2020
DOI: 10.21037/atm-20-4567
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The relationship between estrogen-induced phenotypic transformation and proliferation of vascular smooth muscle and hypertensive intracerebral hemorrhage

Abstract: Background: To explore the effect of estrogen on human cerebral vascular smooth muscle cells (VSMCs) and to clarify the molecular mechanism of estrogen inhibition of VSMC proliferation, which could provide an important reference basis for the clinical treatment of hypertensive intracerebral hemorrhage. Method: Firstly, the effects of different concentrations of estradiol and estrogen receptor (ESR) blocker (tamoxifen) on the proliferation of human VSMCs and the expression of estrogen-related receptor gene (… Show more

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Cited by 14 publications
(14 citation statements)
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“…1c). Among these 21 genes, MYC associated factor X [49], Sp1 transcription factor [50], cyclic adenosine monophosphate responsive element binding protein 1 [51], homeobox A4 [52], and estrogen receptor 1 [53] were previously reported to participate in the switch of ASMC phenotype. It was proposed that miR-22-3p might indirectly regulate CHD9 expression via these factors.…”
Section: Discussionmentioning
confidence: 99%
“…1c). Among these 21 genes, MYC associated factor X [49], Sp1 transcription factor [50], cyclic adenosine monophosphate responsive element binding protein 1 [51], homeobox A4 [52], and estrogen receptor 1 [53] were previously reported to participate in the switch of ASMC phenotype. It was proposed that miR-22-3p might indirectly regulate CHD9 expression via these factors.…”
Section: Discussionmentioning
confidence: 99%
“…However, in the state of vascular injury or inflammation, VSMCs switch from the contractile phenotype to the synthetic phenotype, thereby playing an important role in vascular remodeling [ 39 , 40 , 41 ]. Estrogen can effectively prevent this switch [ 42 ]. As previously described, estrogen inhibits many processes, including VSMC migration and proliferation, via genomic and non-genomic mechanisms during vascular remodeling [ 3 , 35 , 36 ].…”
Section: Resultsmentioning
confidence: 99%
“…On the other hand, it has been discovered by recent studies that TLR4/MyD88/NF-κB(p65) signal pathway could effectively regulate expression of SRF and Myocardin [20]. Olson Lab detected the most effective SRF coactivator by far-Myocardin which could initialize the phenotypic transformation procedure of smooth muscle cell (SMC) and activate the transcription of a series of SRF-regulated and codified cell scaffolding proteins and contraction-associated proteins so as to regulate the SMC phenotyping [20]. In this study, the findings suggest upon ILK overexpression, TGF-β1 stimulation and TLR4/MyD88/NF-κB(p65) activation, downstream SRF and Myocardin gene and proteins change in their expression.…”
Section: Discussionmentioning
confidence: 99%