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学科主题: 临床医学
题名:
Hydrogen sulfide upregulates K-ATP channel expression in vascular smooth muscle cells of spontaneously hypertensive rats
作者: Sun, Yan1; Huang, Yaqian1; Zhang, Rongyuan1; Chen, Qinghua1; Chen, Jie2; Zong, Yanfang1; Liu, Jia1; Feng, Shasha1; Liu, Angie Dong3; Holmberg, Lukas3; Liu, Die1; Tang, Chaoshu4,5; Du, Junbao1,5; Jin, Hongfang1
关键词: Hydrogen sulfide ; Vasorelaxation ; ATP-sensitive potassium channels ; Smooth muscle cell ; Hypertension
刊名: JOURNAL OF MOLECULAR MEDICINE-JMM
发表日期: 2015-04-01
DOI: 10.1007/s00109-014-1227-1
卷: 93, 期:4, 页:439-455
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Genetics & Heredity ; Medicine, Research & Experimental
研究领域[WOS]: Genetics & Heredity ; Research & Experimental Medicine
关键词[WOS]: NITRIC-OXIDE ; POTASSIUM CHANNELS ; H2S ; KIR6.1 ; MICE ; GAS ; CARDIOMYOCYTES ; VASORELAXANT ; PATHOGENESIS ; REAPPRAISAL
英文摘要:

The study was designed to investigate whether H2S could upregulate expression of K-ATP channels in vascular smooth muscle cells (VSMCs), and by this mechanism enhances vasorelaxation in spontaneously hypertensive rats (SHR). Blood pressure, vascular structure, and vasorelaxation were analyzed. Plasma H2S was detected using polarographic sensor. SUR2B and Kir6.1 expressions were detected in VSMCs of SHR and in A7r5 cells as well as primarily cultured ASMCs using real-time PCR, western blot, immunofluorescence, and confocal imaging. Nuclear translocation of forkhead transcription factors FOXO1 and FOXO3a in ASMCs was detected using laser confocal microscopy, and their binding activity with SUR2B and Kir6.1 promoters was examined by chromatin immunoprecipitation. SHR developed hypertension at 18 weeks. They showed downregulated vascular SUR2B and Kir6.1 expressions in association with a decreased plasma H2S level. H2S donor, however, could upregulate vascular SUR2B and Kir6.1 expressions, causing a left shift of the vasorelaxation curve to pinacidil and lowered tail artery pressure in the SHR. Also, H2S antagonized endothelin-1 (ET-1)-inhibited K-ATP expression in A7r5 cells and cultured ASMCs. Mechanistically, H2S inhibited ET-1-stimulated p-FOXO1 and p-FOXO3a expressions (inactivated forms), but increased their nuclear translocation and the ET-1-inhibited binding of FOXO1 and FOXO3a with Kir6.1 and SUR2B promoters in ASMCs. Hence, H2S promotes vasorelaxation of SHR, at least in part, through upregulating the expression of K-ATP subunits by inhibiting phosphorylation of FOXO1 and FOXO3a, and stimulating FOXO1 and FOXO3a nuclear translocation and their binding activity with SUR2B and Kir6.1 promoters.

H2S increased vascular SUR2B and Kir6.1 expression of SHR, promoting vasorelaxation.

H2S antagonized ET-1-inhibited K-ATP expression in A7r5 cells and cultured ASMCs.

H2S inhibited ET-1-induced FOXO1 and FOXO3a phosphorylation in ASMCs.

H2S promoted FOXO1 and FOXO3a nuclear translocation and binding with target gene promoters.

语种: 英语
所属项目编号: 2012CB517806 ; 2013CB933801 ; 81100181 ; 81121061 ; 7121014 ; 7122184 ; 20130001120047 ; NCET-11-0005
项目资助者: Major Basic Research Development Program of People&prime ; s Republic of China ; National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Ministry of Education, China ; Program for New Century Excellent Talents of Ministry of Education, China
WOS记录号: WOS:000351518100009
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55304
Appears in Collections:北京大学第一临床医学院_儿科_期刊论文

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作者单位: 1.Peking Univ First Hosp, Dept Pediat, Beijing 100034, Peoples R China
2.Fujian Med Univ, Prov Sch Clin Med, Dept Pediat, Fuzhou, Peoples R China
3.Linkoping Univ, Dept Med & Hlth Sci, Linkoping, Sweden
4.Peking Univ First Hosp, Inst Cardiovasc Dis, Beijing, Peoples R China
5.Minist Educ, Key Lab Mol Cardiol, Beijing, Peoples R China

Recommended Citation:
Sun, Yan,Huang, Yaqian,Zhang, Rongyuan,et al. Hydrogen sulfide upregulates K-ATP channel expression in vascular smooth muscle cells of spontaneously hypertensive rats[J]. JOURNAL OF MOLECULAR MEDICINE-JMM,2015,93(4):439-455.
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