The relationship between estrogen-induced phenotypic transformation and proliferation of vascular smooth muscle and hypertensive intracerebral hemorrhage
| Autor: | Xuenong He, Chang Liu, Guanyu Wang, Xiaohui Xia, Xiaochuan Sun, Changlong Zhou |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Vascular smooth muscle medicine.drug_class Chemistry Estrogen receptor General Medicine 030204 cardiovascular system & hematology Angiotensin II 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Endocrinology Estrogen Myocardin Internal medicine medicine cardiovascular system Original Article Estrogen receptor alpha GPER Tamoxifen hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | Ann Transl Med |
| Popis: | 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 (ESR: ESR1, ESR2, GPER), myocardin (MYOCD), serum reaction factor (SRF), and apoptosis gene caspase-3 were measured to discover the effect and mechanism of tamoxifen on the proliferation and apoptosis of VSMCs. Secondly, the effects of estradiol on human VSMCs treated with angiotensin II (Ang II) were observed by measuring the expression of vascular smooth muscle markers, α-smooth muscle actin (α-SMA), SM22α, FLN, MCP-1, and TLR4. Results Estradiol inhibited the proliferation of VSMCs by upregulating the expression of ESR1, ESR2, and GPER and downregulating the expression of caspase-3, MYOCD, and SRF, thereby inhibiting the apoptosis of vascular smooth muscle. At the same time, tamoxifen had opposite effects. Angiotensin II decreased the expression of α-SMA and SM22α and promoted the expression of FLN, MCP-1, and TLR4 protein, while estrogen had the opposite effects. Conclusions Estrogen suppresses apoptosis by inhibiting the proliferation of human VSMCs and preventing it from changing from contractile to synthetic. Estrogen can further prevents vascular damage and regulate peripheral inflammatory reaction, thereby producing a protective effect on cardiovascular and cerebrovascular. |
| Databáze: | OpenAIRE |
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