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논문 기본 정보

자료유형
학술저널
저자정보
Ke Tao (Department of General Surgery Changshu Hospital Affiliated to Soochow University Changshu 215500 Ch) Ming Li (Department of General Surgery Changshu Hospital Affiliated to Soochow University Changshu 215500 Ch) Xuefeng Gu (Department of General Surgery Changshu Hospital Affiliated to Soochow University Changshu 215500 Ch) Ming Wang (Department of General Surgery Changshu Hospital Affiliated to Soochow University Changshu 215500 Ch) Tianwei Qian (Department of General Surgery Changshu Hospital Affiliated to Soochow University Changshu 215500 Ch) Lijun Hu (Department of General Surgery Changshu Hospital Affiliated to Soochow University Changshu 215500 Ch) Jiang Li (Department of Vascular Surgery The Affiliated Suzhou Hospital of Nanjing Medical University Suzhou)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제5호
발행연도
2022.9
수록면
347 - 355 (9page)
DOI
10.4196/kjpp.2022.26.5.347

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Abdominal aortic aneurysm (AAA) is a life-threatening disorder worldwide. Fibroblast growth factor 21 (FGF21) was shown to display a high level in the plasma of patients with AAA; however, its detailed functions underlying AAA pathogenesis are unclear. An in vitro AAA model was established in human aortic vascular smooth muscle cells (HASMCs) by angiotensin II (Ang-II) stimulation. Cell counting kit-8, wound healing, and Transwell assays were utilized for measuring cell proliferation and migration. RT-qPCR was used for detecting mRNA expression of FGF21 and activating transcription factor 4 (ATF4). Western blotting was utilized for assessing protein levels of FGF21, ATF4, and markers for the contractile phenotype of HASMCs. ChIP and luciferase reporter assays were implemented for identifying the binding relation between AFT4 and FGF21 promoters. FGF21 and ATF4 were both upregulated in Ang-II-treated HASMCs. Knocking down FGF21 attenuated Ang-IIinduced proliferation, migration, and phenotype switch of HASMCs. ATF4 activated FGF21 transcription by binding to its promoter. FGF21 overexpression reversed AFT4 silencing-mediated inhibition of cell proliferation, migration, and phenotype switch. ATF4 transcriptionally upregulates FGF21 to promote the proliferation, migration, and phenotype switch of Ang-II-treated HASMCs.

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