Upregulation of TGF-β type II receptor in high glucose-induced vascular smooth muscle cells

Mohammadi, Asghar; Zamani-Garmsiri, Fahimeh; Soleimani, Ali Akbar; Najafi, Mohammad

doi:10.1007/s11033-021-07100-7

Cited by 7 publications

(6 citation statements)

References 30 publications

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“…It was in agreement with the previous report that the cell viability and migration do not correlate with glucose values up to 50 mM. 28 It was proposed that the changes of VSMC phenotype in high glucose conditions are related to molecular intermediates produced by other cells, 4 so that it was proposed to study in animal models.…”

Section: F I G U R Esupporting

confidence: 91%

Focal adhesion kinase–related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions

Soleimani

Ghasmpour

Mohammadi

et al. 2022

Endocrino Diabet & Metabol

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Cardiovascular diseases account for approximately 65 percent of deaths in patients with diabetes mellitus. 1 It is well known that the pathogenesis of atherosclerosis is related to the proliferation and migration of vascular smooth muscle cells (VSMCs) within the media layer of arteries, so that these events promote atherogenic plaques led to vessel stenosis and restenosis. Molecular mechanisms behind VSMC proliferation and migration remain unclear. 2,3 Hyperglycemia, however, is not the only factor involved in the progression of cardiovascular diseases in diabetics but it is involved in several pathways including the activation of protein kinase C, the formation of advanced glycation end-products (AGEs) and the stimulation of lipoxygenase synthesis pathway. 4

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Section: F I G U R Esupporting

confidence: 91%

Focal adhesion kinase–related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions

Soleimani

Ghasmpour

Mohammadi

et al. 2022

Endocrino Diabet & Metabol

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“…26 In contrast with the above studies, the VSMC proliferation and migration were not observed in HG conditions in a study, so that it proposed other subendothelial cells and modified compounds related to high blood sugar might be essential to improve the VSMC proliferation and migration. 27 BARR2, as a tumour suppressor, suppresses the mitogenic signalling pathway in prostate cancer cells. BARR2 also inhibits Src activation by CXCR7, resulting in the inhibition of EGFR-and ERKrelated signalling pathways.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Beta arrestin‐related signalling axes are influenced by dexamethasone and metformin in vascular smooth muscle cells cultured in high glucose condition

Soleimani,

Shokri,

Elahimanesh

et al. 2023

Endocrino Diabet & Metabol

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BackgroundMetformin (Met) and dexamethasone (Dexa) are known to reduce blood sugar levels and anti‐inflammatory effects, respectively. Based on the acceleration of atherosclerosis process in diabetes, the β‐arrestin 2 (BARR2) gene and protein expression levels were evaluated in vascular smooth muscle cells (VSMCs) treated with Met and Dexa in high glucose conditions in this study.Methods and MaterialsHuman VSMCs were cultured in Dulbecco's Modified Eagle Medium/Nutrient Mixture F‐12 (DMEM‐F12) medium and, were treated with different values of Met (1 mM, 5 mM and 7 mM) and Dexa (10−7 M, 10−6 M and 10−5 M) in 24‐ and 48‐h periods. The BARR2 gene and protein expression levels were identified with RT‐qPCR and western blotting techniques, respectively. The signalling axes were predicted from gene network made using Cytoscape software and, were annotated with Gene Ontology.ResultsThe BARR2 gene and protein expression levels reduced in VSMCs treated with Dexa and Met after 24‐ and 48‐h periods. These results were more changed after 48 h. Furthermore, many BARR2‐related signalling axes were found from the network genes.ConclusionMet and Dexa suppressed the BARR2 protein and gene expression levels in the VSMCs. Moreover, the gene network suggested some the cellular signalling axes related to BARR2 that may be affected by Met and Dexa.

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“…They were cultured in the complete medium of HASMCs (CM-H081, Procell Technology, Wuhan, Hubei, China) in an incubator at 37℃ and under 95% air and 5% CO 2 conditions. To induce osteogenic differentiation, HASMCs were treated with 10 mM β-GP (Ma et al 2020 ) in the absence or presence of high glucose (30 mM) (Ghasempour et al 2022 ). In the β-GP + EX4 group, EX4 (100 nM) was added to the cell culture medium for 14 days (Takaku et al 2021 ), and the calcium deposition was visualized using a calcium assay kit (ab102505, Abcam, Cambridge, UK) and ARS staining.…”

Section: Methodsmentioning

confidence: 99%

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway

Chen,

Jin,

et al. 2024

Mol Med

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Background Vascular calcification (VC) is a complication in diabetes mellitus (DM) patients. Osteogenic phenotype switching of vascular smooth muscle cells (VSMCs) plays a critical role in diabetes-related VC. Mitophagy can inhibit phenotype switching in VSMCs. This study aimed to investigate the role of the glucagon-like peptide-1 receptor (GLP-1R) agonist exendin 4 (EX4) in mitophagy-induced phenotype switching. Materials and methods The status of VC in T2DM mice was monitored using Von Kossa and Alizarin Red S (ARS) staining in mouse aortic tissue. Human aortic smooth muscle cells were cultured in high glucose (HG) and β-glycerophosphate (β-GP) conditioned medium. Accumulation of LC3B and p62 was detected in the mitochondrial fraction. The effect of EX4 in vitro and in vivo was investigated by knocking down AMPKα1. Results In diabetic VC mice, EX4 decreased the percentage of von Kossa/ARS positive area. EX4 inhibited osteogenic differentiation of HG/β-GP-induced VSMCs. In HG/β-GP-induced VSMCs, the number of mitophagosomes was increased, whereas the addition of EX4 restored mitochondrial function, increased the number of mitophagosome-lysosome fusions, and reduced p62 in mitochondrial frictions. EX4 increased the phosphorylation of AMPKα (Thr172) and ULK1 (Ser555) in HG/β-GP-induced VSMCs. After knockdown of AMPKα1, ULK1 could not be activated by EX4. The accumulation of LC3B and p62 could not be reduced after AMPKα1 knockdown. Knockdown of AMPKα1 negated the therapeutic effects of EX4 on VC of diabetic mice. Conclusion EX4 could promote mitophagy by activating the AMPK signaling pathway, attenuate insufficient mitophagy, and thus inhibit the osteogenic phenotype switching of VSMCs.

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Upregulation of TGF-β type II receptor in high glucose-induced vascular smooth muscle cells

Cited by 7 publications

References 30 publications

Focal adhesion kinase–related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions

Focal adhesion kinase–related pathways may be suppressed by metformin in vascular smooth muscle cells in high glucose conditions

Beta arrestin‐related signalling axes are influenced by dexamethasone and metformin in vascular smooth muscle cells cultured in high glucose condition

Glucagon-like peptide-1 receptor agonist exendin 4 ameliorates diabetes-associated vascular calcification by regulating mitophagy through the AMPK signaling pathway

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