related to osteoblast apoptosis. OBJECTIVE: To investigate the role of long non-coding RNA H19 (lncRNA H19) in dexamethasone-induced osteoblast apoptosis. METHODS: Mouse osteoblasts (MC3T3-E1) were cultured and divided into control group (no treatment) and dexamethasone group (treated with 1 μmol/L dexamethasone for 24 hours). Western blot was used to detect the protein expression levels of Bax, Bcl-2, and p-ERK1/2/ERK1/2. Flow cytometry and cell viability staining were used to detected cell apoptosis. qRT-PCR was performed to detect the expression of lncRNA H19. lncRNA H19 negative control plasmid (ad-NC) and lncRNA H19 overexpression plasmid (ad-lncRNA H19) were transfected into MC3T3-E1 cells, followed by 24 hours of dexamethasone intervention. Cell apoptosis of MC3T3-E1 was detected using cell viability staining, western blot assay, and flow cytometry. MC3T3-E1 cells were treated with MAPK-ERK pathway inhibitor (PD98059) for 24 hours and western blot was used to detect the protein expression levels of Bax and Bcl-2. RESULTS AND CONCLUSION: Compared with the control group, the apoptotic rate of MC3T3-E1 cells was increased in the dexamethasone group (P < 0.01), while the expression of lncRNA H19 was decreased (P < 0.01) and the MAPK/ERK signaling pathway was inhibited. Up-regulation of lncRNA H19 in MC3T3-E1 cells reduced the apoptosis of cells (P < 0.01) and activated the MAPK/ERK signaling pathway. MC3T3-E1 cells treated with dexamethasone+ad-lncRNA H19+PD98059 showed an increase in the expression of Bax (P < 0.01) and a decrease in the expression of Bcl-2 (P < 0.01) compared with the cells treated with dexamethasone+ad-lncRNA H19. These findings indicate that overexpression of lncRNA H19 can inhibit dexamethasone-induced apoptosis in MC3T3-E1 cells by activating the MAPK-ERK signaling pathway. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景: 激素性股骨头坏死的发病机制尚不清楚, 成骨细胞凋亡与其关系密切. 目的: 探讨长链非编码RNA H19(long Non-Coding RNA H19, lncRNA H19)在地塞米松促进成骨细胞凋亡中的作用. 方法: 培养小鼠成骨细胞MC3T3-E1, 分为对照组(不处理)和地塞米松组(1 μmol/L 地塞米松处理24 h), 采用Western blot检测各组细胞Bax、 Bcl-2和细胞外调节蛋白激酶(p-ERK1/2/ERK1/2)蛋白的表达, 流式细胞术和细胞活力染色检测细胞凋亡情况, qRT-PCR检测lncRNA H19的表 达. 转染lncRNA H19阴性对照(ad-NC)和lncRNA H19过表达质粒(ad-lncRNA H19)并给予地塞米松干预24 h后, 采用细胞活力染色、Western blot和流式细胞术检测MC3T3-E1细胞凋亡情况; 使用MAPK-ERK通路抑制剂PD98059处理MC3T3-E1细胞24 h, Western blot检测各组细胞Bax 和Bcl-2蛋白的表达. 结果与结论: ①与对照组相比, 地塞米松组MC3T3-E1细胞凋亡率升高, lncRNA H19相对表达降低(P < 0.01), MAPK/ERK信号通路被抑制; ②上调MC3T3-E1细胞lncRNA H19后, 细胞凋亡率降低(P < 0.01), MAPK/ERK信号通路被激活; ③与地塞米松+ad-lncRNA H19组相比, 地塞米 松+ad-lncRNA H19+PD98059组细胞Bax蛋白表达增加(P < 0.01), Bcl-2蛋白表达降低(P < 0.01); ④提示过表达lncRNA H19通过激活MAPK-ERK信 号通路抑制地塞米松诱导的MC3T3-E1细胞凋亡. [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: Role of LncRNA MALAT1 in myocardial autophagy reduction in aging rats after ischemic postconditioning. (English)

المؤلفون: 杨慧霞, 揭育祯, 白志刚, 焦 运, 杨 勇, 马天龙, 马胜超, 姜怡邓

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 7/18/2023, Vol. 27 Issue 20, p3173-3179, 7p

