Journal: Diabetes & Metabolism Journal

Article Title: 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

doi: 10.4093/dmj.2022.0363

Figure Lengend Snippet: Exendin-4, liraglutide, and dulaglutide inhibit the migration and proliferation of vascular smooth muscle cells (VSMCs) treated with angiotensin II (Ang II). A-10 cells are treated with 1 μM Ang II, followed by treatment with or without 100 nM exendin-4 (Ex-4), liraglutide (Lira), and dulaglutide (Dula) for 48 hours. (A, B) VSMC migration is determined using scratch wound healing assay and transwell migration assay, and (C) VSMC proliferation is determined using MTT assay. a P <0.05 and b P <0.01 when compared with the control cells, c P <0.05 and d P <0.01 when compared with the Ang II-treated cells.

Article Snippet: To examine the protective effects of GLP-1RAs on proliferation and migration of VSMCs induced by Ang II (Sigma-Aldrich, St. Louis, MO, USA), the cells were pretreated with either 100 nM exendin-4 (Sigma-Aldrich), liraglutide, or dulaglutide (MedChemExpress, Monmouth Junction, NJ, USA) 1 hour before Ang II treatment.

Techniques: Migration, Wound Healing Assay, Transwell Migration Assay, MTT Assay, Control

Journal: Diabetes & Metabolism Journal

Article Title: 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

doi: 10.4093/dmj.2022.0363

Figure Lengend Snippet: Exendin-4, liraglutide, and dulaglutide inhibit extracellular signal-regulated kinase (Erk) and c-JUN N-terminal kinase (JNK) signaling pathways and the expression of proliferation marker genes in vascular smooth muscle cells (VSMCs) treated with angiotensin II (Ang II). (A, B) A-10 cells are treated with various concentrations of Ang II for 24 hours. (C, D) A-10 cells are treated with 1 μM Ang II, followed by treatment with or without 100 nM exendin-4 (Ex-4), liraglutide (Lira), and dulaglutide (Dula) for 24 hours. p-Erk, p-JNK, and phospho-phosphatidylinositol 3-kinase (p-Pi3k) levels are analyzed using Western blotting. The mRNA expression levels of the genes encoding marker of proliferation Ki-67 ( Mki-67 ), proliferating cell nuclear antigen ( Pcna ), and cyclin D1 ( Ccnd1 ) are analyzed with quantitative real-time polymerase chain reaction and normalized to that of the glyceraldehyde3-phosphate dehydrogenase ( Gapdh ) gene. a P <0.05 and b P <0.01 when compared with the control (CON) cells, c P <0.05 and d P <0.01 when compared with the Ang II-treated cells.

Article Snippet: To examine the protective effects of GLP-1RAs on proliferation and migration of VSMCs induced by Ang II (Sigma-Aldrich, St. Louis, MO, USA), the cells were pretreated with either 100 nM exendin-4 (Sigma-Aldrich), liraglutide, or dulaglutide (MedChemExpress, Monmouth Junction, NJ, USA) 1 hour before Ang II treatment.

Techniques: Protein-Protein interactions, Expressing, Marker, Western Blot, Real-time Polymerase Chain Reaction, Control

Journal: Diabetes & Metabolism Journal

Article Title: 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

doi: 10.4093/dmj.2022.0363

Figure Lengend Snippet: Inhibitory effects of exendin-4 (Ex-4), liraglutide (Lira), and dulaglutide (Dula) on the expression of extracellular signal-regulated kinase (Erk) and c-JUN N-terminal kinase (JNK) are mediated by glucagon-like peptide-1 receptor (GLP-1R). A-10 cells pre-exposed to (A) 50 μM Erk inhibitor (PD98059) or (B) 50 μM JNK inhibitor (SP600125) for 1 hour are treated with 1 μM angiotensin II (Ang II), followed by treatment with or without Ex-4 (100 nM), Lira (100 nM), and Dula (100 nM) for 24 hours. (C) A-10 cells, transfected with 50 nM GLP-1R siRNA or scrambled (Scr) siRNA for 24 hours, are treated with Ang II, followed by treatment with or without Ex-4, Lira, and Dula for 24 hours. Expression levels of phosphor-Erk (p-Erk), p-JNK, proliferating cell nuclear antigen ( Pcna ), and cyclin D1 are analyzed using Western blotting, and glyceraldehyde-3-phosphate dehydrogenase (Gapdh) is used as the loading control. a P <0.05 and b P <0.01 when compared with the control cells, c P <0.05 and d P <0.01 when compared with the Ang II-treated cells.

