المؤلفون: Akinmolayemi, Oludamilola, Ozdemir, Denizhan, Pibarot, Philippe, Hahn, Rebecca T.

المصدر: JACC: Cardiovascular Imaging ; volume 16, issue 1, page 139-140 ; ISSN 1936-878X

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine, Radiology, Nuclear Medicine and imaging

الإتاحة: https://doi.org/10.1016/j.jcmg.2022.11.007Test
https://api.elsevier.com/content/article/PII:S1936878X22006751?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1936878X22006751?httpAccept=text/plainTest

المؤلفون: Akinmolayemi, Oludamilola, Ozdemir, Denizhan, Pibarot, Philippe, Zhao, Yanglu, Leipsic, Jonathon, Douglas, Pamela S., Jaber, Wael A., Weissman, Neil J., Blanke, Philipp, Hahn, Rebecca T.

المصدر: JACC: Cardiovascular Imaging ; volume 16, issue 1, page 1-9 ; ISSN 1936-878X

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine, Radiology, Nuclear Medicine and imaging

الإتاحة: https://doi.org/10.1016/j.jcmg.2022.05.010Test
https://api.elsevier.com/content/article/PII:S1936878X22003448?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S1936878X22003448?httpAccept=text/plainTest

المؤلفون: Petrossian, Gregory, Ozdemir, Denizhan, Galougahi, Keyvan Karimi, Scheiner, Jonathan, Thomas, Susan V, Shlofmitz, Richard, Shlofmitz, Evan, Jeremias, Allen, Ali, Ziad A

المصدر: US Cardiology Review ; volume 16 ; ISSN 1758-390X 1758-3896

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine

الوصف: Intravascular imaging with optical coherence tomography (OCT) and intravascular ultrasound provides superior visualization of the culprit plaques for acute coronary syndromes (ACS) compared with coronary angiography. Combined with angiography, intravascular imaging can be used to instigate ‘precision therapy’ for ACS. Post-mortem histopathology identified atherothrombosis at the exposed surface of a ruptured fibrous cap as the main cause of ACS. Further histopathological studies identified intact fibrous caps and calcified nodules as other culprit lesions for ACS. These plaque types were subsequently also identified on intravascular imaging, particularly with the high-resolution OCT. The less-common non-atherothrombotic causes of ACS are coronary artery spasm, coronary artery dissection, and coronary embolism. In this review, the authors provide an overview of clinical studies using intravascular imaging with OCT in the diagnosis and management of ACS.

الإتاحة: https://doi.org/10.15420/usc.2022.03Test
https://www.uscjournal.com/articleindex/usc.2022.03Test

المؤلفون: Becker-Greene, Dakota, Li, Hao, Pérez Cremades, Daniel, Wu, Winona, Bestepe, Furkan, Ozdemir, Denizhan, Niosi, Carolyn E., Aydogan, Ceren, Orgill, Dennis P., Feinberg, Mark W., Icli, Basak

المصدر: Becker-Greene, Dakota Li, Hao Pérez Cremades, Daniel Wu, Winona Bestepe, Furkan Ozdemir, Denizhan Niosi, Carolyn E. Aydogan, Ceren Orgill, Dennis P. Feinberg, Mark W. Icli, Basak 2021 MiR-409-3p regulates angiogenesis, white to brown adipose tissue transition, and insulin resistance through MAP4K3 and ZEB1 signaling pathways. Cellular and Molecular Life Sciences 78 7663 7679

مصطلحات موضوعية: Fisiologia

الوصف: Endothelial cells (ECs) within the microvasculature of brown adipose tissue (BAT) are important in regulating the plasticity of adipocytes in response to increased metabolic demand by modulating the angiogenic response. However, the mechanism of EC-adipocyte crosstalk during this process is not completely understood. We used RNA sequencing to profile microRNAs derived from BAT ECs of obese mice and identified an anti-angiogenic microRNA, miR-409-3p. MiR-409-3p overexpres- sion inhibited EC angiogenic properties; whereas, its inhibition had the opposite effects. Mechanistic studies revealed that miR-409-3p targets ZEB1 and MAP4K3. Knockdown of ZEB1/MAP4K3 phenocopied the angiogenic effects of miR-409-3p. Adipocytes co-cultured with conditioned media from ECs deficient in miR-409-3p showed increased expression of BAT markers, UCP1 and CIDEA. We identified a pro-angiogenic growth factor, placental growth factor (PLGF), released from ECs in response to miR-409-3p inhibition. Deficiency of ZEB1 or MAP4K3 blocked the release of PLGF from ECs and PLGF stimulation of 3T3-L1 adipocytes increased UCP1 expression in a miR-409-3p dependent manner. MiR-409-3p neutraliza- tion improved BAT angiogenesis, glucose and insulin tolerance, and energy expenditure in mice with diet-induced obesity. These findings establish miR-409-3p as a critical regulator of EC-BAT crosstalk by modulating a ZEB1-MAP4K3-PLGF signaling axis, providing new insights for therapeutic intervention in obesity.