مصطلحات موضوعية: LINCRNA, ISCHEMIC postconditioning, SPRAGUE Dawley rats, REPERFUSION injury, PROTEIN expression

الملخص (بالإنجليزية): BACKGROUND: Ischemic postconditioning can alleviate myocardial ischemia-reperfusion injury, but the specific mechanism is not clear. OBJECTIVE: To investigate the mechanism of long non-coding RNA (lncRNA) MALAT1 in the reduction of autophagy levels in aging myocardium induced by ischemic postconditioning. METHODS: Twenty-seven Sprague-Dawley rats aged 22-24 months were randomly divided into three groups, with nine rats in each group: sham operation, ischemia-reperfusion, and ischemic postconditioning groups. Morphological changes of myocardial tissue were observed by hematoxylin-eosin staining and Masson staining. Rat myocardial cells (H9C2) were induced in vitro with 8 mg/mL D-galactose for 9 days and then divided into normoxia, hypoxia-reoxygenation, and hypoxia postconditioning groups. Western blot was used to detect the protein expression levels of LC3II/I and p62. Fluorescence quantitative PCR was used to detect the expression of lncRNA MALAT1 in aging myocardium and aging cardiomyocytes. Autophagy double-labeled adenovirus (RFP-GFP-LC3) was used to observe the changes of autophagic flux in aging cardiomyocytes. lncRNA MALAT1 interference fragment and overexpression plasmid were transfected into aging cardiomyocytes and the protein expression levels of LC3II/I and p62 were detected by western blot. RESULTS AND CONCLUSION: Compared with the ischemia-reperfusion group, the myocardial tissue structure of the ischemic postconditioning group was basically clear, the nucleus was intact, and the deposition of blue collagen fibers in the myocardial tissue was reduced. Compared with the ischemia-reperfusion group, the expression of LC3II/I was decreased and the expression of p62 was increased in the ischemic postconditioning group (P < 0.05). Compared with the hypoxia-reperfusion group, the expression of LC3II/I was decreased (P < 0.01) and the expression of p62 was increased (P < 0.05) in the hypoxia postconditioning group, and the number of intracellular autophagosomes and autophagolysosomes was decreased (P < 0.05). Compared with the ischemiareperfusion group, the expression of MALAT1 in the aging myocardial tissue was decreased the ischemic postconditioning group (P < 0.01); compared with the hypoxia-reperfusion group, the expression of MALAT1 in aging cardiomyocytes was decreased in the hypoxic postconditioning group (P < 0.01). Compared with the hypoxia postconditioning+si-NC group, the expression of LC3II/I was decreased and the expression of p62 was increased in the hypoxia postconditioning +si-lncRNA MALAT1 (P < 0.01); compared with the hypoxia postconditioning+ad-NC group, the expression of LC3II/I was increased and the expression of p62 was decreased in the hypoxia postconditioning+ad-lncRNA MALAT1 group (P < 0.01). To conclude, the lncRNA MALAT1 mediated reduction of autophagy levels is an important mechanism underlying the protective effect of ischemic postconditioning in aging myocardium. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：缺血后处理可缓解心肌缺血再灌注损伤，但是其具体机制尚不清楚。 目的：探讨lncRNA MALAT1在缺血后处理所引起衰老心肌自噬水平降低中的作用。 方法： 27只22-24月龄SD大鼠随机分为3组：假手术组、缺血再灌注组和缺血后处理组，每组9只，采用苏木精-伊红染色和Masson染色 观察心肌组织形态学变化； 体外使用8 mg/mL D-半乳糖诱导大鼠心肌(H9C2)细胞9 d后，分为正常氧组、缺氧复氧组和缺氧后处理组。 Western blot检测衰老心肌组织及衰老心肌细胞中LC3Ⅱ/Ⅰ和p62蛋白的表达；采用qRT-PCR检测衰老心肌组织和衰老心肌细胞中MALAT1相 对表达；转染自噬双标腺病毒(RFP-GFP-LC3)观察衰老心肌细胞自噬流的变化；衰老心肌细胞转染MALAT1干扰片段和过表达质粒，Western blot检测各组细胞中LC3Ⅱ/Ⅰ和p62蛋白的表达。 结果与结论： 与缺血再灌注组比较，缺血后处理组心肌组织结构基本清晰，细胞核完整，心肌组织间蓝色胶原纤维沉积减少； 与缺 血再灌注组比较，缺血后处理组LC3Ⅱ/Ⅰ表达降低且p62表达增高(P < 0.05)； 与缺氧复氧组比较，缺氧后处理组LC3Ⅱ/Ⅰ表达降低(P < 0.01)且p62表达增加(P < 0.05)，细胞内自噬体和自噬溶酶体数量均减少(P < 0.01)； 与缺血再灌注组比较，缺血后处理组衰老心肌组织的 MALAT1表达降低(P < 0.01)；与缺氧复氧组比较，缺氧后处理组衰老心肌细胞的MALAT1表达降低(P < 0.01)； 衰老心肌细胞转染MALAT1 干扰片段和过表达质粒后，与缺氧复氧+si-NC组比较，缺氧复氧+si-MALAT1组LC3Ⅱ/Ⅰ表达降低且p62表达增加(P < 0.01)；与缺氧后处理+ ad-NC组比较，缺氧后处理+ad-MALAT1组LC3Ⅱ/Ⅰ表达增加且p62表达降低(P < 0.01)； 结果表明：lncRNA MALAT1介导的自噬水平降低是 衰老大鼠心肌缺血后处理发挥保护作用的重要机制。 [ABSTRACT FROM AUTHOR]

: Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

العنوان البديل: miR-382-3p inhibits the proliferation of human hypertrophic scar fibroblasts. (English)

المؤلفون: 贺 茜, 马 芳, 万 瑀, 唐玉婷, 马胜超, 姜怡邓, 沈江涌

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 4/18/2023, Vol. 27 Issue 11, p1758-1764, 7p

مصطلحات موضوعية: PROLIFERATING cell nuclear antigen, HYPERTROPHIC scars, CYCLIN-dependent kinase inhibitors, STAT proteins, GENE expression, FIBROBLASTS, CYCLIN-dependent kinases

الملخص (بالإنجليزية): BACKGROUND: At present, numerous studies have shown that miRNA is involved in the occurrence and development of hypertrophic scars and STAT1 is involved in the proliferation of scar fibroblasts. It is speculated that miR-382-3p may also be related to the occurrence and development of hypertrophic scars. OBJECTIVE: To investigate the mechanism of miR-382-3p on the proliferation of human hypertrophic scar fibroblasts. METHODS: Hypertrophic scar and normal skin of the same individual were collected from the Department of Burn Plastic Surgery, General Hospital of Ningxia Medical University, and human hypertrophic scar fibroblasts and human normal skin fibroblasts were then extracted. Cell transfection was conducted as follows: (1) the cells were divided into control group (no treatment), miR-382-3p negative control group, and miR-382-3p overexpression group; (2) the cells were divided into control group (no treatment), STAT1 interference control group (si-NC) and STAT1 interference groups (si-STAT1-1, si-STAT1-2, si-STAT1-3). Hematoxylin-eosin staining was used to identify normal skin and hypertrophic scar, and immunofluorescence was used to identify fibroblasts. Quantitative realtime PCR was applied to detect the mRNA expression of miR-382-3p, STAT1, proliferating cell nuclear antigen (PCNA) and cyclin-dependent kinase inhibitor (p27). Western blot assay was performed to detect the protein expressions of STAT1, PCNA and p27. Cell counting kit-8 and EdU were used to detect cell proliferation activity and proliferation level. Targetscan was used to predict the downstream target genes of miR-382-3p and dual luciferase was used to verify the binding of miR-382-3p to STAT1. RESULTS AND CONCLUSION: Compared with normal skin and normal skin fibroblasts, miR-382-3p was lowly expressed in hypertrophic scar and hypertrophic scar fibroblasts (tissue: P < 0.01, cell: P < 0.01), and STAT1 was highly expressed in hypertrophic scar and hypertrophic scar fibroblasts (mRNA level in tissue: P < 0.01, protein level in tissue: P < 