دورية أكاديمية
Glucagon-Like Peptide Receptor Agonist Inhibits Angiotensin II-Induced Proliferation and Migration in Vascular Smooth Muscle Cells and Ameliorates Phosphate-Induced Vascular Smooth Muscle Cells Calcification
| العنوان: | Glucagon-Like Peptide Receptor Agonist Inhibits Angiotensin II-Induced Proliferation and Migration in Vascular Smooth Muscle Cells and Ameliorates Phosphate-Induced Vascular Smooth Muscle Cells Calcification |
|---|---|
| المؤلفون: | Jinmi Lee, Seok-Woo Hong, Min-Jeong Kim, Sun Joon Moon, Hyemi Kwon, Se Eun Park, Eun-Jung Rhee, Won-Young Lee |
| المصدر: | Diabetes & Metabolism Journal, Vol 48, Iss 1, Pp 83-96 (2024) |
| بيانات النشر: | Korean Diabetes Association, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Diseases of the endocrine glands. Clinical endocrinology |
| مصطلحات موضوعية: | angiotensin ii, cell migration inhibition, cell proliferation, glucagon-like peptide 1, muscle, smooth, vascular, Diseases of the endocrine glands. Clinical endocrinology, RC648-665 |
| الوصف: | Background Glucagon-like peptide-1 receptor agonist (GLP-1RA), which is a therapeutic agent for the treatment of type 2 diabetes mellitus, has a beneficial effect on the cardiovascular system. Methods To examine the protective effects of GLP-1RAs on proliferation and migration of vascular smooth muscle cells (VSMCs), A-10 cells exposed to angiotensin II (Ang II) were treated with either exendin-4, liraglutide, or dulaglutide. To examine the effects of GLP-1RAs on vascular calcification, cells exposed to high concentration of inorganic phosphate (Pi) were treated with exendin-4, liraglutide, or dulaglutide. Results Ang II increased proliferation and migration of VSMCs, gene expression levels of Ang II receptors AT1 and AT2, proliferation marker of proliferation Ki-67 (Mki-67), proliferating cell nuclear antigen (Pcna), and cyclin D1 (Ccnd1), and the protein expression levels of phospho-extracellular signal-regulated kinase (p-Erk), phospho-c-JUN N-terminal kinase (p-JNK), and phospho-phosphatidylinositol 3-kinase (p-Pi3k). Exendin-4, liraglutide, and dulaglutide significantly decreased the proliferation and migration of VSMCs, the gene expression levels of Pcna, and the protein expression levels of p-Erk and p-JNK in the Ang II-treated VSMCs. Erk inhibitor PD98059 and JNK inhibitor SP600125 decreased the protein expression levels of Pcna and Ccnd1 and proliferation of VSMCs. Inhibition of GLP-1R by siRNA reversed the reduction of the protein expression levels of p-Erk and p-JNK by exendin-4, liraglutide, and dulaglutide in the Ang II-treated VSMCs. Moreover, GLP-1 (9-36) amide also decreased the proliferation and migration of the Ang II-treated VSMCs. In addition, these GLP-1RAs decreased calcium deposition by inhibiting activating transcription factor 4 (Atf4) in Pi-treated VSMCs. Conclusion These data show that GLP-1RAs ameliorate aberrant proliferation and migration in VSMCs through both GLP-1R-dependent and independent pathways and inhibit Pi-induced vascular calcification. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2233-6079 2233-6087 |
| العلاقة: | http://e-dmj.org/upload/pdf/dmj-2022-0363.pdfTest; https://doaj.org/toc/2233-6079Test; https://doaj.org/toc/2233-6087Test |
| DOI: | 10.4093/dmj.2022.0363 |
| الوصول الحر: | https://doaj.org/article/511119968529429f8f90173d05c1966cTest |
| رقم الانضمام: | edsdoj.511119968529429f8f90173d05c1966c |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 22336079 22336087 |
|---|---|
| DOI: | 10.4093/dmj.2022.0363 |