Article Snippet: To examine the protective effects of GLP-1RAs on proliferation and migration of VSMCs induced by Ang II (Sigma-Aldrich, St. Louis, MO, USA), the cells were pretreated with either 100 nM exendin-4 (Sigma-Aldrich), liraglutide, or dulaglutide (MedChemExpress, Monmouth Junction, NJ, USA) 1 hour before Ang II treatment.

Techniques: Expressing, Transfection, Western Blot, Control

Journal: Diabetes & Metabolism Journal

Article Title: 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

doi: 10.4093/dmj.2022.0363

Figure Lengend Snippet: Exendin-4 (Ex-4), liraglutide (Lira), and dulaglutide (Dula) inhibit high inorganic phosphate (Pi)-induced vascular calcification in vascular smooth muscle cells. A-10 cells are treated with 4 mM Pi, followed by treatment with or without 100 nM Ex-4, Lira, or Dula for 7 days. Levels of calcium deposition are assessed by (A) alizarin red S staining and (B) calcium assays. (C, D) The protein and gene expressions of endoplasmic reticulum (ER) stress markers are analyzed using Western blotting and quantitative real-time polymerase chain reaction, respectively. (E, F) A-10 cells transfected with 10 nM activating transcription factor 4 (Atf4) siRNA or scramble (Scr) siRNA are treated with 4 mM Pi, followed by treatment with or without 100 nM Ex-4, Lira, or Dula. Expression levels of Atf4, bone morphogenic protein 2 (Bmp2), and runt-related transcription factor-2 (Runx2) are analyzed using Western blotting, and glyceraldehyde-3-phosphate dehydrogenase ( Gapdh ) is used as the loading control (CON). Levels of calcium deposition are assessed by calcium assays. Grp78 , 78 kDa glucose-regulated protein; Perk , protein kinase RNA-like endoplasmic reticulum kinase; Ire1 , inositol-requiring protein 1; CHOP , C/EBP homologous protein. a P <0.05 and b P <0.01 when compared with the CON cells, c P <0.05 and d P <0.01 when compared with the Pi-treated cells, e P <0.05 and f P <0.01 when compared with each siRNA-untreated groups.

Article Snippet: To examine the protective effects of GLP-1RAs on proliferation and migration of VSMCs induced by Ang II (Sigma-Aldrich, St. Louis, MO, USA), the cells were pretreated with either 100 nM exendin-4 (Sigma-Aldrich), liraglutide, or dulaglutide (MedChemExpress, Monmouth Junction, NJ, USA) 1 hour before Ang II treatment.

Techniques: Staining, Western Blot, Real-time Polymerase Chain Reaction, Transfection, Expressing, Control

Journal: Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry

Article Title: The Antidiabetic Mechanisms of Polyphenols Related to Increased Glucagon-Like Peptide-1 (GLP1) and Insulin Signaling

doi: 10.3390/molecules22060903

Figure Lengend Snippet: Pharmacological agents to treat type-2 diabetes mellitus (T2DM) that act on glucagon-like peptide-1 (GLP1), insulin or insulin sensitivity.

Article Snippet: GLP1R agonists (incretin mimetics) , Mimic GLP1 signaling , Exenatide, liraglutide, lixisenatide, albiglutide, dulaglutide , [ ] .

Techniques: