Bves maintains vascular smooth muscle cell contractile phenotype and protects against transplant vasculopathy via Dusp1-dependent p38MAPK and ERK1/2 signaling

Liu, Jinxin; Huang, Tong; Xie, Dawei; Yu, Qihong

doi:10.1016/j.atherosclerosis.2022.08.010

Cited by 3 publications

(3 citation statements)

References 50 publications

(79 reference statements)

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“…Erk1 and 2 are widely known as the main molecules responsible for initiating the signaling pathway involved in VSMC proliferation and differentiation. 29 – 31 A previous study found that the mechanism by which LncRNA H19 promotes vascular calcification might be related to the Erk1/2 pathways, but it did not confirm this process. 32 In the present study, we found that after 7 days of culture with β-GP, p-Erk1/2 expression was increased.…”

Section: Discussionmentioning

confidence: 96%

Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways

Wang,

Cheng,

Jin

et al. 2024

J Int Med Res

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Objective Vascular calcification is a common chronic kidney disease complication. This study aimed to investigate the function of long non-coding RNA (LncRNA) H19 in vascular calcification to explore new therapeutic strategies. Methods We induced osteogenic differentiation and calcification of vascular smooth muscle cells (VSMCs) using β-glycerophosphate. Then, we detected the LncRNA H19 promoter methylation status and Erk1/2 pathways using methylation-specific polymerase chain reaction and western blotting, respectively. Results Compared with the control group, high phosphorus levels induced VSMC calcification, accompanied by increases in LncRNA H19 and the osteogenic marker Runx2 and reduction of the contractile phenotype marker SM22a. LncRNA H19 knockdown inhibited osteogenic differentiation and calcification of VSMCs. However, the suppressed role of VSMC calcification caused by shRNA H19 was partially reversed by simultaneous activation of the Erk1/2 pathways. Mechanically, we found that the methylation rate of CpG islands in the LncRNA H19 promoter region was significantly lower in the high-phosphorus group, and the hypomethylation state elevated LncRNA H19 levels, which in turn regulated phosphorylated Erk1/2 expression. Conclusions LncRNA H19 promoted osteogenic differentiation and calcification of VSMCs by regulating the Erk1/2 pathways. Additionally, hypomethylation of LncRNA H19 promoter CpG islands upregulated LncRNA H19 levels and subsequently activated Erk1/2 phosphorylation.

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Section: Discussionmentioning

confidence: 96%

Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways

Wang,

Cheng,

Jin

et al. 2024

J Int Med Res

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“…Research by Liu et al ( 37 ) highlights the protective effect of inhibiting MAPK pathway activation on the preservation of the contractile phenotype in VSMCs. This suggests that MAPK pathway activity can drive VSMCs away from their contractile, quiescent state towards a more active, synthetic state.…”

Section: Introductionmentioning

confidence: 99%

“…Key signaling pathways such as TGF-β, mediated through Smad proteins, generally sustain the contractile phenotype but can shift toward a synthetic phenotype influenced by factors like Smad7 ( 30 ). The Notch ( 33 ), Wnt ( 41 ), and MAPK ( 37 ) pathways also critically maintain VSMC phenotype stability and regulate cellular behavior in response to external stimuli.…”

Section: Introductionmentioning

confidence: 99%

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications

Xin,

Zhang,

et al. 2024

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVD) are the leading cause of death worldwide, despite advances in understanding cardiovascular health. Significant barriers still exist in effectively preventing and managing these diseases. Vascular smooth muscle cells (VSMCs) are crucial for maintaining vascular integrity and can switch between contractile and synthetic functions in response to stimuli such as hypoxia and inflammation. These transformations play a pivotal role in the progression of cardiovascular diseases, facilitating vascular modifications and disease advancement. This article synthesizes the current understanding of the mechanisms and signaling pathways regulating VSMC phenotypic transitions, highlighting their potential as therapeutic targets in cardiovascular disease interventions.

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Dual-specificity phosphatase 1 inhibits Singapore grouper iridovirus replication via regulating apoptosis in Epinephelus coioides

He,

Cai,

et al. 2024

Fish & Shellfish Immunology

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Bves maintains vascular smooth muscle cell contractile phenotype and protects against transplant vasculopathy via Dusp1-dependent p38MAPK and ERK1/2 signaling

Cited by 3 publications

References 50 publications

Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways

Hypomethylation of the LncRNA H19 promoter accelerates osteogenic differentiation of vascular smooth muscle cells by activating the Erk1/2 pathways

Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications

Dual-specificity phosphatase 1 inhibits Singapore grouper iridovirus replication via regulating apoptosis in Epinephelus coioides

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