العلاقة: Cellular and Molecular Life Sciences, 2021, vol. 78, p. 7663-7679; https://hdl.handle.net/10550/82136Test; 151052

الإتاحة: https://hdl.handle.net/10550/82136Test

المؤلفون: Gogia, Shawn, Edens, Madison, Fall, Khady, Ozdemir, Denizhan, Rahim, Hussein, Moses, Jeffrey, Karmpaliotis, Dimitrios, Kirtane, Ajay, Ben-Yehuda, Ori, Redfors, Bjorn, Leon, Martin, Matsumura, Mitsuaki, Jeremias, Allen, Maehara, Akiko, Mintz, Gary, Ali, Ziad

المصدر: Journal of the American College of Cardiology ; volume 77, issue 18, page 936 ; ISSN 0735-1097

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine

الإتاحة: https://doi.org/10.1016/s0735-1097Test(21)02295-6
https://api.elsevier.com/content/article/PII:S0735109721022956?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0735109721022956?httpAccept=text/plainTest

المؤلفون: Rahim, Muhammed, Rahim, Hussein, Gogia, Shawn, Ozdemir, Denizhan, Flattery, Erin, Parikh, Sahil, Kirtane, Ajay, Nazif, Tamim, Vahl, Torsten, Karmpaliotis, Dimitrios, Ben-Yehuda, Ori, Jeremias, Allen, Shlofmitz, Evan, Shlofmitz, Richard, Fall, Khady, Matsumura, Mitsuaki, Redfors, Bjorn, Moses, Jeffrey, Stone, Gregg, Maehara, Akiko, Leon, Martin, Rao, Sunil, Mahmud, Ehtisham, Mintz, Gary, Ali, Ziad

المصدر: Journal of the American College of Cardiology ; volume 77, issue 18, page 3359 ; ISSN 0735-1097

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine

الإتاحة: https://doi.org/10.1016/s0735-1097Test(21)04713-6
https://api.elsevier.com/content/article/PII:S0735109721047136?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0735109721047136?httpAccept=text/plainTest

المؤلفون: Gogia, Shawn, Edens, Madison, Fall, Khady, Ozdemir, Denizhan, Rahim, Hussein, Patel, Amisha, Karmpaliotis, Dimitrios, Kirtane, Ajay, Ben-Yehuda, Ori, Redfors, Bjorn, Leon, Martin, Matsumura, Mitsuaki, Maehara, Akiko, Mintz, Gary, Ali, Ziad

المصدر: Journal of the American College of Cardiology ; volume 77, issue 18, page 1017 ; ISSN 0735-1097

مصطلحات موضوعية: Cardiology and Cardiovascular Medicine

الإتاحة: https://doi.org/10.1016/s0735-1097Test(21)02376-7
https://api.elsevier.com/content/article/PII:S0735109721023767?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0735109721023767?httpAccept=text/plainTest

المؤلفون: Manica, Andre, Marchini, Julio F., Orgill, Dennis P., Wu, Winona, Ozdemir, Denizhan, Feinberg, Mark W., Perez-Cremades, Daniel, Li, Hao, Guimaraes, Raphael Boesch, Haemmig, Stefan, Icli, Basak

الوصف: Neoangiogenesis is critical for tissue repair in response to injury such as myocardial ischemia or dermal wound healing. MicroRNAs are small noncoding RNAs and important regulators of angiogenesis under physiological and pathological disease states. Therefore, identification of microRNAs that may restore impaired angiogenesis in response to tissue injury may provide new targets for therapy. Using a microRNA microarray profiling approach, we identified a human-specific microRNA, miR-4674, that was significantly decreased in patients after myocardial tissue injury and had an endothelial cell (EC)-enriched expression pattern. Functionally, overexpression of miR-4674 markedly attenuated EC proliferation, migration, network tube formation, and spheroid sprouting, whereas blockade of miR-4674 had the opposite effects. Transcriptomic profiling, gene set enrichment analyses, bioinformatics, 3'-untranslated region (3'-UTR) reporter and microribonucleoprotein immunoprecipitation (miRNP-IP) assays, and small interfering RNA dependency studies revealed that miR-4674 regulates VEGF stimulated-p38 mitogen-activated protein kinase (MAPK) signaling and targets interleukin 1 receptor-associated kinase 1 (Irak1) and BICD cargo adaptor 2 (Bicd2) in ECs. Furthermore, Irak1 and Bicd2 were necessary for miR-4674-driven EC proliferation and migration. Finally, neutralization of miR-4674 increased angiogenesis, Irak1 and Bicd2 expression, and p38 phosphorylation in human skin organoids as a model of tissue injury. Collectively, targeting miR-4674 may provide a novel therapeutic target for tissue repair in pathological disease states associated with impaired angiogenesis.

العلاقة: 3efa366d-7e23-41ff-9fc0-6b81b2b678a4; https://avesis.hacettepe.edu.tr/publication/details/3efa366d-7e23-41ff-9fc0-6b81b2b678a4/oaiTest

الإتاحة: https://doi.org/10.1152/ajpcell.00542.2019Test
https://avesis.hacettepe.edu.tr/publication/details/3efa366d-7e23-41ff-9fc0-6b81b2b678a4/oaiTest

المؤلفون: Icli, Basak, Li, Hao, Perez-Cremades, Daniel, Wu, Winona, Ozdemir, Denizhan, Haemmig, Stefan, Guimaraes, Raphael Boesch, Manica, Andre, Marchini, Julio F., Orgill, Dennis P., Feinberg, Mark W.

