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Your search keyword '"Zheng, Hua-Qing"' showing total 8 results
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8 results on '"Zheng, Hua-Qing"'

3. TMEM16A ameliorates vascular remodeling by suppressing autophagy via inhibiting Bcl-2-p62 complex formation

Author

Lv, Xiao-Fei, primary, Zhang, Ya-Juan, additional, Liu, Xiu, additional, Zheng, Hua-Qing, additional, Liu, Can-Zhao, additional, Zeng, Xue-Lin, additional, Li, Xiang-Yu, additional, Lin, Xiao-Chun, additional, Lin, Cai-Xia, additional, Ma, Ming-Ming, additional, Zhang, Fei-Ran, additional, Shang, Jin-Yan, additional, Zhou, Jia-Guo, additional, Liang, Si-Jia, additional, and Guan, Yong-Yuan, additional

Published
2020
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7. WNK1 is required for proliferation induced by hypotonic challenge in rat vascular smooth muscle cells

Author

Zhang, Ya-juan, Zheng, Hua-qing, Chen, Bao-yi, Sun, Lu, Ma, Ming-ming, Wang, Guan-lei, and Guan, Yong-yuan

Abstract

Hypotonic challenge evoked vascular cell proliferation through activation of volume-regulated Cl−channel (VRCC), leading to a decrease in the intracellular Cl−concentration ([Cl−]i). We hypothesize that the decrease in [Cl−]imay activate one or several Cl−-sensitive kinases, resulting in a subsequent signaling cascade. In this study we demonstrated that WNK1, a Cl−-sensitive kinase, was involved in VRCC-induced proliferative signaling pathway in A10 vascular smooth muscle cells in vitro. A10 cells were exposed to a hypotonic challenge (225 mosmol·kg−1·H20), which caused significantly increase in WNK1 phosphorylation without altering WNK1 protein expression. WNK1 overexpression significantly increased hypotonic-induced A10 cell proliferation, whereas silencing of WNK1 caused an opposite action. WNK1 mutation did not affect hypotonic-induced WNK1 phosphorylation and cell proliferation. Silencing of WNK1 caused cell cycle arrest at G0/G1phase and prevented transition from G1to S phase, whereas the WNK1 overexpression accelerated cell cycle transition from G1to S phase. Silencing of WNK1 significantly inhibited cyclin D1/cyclin E1 expression and increased p27kip/p21cip expression. WNK1 overexpression significantly increased cyclin D1/cyclin E1 expression and reduced p27KIP/p21CIPexpression. In addition, WNK1 knockdown or overexpression significantly attenuated or increased the hypotonic-induced phosphorylation of Akt and PI3K respectively.In conclusion, the reduction in [Cl−]icaused by hypotonic challenge-induced VRCC opening evokes WNK1 phosphorylation in A10 VSMCs, which mediates cell cycle transition from G0/G1to S phase and proliferation through the PI3K-Akt signaling pathway.

Published
2018
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8. [A1166C polymorphism of the angiotensin II type 1 receptor gene and essential hypertension in Han, Tibetan and Yi populations].

Author

Liu Y, Shan GL, Cui CY, Hou SQ, Zhuoma C, Cen WJ, Cai D, Zheng HQ, Xiao ZS, Wu ZL, Zhou WY, and Qiu CC

Subjects
Alleles, China ethnology, DNA analysis, Female, Genetic Predisposition to Disease, Genetics, Population, Genotype, Humans, Male, Polymorphism, Single Nucleotide, Tibet, Asian People genetics, Blood Pressure genetics, Gene Frequency, Hypertension genetics, Polymorphism, Genetic, Receptor, Angiotensin, Type 1 genetics
Abstract

Objective: To clarify whether A1166C polymorphism of the angiotensin II type 1 receptor (AT(1)R) gene is associated with susceptibility to essential hypertension in Han, Tibetan and Yi populations in China., Methods: This study involved 302 normotensive and 446 hypertensive subjects. The polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism in genomic DNA. The data were analyzed by ANCOVA, chi-square test, and multiple logistic regression., Results: In normotensive controls, the A1166 allele frequencies were 0.979, 0.939 and 0.965 in Han, Tibetan and Yi participants, respectively. There was no significant intergroup variation in frequency of the allele in normotensives (chi-square=4.166, P=0.125). The frequency of the A1166 allele in Tibetan male hypertensives was significantly higher than that in normotensives (chi-square=11.46, P=0.001). There was no significant difference in A1166C genotype distribution and allele frequency between normotensives and hypertensives either in the Han (P=0.465) or Yi (P=0.357) populations. Body mass index in the Han and Yi populations (P=0.0001), age in the Tibetan and Yi populations (P=0.0001), and AA genotype in the Tibetan male population (P=0.0034) all were independent risk factors for hypertension. Diastolic blood pressure levels were significantly higher in Tibetan male subjects with the AA genotype than in those with the AC+CC genotype (P=0.0040)., Conclusion: The A1166 allele is very common in Han, Tibetan and Yi populations, approximately 1.35-fold more common than in Caucasians. The A1166 allele of the AT(1)R gene may be a predisposing factor for essential hypertension in Tibetan males. A1166C polymorphism of the AT(1)R gene is probably not involved in the pathogenesis of essential hypertension in Han and Yi populations.

Published
2003

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