0.01; mRNA level in cells: P < 0.01, protein level in tissue: P < 0.01). After overexpression of miR-382-3p, the cell proliferation ability was weakened (P < 0.05), the number of EdU positive cells was decreased (P < 0.01), the expression of PCNA was decreased (mRNA: P < 0.01, protein: P < 0.05), and the expression of p27 was increased (mRNA: P < 0.05, protein: P < 0.05). miR-382-3p could target and regulate the expression of STAT1 (P < 0.01), and overexpression of miR-382-3p could reduce the expression of STAT1 (mRNA: P < 0.01, protein: P < 0.01). Interference with STAT1 reduced the expression of PCNA (P < 0.05), increased the expression of p27 (P < 0.05), and reduced the number of EdU positive cells (P < 0.01). To conclude, miR-382-3p could inhibit the proliferation of hypertrophic scar fibroblasts by inhibiting the expression of STAT1, which provides a certain theoretical basis for identifying effective targets for the treatment of hypertrophic scars. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：目前多项研究证实了miRNA影响增生性瘢痕的发生发展，STAT1参与瘢痕成纤维细胞的增殖过程，猜测miR-382-3p也有可能与增生性 瘢痕的发生发展有关系。目的：探讨miR-382-3p对人增生性瘢痕成纤维细胞增殖的作用机制。方法：收集宁夏医科大学总医院烧伤整形外科提供的增生性瘢痕和同一个体正常皮肤，提取人增生性瘢痕成纤维细胞和人正常皮肤成纤 维细胞；细胞转染分别设置：①对照组(不做处理)、miR-382-3p阴性对照组、miR-382-3p过表达组；②对照组(不做处理)、STAT1干扰对照 组(si-NC)和STAT1干扰组(si-STAT1-1、si-STAT1-2、si-STAT1-3)。苏木精-伊红染色鉴定正常皮肤和增生性瘢痕；免疫荧光鉴定成纤维细胞； qRT-PCR检测miR-382-3p、STAT1、增殖细胞核抗原及细胞周期依赖性激酶抑制物(p27)mRNA表达；Western blot检测STAT1、增殖细胞核抗原 及p27蛋白表达；CCK8、EdU检测细胞增殖活力和增殖水平；Targetscan预测miR-382-3p的下游靶基因，双荧光素酶验证miR-382-3p与STAT1 的结合情况。 结果与结论：①与正常皮肤和正常皮肤成纤维细胞相比，miR-382-3p在增生性瘢痕和增生性瘢痕成纤维细胞中呈低表达(组织：P < 0.01，细胞：P < 0.01)，STAT1在增生性瘢痕和增生性瘢痕成纤维细胞中呈高表达(组织水平mRNA：P < 0.01，组织水平蛋白：P < 0.01；细胞水平 mRNA：P < 0.01，细胞水平蛋白：P < 0.01)；②过表达miR-382-3p后细胞增殖能力减弱(P < 0.05)，EdU阳性细胞数减少(P < 0.01)，增殖细胞 核抗原的表达减少(mRNA：P < 0.01，蛋白：P < 0.05)，p27的表达增加(mRNA：P < 0.05，蛋白：P < 0.05)；③miR-382-3p能够靶向调控STAT1 的表达(P < 0.01)，过表达miR-382-3p可导致STAT1的表达减少(mRNA：P < 0.01，蛋白：P < 0.01)；④干扰STAT1后可导致增殖细胞核抗原的表 达减少(P < 0.05)，p27的表达增加(P < 0.05)，EdU阳性细胞数减少(P < 0.01)；⑤结果表明：miR-382-3p可通过抑制STAT1的表达进而抑制增生 性瘢痕成纤维细胞的增殖，为未来增生性瘢痕的治疗寻找有效靶点提供一定的理论依据。 [ABSTRACT FROM AUTHOR]

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العنوان البديل: Ephrin A receptor 2 DNA methylation increases in pancreatic beta cell apoptosis induced by homocysteine. (English)

المؤلفون: 张 晴, 高春兰, 于飞飞, 张正皓, 马 芳, 高 源, 李桂忠, 姜怡邓, 马胜超

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 2/18/2023, Vol. 27 Issue 5, p714-719, 6p

مصطلحات موضوعية: EPHRIN receptors, DNA methylation, BAX protein, PROTEIN expression, ISLANDS of Langerhans

الملخص (بالإنجليزية): BACKGROUND: Increased homocysteine levels lead to apoptosis of pancreatic β cells, but the exact mechanism remains unclear. OBJECTIVE: To explore the specific mechanism of DNA hypermethylation of Ephrin A receptor 2 (EphA2) and its promoter region in pancreatic β cells. METHODS: Mouse insulinoma cell lines (Min6) were cultured in vitro and divided into control group (0 µmol/L homocysteine) and homocysteine group (120 µmol/L homocysteine). After 48 hours of intervention in the cells, immunofluorescence and western blot were used to test the expression of apoptosisrelated proteins Bax, Bcl-2, and Caspase-3 in pancreatic islet β cells of the two groups. The expression levels of DNA methylation-related proteins DNMT1 and DNMT3a were detected by western blot. Real-time fluorescent quantitative PCR (qRT- PCR) was used to detect the level of EphA2 mRNA. Western blot was used to detect the protein expression of EphA2. Nested methylation-specific PCR was used to detect the level of DNA methylation in the promoter region of EphA2. RESULTS AND CONCLUSION: Compared with the control group, the expression of apoptosis-related proteins Bax and Caspase-3 in the pancreatic β cells was significantly increased in the homocysteine group, and the expression of Bcl-2 was significantly decreased; the mRNA and protein expression levels of EphA2 were significantly decreased (P < 0.05). Compared with the control group, the EphA2 DNA methylation level and the expression of DNMT1 protein in the pancreatic β cells were significantly higher in the homocysteine group (P < 0.05). To conclude, EphA2 DNA hypermethylation plays a significant role in homocysteine-induced pancreatic β cell apoptosis and DNMT1 may be involved in its hypermethylation process [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：同型半胱氨酸水平增加会导致胰岛β细胞发生凋亡，但其具体机制尚不明确。 目的：探讨胰岛β细胞中肝配蛋白A型受体2及其启动子区DNA高甲基化的具体机制。 方法：体外培养小鼠胰岛β细胞株Min6，将其分为对照组(0 μmol/L同型半胱氨酸)和同型半胱氨酸组(120 μmol/L同型半胱氨酸)。干预细胞 48 h后，采用免疫荧光和Western blot法检测2组细胞中凋亡相关蛋白Bax、Bcl-2、半胱氨酰天冬氨酸特异性蛋白酶3表达情况；Western blot 法检测DNA甲基化相关蛋白DNMT1、DNMT3a的表达水平；实时荧光定量PCR检测两组细胞中肝配蛋白A型受体2 mRNA水平；Western blot 检测肝配蛋白A型受体2的蛋白表达情况；巢式甲基化特异性PCR检测EphA2启动子区DNA甲基化水平。 结果与结论：①与对照组相比，同型半胱氨酸组胰岛β细胞中凋亡相关蛋白Bax和半胱氨酰天冬氨酸特异性蛋白酶3表达明显升高，Bcl-2表 达明显下降；肝配蛋白A型受体2的mRNA和蛋白表达水平明显下降(P < 0.05)； ②与对照组相比，同型半胱氨酸组肝配蛋白A型受体2 DNA甲 基化水平明显升高(P < 0.05)，同型半胱氨酸组胰岛β细胞中DNMT1蛋白表达明显增高(P < 0.05)；③提示肝配蛋白A型受体2 DNA高甲基化在 同型半胱氨酸致胰岛β细胞凋亡中的作用明显，而DNMT1可能参与其高甲基化过程。 [ABSTRACT FROM AUTHOR]

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المؤلفون: 韩睿, 赵孟良, 马胜超, 李莉

المصدر: 《分子植物育种》网络版; MPB 2012 VOL10

مصطلحات موضوعية: 菊芋；SRAP-PCR；反应体系；优化；引物筛选

الوصف: 本研究以菊芋为材料，通过单因子优化试验和L16(45)正交试验设计对影响SRAP-PCR扩增结果的重要参数进行探讨，建立了适合菊芋SRAP-PCR分析的反应体系，即20 μL反应体系中含10×PCR 扩增缓冲液，2.5 mmol/L Mg2+，0.24 mmol/L dNTPs，0.25 μmol/L正反引物，0.8 U TaqDNA聚合酶和80 ng模板DNA。利用该优化体系进行稳定性检测，并从110 个SRAP 引物组合中筛选出100个具有扩增条带清晰丰富且重复性好的引物组合和22个清晰且多态性高的引物组合，表明该体系稳定可靠，并且能够有效地用于菊芋种质资源鉴定及遗传多样性分析等研究。

وصف الملف: application/pdf

العلاقة: https://biopublisher.cn/index.php/mpb/article/view/735/pdf_84Test; https://biopublisher.cn/index.php/mpb/article/downloadSuppFile/735/166Test; https://biopublisher.cn/index.php/mpb/article/downloadSuppFile/735/167Test; https://biopublisher.cn/index.php/mpb/article/view/735Test

الإتاحة: https://biopublisher.cn/index.php/mpb/article/view/735Test

العنوان البديل: Mechanism of hyperhomocysteinemia induced renal injury in Cbs^+/- mice. (English)

المؤلفون: 吴 凯, 刘 昆, 谢 琳, 卢冠军, 马胜超, 李桂忠, 曹 军, 揭育祯1,2,3，, 姜怡邓, 郝银菊

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; 4/18/2021, Vol. 25 Issue 11, p1728-1732, 5p

مصطلحات موضوعية: TRANSMISSION electron microscopes, BASAL lamina, CHRONIC kidney failure, APOPTOSIS, PROTEIN expression, BCL genes

الملخص (بالإنجليزية): BACKGROUND: In chronic kidney disease, there is often an increase in the level of homocysteine, which can lead to podocyte apoptosis, but the specific mechanism is not clear. OBJECTIVE: To investigate the mechanism of hyperhomocysteinemia-induced renal injury in Cbs^+/- mice. METHODS: Cbs^+/+ mice (control group) and Cbs^+/- mice (model group) with similar body weight were selected, with 10 mice in each group, and were fed with high methionine diet. After 8 weeks, the mice were killed, the serum was separated and the kidney tissue was obtained. The levels of serum homocysteine, urea nitrogen and creatinine were measured by automatic biochemical analyzer. The renal injury was observed by Periodic Acid-Schiff staining and transmission electron microscope. TUNEL staining was used to observe the apoptosis of glomeruli. The protein expression levels of Bax, Bcl-2 and caspase12 were detected by western blot. RESULTS AND CONCLUSION: Compared with Cbs^+/+ mice, the level of serum homocysteine, urea nitrogen and creatinine in Cbs^+/- mice were significantly increased (P < 0.01). The Periodic Acid-Schiff staining results showed that the glomerular basement membrane of Cbs^+/+ mice was clear and the thickness was uniform, while the Cbs^+/- mouse glomerular basement membrane showed varying degrees of uneven thickness, widening of membrane area and thickening of matrix. Under the transmission electron microscope, the glomerular basement membrane of Cbs^+/+ mice was clear and the foot process was regular, while the glomerular basement membrane of Cbs^+/- mice was locally thickened and the foot process was irregular fusion. TUNEL staining showed that the number of apoptotic cells in glomeruli of Cbs^+/- mice was significantly increased compared with Cbs^+/+ mice; meanwhile, western blot detection showed that the protein levels of Bax/Bcl-2 and caspase12 were significantly increased (P < 0.05). To conclude, podocyte apoptosis plays an important role in hyperhomocysteinemiainduced renal injury in Cbs^+/- mice [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：在慢性肾脏病中常常伴有同型半胱氨酸水平升高，导致足细胞凋亡，但是其具体机制还尚未清楚。 目的：探讨高同型半胱氨酸血症诱导Cbs^+/-小鼠肾损伤的作用机制。 方法：选取体质量相近的Cbs+/+小鼠(对照组)和Cbs^+/-小鼠(模型组)，每组10只，两组小鼠均饲以高蛋氨酸饮食，8周后处死，分离血清，留 取肾脏组织。采用全自动生化分析仪检测血清同型半胱氨酸、尿素氮、肌酐水平；糖原染色法及透射电镜观察肾脏损伤情况；TUNEL染色 观察肾小球中细胞凋亡情况；Western blot检测Bax、Bcl-2和caspase12的蛋白表达水平。 结果与结论：①与Cbs^+/+小鼠比较，Cbs^+/-小鼠血清同型半胱氨酸、尿素氮及肌酐水平均明显升高(P < 0.01)；②糖原染色结果显示，Cbs^+/+小 鼠肾小球基底膜清楚，粗细均匀，而Cbs^+/-小鼠肾小球基底膜则呈现不同程度的粗细不均，膜区增宽、基质增厚；③透射电镜显示，Cbs^+/+ 小鼠肾小球基底膜清晰，足突规则，而Cbs^+/-小鼠肾小球基底膜局灶性增厚，足突不规则融合；④TUNEL染色结果显示，与Cbs^+/+小鼠比 较，Cbs^+/-小鼠肾小球内凋亡细胞数量明显增加；⑤Western blot检测结果显示，Bax/Bcl-2和caspase12的蛋白水平均升高(P < 0.05)；⑥结果 表明：足细胞凋亡在高同型半胱氨酸血症诱导Cbs+/-小鼠肾损伤中发挥着重要的作用。 [ABSTRACT FROM AUTHOR]

