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Journal of Zhejiang University SCIENCE B

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Globular adiponectin-mediated vascular remodeling by affecting the secretion of adventitial-derived tumor necrosis factor induced by urotensin II


Author(s):  Jun LI, Limin LUO, Yonggang ZHANG, Xiao DONG, Shuyi DANG, Xiaogang GUO, Wenhui DING

Affiliation(s):  Department of Cardiology, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China; more

Corresponding email(s):  dwh_rd@126.com

Key Words:  Urotensin II; adiponectin; Signal Transduction; Adventitial Fibroblasts; RNAi; APN-KO


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Jun LI, Limin LUO, Yonggang ZHANG, Xiao DONG, Shuyi DANG, Xiaogang GUO, Wenhui DING. Globular adiponectin-mediated vascular remodeling by affecting the secretion of adventitial-derived tumor necrosis factor induced by urotensin II[J]. Journal of Zhejiang University Science B, 1998, -1(7): .

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publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2200346"
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A1 - Wenhui DING
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Abstract: 
In this study, we explored how adiponectin mediated UII-induced TNF-α and α-SMA expression and ensuing intracellular signaling pathways in AFs. Methods: Growth-arrested AFs and rat tunica adventitia of vessels were incubated with UII and inhibitors of signal transduction pathways for 1 to 24 hours. The cells were then harvested for TNF-α receptor mRNA and TNF-α protein expression determination by RT-PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Adiponectin and adiponectin receptor (adipoR) expression was measured by reverse transcription-PCR (RT-PCR), quantitative real-time RT-PCR (qRT-PCR), immunohistochemical analysis, and cell counting kit-8 (CCK-8) cell proliferation experiments. We then quantified TNF-α and α-SMA mRNA and protein expression levels by qRT-PCR and immunofluorescence staining (IF). RNA interference (RNAi) was used to explore the function of the adipoR genes. To investigate the signaling pathway, we applied western blotting (wb) to examine phosphorylation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK). In vivo, an APN knockout mouse model mimicking adventitial inflammation was generated to measure TNF-α and α-SMA expression by application of qRT-PCR and IF, with the goal of gaining a comprehensive atlas of adiponectin in vascular remodeling. Results: In both cells and tissues, UII promoted TNF-α protein and TNF-α-R secretion in a dose- and time-dependent manner via Rho/PKC pathways. We detected marked expression of adipoR1, T-cadherin, and calreticulin as well as a moderate presence of adipoR2 in AFs, while no adiponectin was observed. gAd fostered the growth of AFs, and acted in concert with UII to induce α-SMA and TNF-α through the AdipoR1/T-cadherin/Calreticulin/AMPK pathway. In AFs, gAd and UII synergistically induced AMPK phosphorylation. In the adventitial inflammation model, APN deficiency up-regulated the expression of α-SMA, UT, and UII while inhibiting TNF-α expression. Conclusions: From the results of our study, we can speculate that UII induces TNF-α protein and TNF-α-R secretion in AFs and rat tunica adventitia of vessels via the Rho and PKC signal transduction pathways. Thus, it is plausible that adiponectin is a major player in adventitial progression and could serve as a novel therapeutic target for cardiovascular disease administration.

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