المصدر: AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 318(3) C524-C535

الوصف: Neoangiogenesis is critical for tissue repair in response to injury such as myocardial ischemia or dermal wound healing. MicroRNAs are small noncoding RNAs and important regulators of angiogenesis under physiological and pathological disease states. Therefore, identification of microRNAs that may restore impaired angiogenesis in response to tissue injury may provide new targets for therapy. Using a microRNA microarray profiling approach, we identified a human-specific microRNA, miR-4674, that was significantly decreased in patients after myocardial tissue injury and had an endothelial cell (EC)-enriched expression pattern. Functionally, overexpression of miR-4674 markedly attenuated EC proliferation, migration, network tube formation, and spheroid sprouting, whereas blockade of miR-4674 had the opposite effects. Transcriptomic profiling, gene set enrichment analyses, bioinformatics, 3'-untranslated region (3'-UTR) reporter and microribonucleoprotein immunoprecipitation (miRNP-IP) assays, and small interfering RNA dependency studies revealed that miR-4674 regulates VEGF stimulated-p38 mitogen-activated protein kinase (MAPK) signaling and targets interleukin 1 receptor-associated kinase 1 (Irak1) and BICD cargo adaptor 2 (Bicd2) in ECs. Furthermore, Irak1 and Bicd2 were necessary for miR-4674-driven EC proliferation and migration. Finally, neutralization of miR-4674 increased angiogenesis, Irak1 and Bicd2 expression, and p38 phosphorylation in human skin organoids as a model of tissue injury. Collectively, targeting miR-4674 may provide a novel therapeutic target for tissue repair in pathological disease states associated with impaired angiogenesis.

العلاقة: https://aperta.ulakbim.gov.tr/record/8135Test; oai:zenodo.org:8135

الإتاحة: https://aperta.ulakbim.gov.tr/record/8135Test

المؤلفون: Icli, Basak, Wu, Winona, Ozdemir, Denizhan, Li, Hao, Haemmig, Stefan, Liu, Xin, Giatsidis, Giorgio, Cheng, Henry S., Avci, Seyma Nazli, Kurt, Merve, Lee, Nathan, Guimaraes, Raphael Boesche, Manica, Andre, Marchini, Julio F., Rynning, Stein Erik, Risnes, Ivar, Hollan, Ivana, Croce, Kevin, Orgill, Dennis P., Feinberg, Mark W.

المساهمون: Tıbbi Biyoloji

الوصف: Angiogenesis is a critical process in repair of tissue injury that is regulated by a delicate balance between pro- and antiangiogenic factors. In disease states associated with impaired angiogenesis, we identified that miR-135a-3p is rapidly induced and serves as an antiangiogenic microRNA (miRNA) by targeting endothelial cell (EC) p38 signaling in vitro and in vivo. MiR-135a-3p overexpression significantly inhibited EC proliferation, migration, and network tube formation in matrigel, whereas miR-135-3p neutralization had the opposite effects. Mechanistic studies using transcriptomic profiling, bioinformatics, 3′-UTR reporter and miRNA ribonucleoprotein complex -immunoprecipitation assays, and small interfering RNA dependency studies revealed that miR-135a-3p inhibits the p38 signaling pathway in ECs by targeting huntingtin-interacting protein 1 (HIP1). Local delivery of miR-135a-3p inhibitors to wounds of diabetic db/db mice markedly increased angiogenesis, granulation tissue thickness, and wound closure rates, whereas local delivery of miR-135a-3p mimics impaired these effects. Finally, through gain- and loss-of-function studies in human skin organoids as a model of tissue injury, we demonstrated that miR-135a-3p potently modulated p38 signaling and angiogenesis in response to VEGF stimulation by targeting HIP1. These findings establish miR-135a-3p as a pivotal regulator of pathophysiological angiogenesis and tissue repair by targeting a VEGF-HIP1-p38K signaling axis, providing new targets for angiogenic therapy to promote tissue repair.—Icli, B., Wu, W., Ozdemir, D., Li, H., Haemmig, S., Liu, X., Giatsidis, G., Cheng, H. S., Avci, S. N., Kurt, M., Lee, N., Guimaraes, R. B., Manica, A., Marchini, J. F., Rynning, S. E., Risnes, I., Hollan, I., Croce, K., Orgill, D. P., Feinberg, M. W. MicroRNA-135a-3p regulates angiogenesis and tissue repair by targeting p38 signaling in endothelial cells.

وصف الملف: application/pdf

العلاقة: The Faseb Journal; http://dx.doi.org/10.1096/fj.201802063RRTest; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6436660Test/; http://hdl.handle.net/11655/24188Test; 33

الإتاحة: https://doi.org/10.1096/fj.201802063RRTest
http://hdl.handle.net/11655/24188Test
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6436660Test/