The transient receptor potential vanilloid‐3 regulates hypoxia‐mediated pulmonary artery smooth muscle cells proliferation via <scp>PI</scp>3K/<scp>AKT</scp> signaling pathway

Zhang, Qianlong; Cao, Yonggang; Luo, Qian; Wang, Peng; Shi, Pilong; Song, Chao; Mingyao, E; Ren, Jing; Fu, Bowen; Sun, Hai‐Ying

doi:10.1111/cpr.12436

Cited by 45 publications

(33 citation statements)

References 57 publications

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“…The PI3K/AKT signaling pathway is important in VSMC proliferation and migration (15,31). Previous studies have reported that PI3K/AKT activation is important in promoting the migration of cultured VSMCs; however, this effect is increased by AKT depletion (32,33). Another study also found that PI3K/AKT inhibition blocked serum-stimulated VSMC lamellipodia formation (15).…”

Section: Discussionmentioning

confidence: 92%

Knockdown of GC binding factor 2 by RNA interference inhibits invasion and migration of vascular smooth muscle cells

Ren

Guan

2019

Mol Med Report

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GC binding factor 2 (GCF2) is a transcriptional repressor that inhibits the transcription of GC-rich promoters, thereby regulating biological processes, including proliferation. However, the role of GCF2 in vascular smooth muscle cells (VSMCs) remains unclear. The level of α-smooth muscle (α-SM) actin was determined by immunofluorescence. Cell viability, migration and invasion were analyzed using Cell Counting Kit-8, wound healing and Transwell assays, respectively. Apoptosis and cell cycle progression were determined using flow cytometry. The expressions of Bcl-2, Bax, cleaved caspase-3, cyclin E, CDK2 and the CDK inhibitor p21 were determined by reverse transcription-quantitative (RT-q)PCR and western blot analysis. RT-qPCR was performed to analyze the levels of GCF2 and western blot analysis was conducted to determine the phosphorylation levels of PI3K and AKT. α-SM actin was found to be expressed in VSMCs. Cell viability, migration and invasion were inhibited by small interfering (si)RNA targeting GCF2. Changes in the expression levels of Bcl-2, Bax and cleaved caspase-3 showed that the pro-apoptotic capacity of the cells was increased by siGCF2. Cell cycle arrest in the G 0 /G 1 phase was induced by siGCF2, which was accompanied by changes in the levels of cyclin E, CDK2 and p21. Furthermore, phosphorylation of PI3K and AKT was suppressed by siGCF2. However, the inhibitory effects of siGCF2 on cell viability, migration and invasion were increased by insulin-like growth factor 1, which is a specific agonist of AKT. The anti-proliferative activity of siGCF2 may be associated with the PI3K/AKT pathway in VSMCs.

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Section: Discussionmentioning

confidence: 92%

Knockdown of GC binding factor 2 by RNA interference inhibits invasion and migration of vascular smooth muscle cells

Ren

Guan

2019

Mol Med Report

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“…It participates in the proliferation of vascular smooth muscle cells ,[ ] the generation of inflammatory factors such as VCAM‐1, and the autophagy of macrophages . In rats with hypoxic pulmonary hypertension, PI3K/Akt is activated, and the associated with protein level increases . LY294002 serves as an inhibitor of PI3K pathways, which can compete with PI3K in ATP binding sites and specifically inhibit PI3K activation.…”

Section: Discussionmentioning

confidence: 99%

Minimally modified low-density lipoprotein upregulates the ETB and α1 receptors in mouse mesenteric arteries in vivo by activating the PI3K/Akt pathway

Zeng

Lin

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives The current study aimed to explore whether minimally modified low‐density lipoprotein (mmLDL) via tail vein injection upregulates the ETB and α1 receptors in mouse mesenteric arteries by activating the PI3K/Akt pathway. Methods The contraction curves of the mesenteric arteries caused by sarafotoxin 6c (S6c, ETB receptor agonist) and phenylephrine (PE, α1 receptor agonist) were measured by a myograph system. Serum oxLDL was detected using enzyme‐linked immunosorbent assays. The levels of the ETB receptor, the α1 receptor, PI3K, p‐PI3K and p‐Akt were detected using real‐time polymerase chain reaction and Western blot analyses. Key findings Minimally modified low‐density lipoprotein noticeably enhanced the contraction effect curves of S6c and PE, with significantly increased Emax values (P < 0.01), compared to those of the control group. This treatment significantly increased the mRNA expression and protein levels of the ETB and α1 receptors and the protein levels of p‐PI3K and p‐Akt in the vessel wall (P < 0.01). LY294002 inhibited the effect of mmLDL. Conclusions An increase in mmLDL activated the PI3K/Akt pathway, which upregulated the expression of the ETB and α1 receptors and enhanced the ETB and α1‐receptor‐mediated contractile function.

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“…Aijima et al argued that knockdown of TRPV3 suppressed proliferation of oral epithelia in mice [14]. Zhang et al revealed that TRPV3 promotes hypoxia-mediated pulmonary artery smooth muscle cells proliferation via increased [Ca 2+ ]i [15].Here, we investigated if TRPV3 plays a role in endothelial cell (EC) proliferation and tumor angiogenesis.…”

Section: Introductionmentioning

confidence: 92%

Non-Small Cell Lung Cancer A549 cells induces HUVECs proliferation and migration through TRPV3 promoting the secretion of VEGF

2019

Preprint

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The transient receptor potential vanilloid‐3 regulates hypoxia‐mediated pulmonary artery smooth muscle cells proliferation via PI3K/AKT signaling pathway

Abstract: These findings suggest that TRPV3 is involved in hypoxia-induced pulmonary vascular remodeling and promotes proliferation of PASMCs and the effect is, at least in part, mediated via the PI3K/AKT pathway.

Cited by 45 publications

References 57 publications

Knockdown of GC binding factor 2 by RNA interference inhibits invasion and migration of vascular smooth muscle cells

Knockdown of GC binding factor 2 by RNA interference inhibits invasion and migration of vascular smooth muscle cells

Minimally modified low-density lipoprotein upregulates the ETB and α1 receptors in mouse mesenteric arteries in vivo by activating the PI3K/Akt pathway

Non-Small Cell Lung Cancer A549 cells induces HUVECs proliferation and migration through TRPV3 promoting the secretion of VEGF

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