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العنوان البديل: Increased FoxO1 DNA methylation level in homocysteine-induced podocyte apoptosis. (English)

المؤلفون: 刘 昆, 谢 琳, 曹 军, 丁 宁, 徐灵博, 马胜超, 李桂忠, 姜怡邓, 卢冠军

المصدر: Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu; Jan2021, Vol. 25 Issue 2, p269-273, 5p

مصطلحات موضوعية: HOMOCYSTEINE, BAX protein, BCL-2 proteins, DNA methylation, APOPTOSIS, PROTEIN expression

الملخص (بالإنجليزية): BACKGROUND: The increase of homocysteine can lead to renal injury and podocyte apoptosis, but the specific mechanism is not clear. OBJECTIVE: To investigate the effect of Forkhead box O1 (FoxO1) and its DNA methylation in podocyte apoptosis induced by homocysteine. METHODS: Mouse renal podocytes (MPC-5) were cultured in vitro and divided into control group (0 μmol/L homocysteine) and homocysteine group (80 μmol/L homocysteine). After 48 hours of intervention, the expression of podocyte apoptosis-related proteins Bax, caspase12 and Bcl-2 was detected by immunofluorescence technique; the expression level of FoxO1 mRNA was detected by real-time fluorescence quantitative PCR; the protein expression levels of FoxO1 and DNMT1 were detected by western blot; DNA methylation level of FoxO1 was detected by nested methylation-specific PCR. RESULTS AND CONCLUSION: Compared with the control group, the expression levels of Bax and caspase12 protein in podocytes of the homocysteine group were significantly increased, while the expression of Bcl-2 protein was significantly decreased. The expression levels of FoxO1 mRNA and protein were significantly decreased in the homocysteine group compared with the control group (P < 0.01). At the same time, the methylation level of FoxO1 DNA in the homocysteine group was significantly higher than that in the control group (P < 0.01), and the expression of DNMT1 protein in podocytes in the homocysteine group was significantly higher than that in the control group (P < 0.01). To conclude, FoxO1 DNA hypermethylation plays a significant role in podocyte apoptosis induced by homocysteine, whereas DNMT1 participates in homocysteine-induced podocyte apoptosis. [ABSTRACT FROM AUTHOR]

Abstract (Chinese): 背景：同型半胱氨酸增多会引起肾损伤并导致足细胞凋亡，但是其具体机制还尚不清楚。 目的：探讨叉头框转录因子 O1 (forkhead box O，FoxO1) 及其 DNA 甲基化在同型半胱氨酸致足细胞凋亡中的作用。 方法：体外培养小鼠肾脏足细胞 (MPC-5)，将其分为对照组(0 μmol/L同型半胱氨酸)和同型半胱氨酸组 (80 μmol/L 同型半胱氨酸)。干预细胞 48 h后，采用免疫荧光技术检验足细胞凋亡相关蛋白Bax、caspase12 和 Bcl-2 的表达情况；采用实时荧光定量 PCR(qRT-PCR) 检测 FoxO1 mRNA 水平；采用 Western blot 检测 FoxO1和DNMT1蛋白表达水平；采用巢式降落式特异性 PCR(nMS-PCR) 测验 FoxO1 的 DNA甲基化水平。 结果与结论：①与对照组相比，同型半胱氨酸组足细胞中 Bax 和 caspase12 表达明显增高，Bcl-2 表达明显降低；②FoxO1的mRNA和蛋白表达 水平明显降低(P < 0.01)；③与对照组相比，同型半胱氨酸组 FoxO1 DNA 甲基化水平明显升高 (P < 0.01)，同型半胱氨酸组足细胞中DNMT1蛋 白表达明显增高 (P < 0.01)；④结果表明：FoxO1 DNA 高甲基化在同型半胱氨酸致足细胞凋亡中作用显著，而 DNMT1 参与同型半胱氨酸诱导 的足细胞凋亡过程。 [ABSTRACT FROM AUTHOR]

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