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Adiponectin and its receptors are involved in hypertensive vascular injury

Adipocyte-derived adiponectin (APN) is involved in the protection against cardiovascular disease, but the endogenous APN and its receptor expression in the perivascular adipocytes and their role in hypertensive vascular injury remain unclear. The present study aimed to detect endogenous APN and its... Full description

Journal Title: Molecular Medicine Reports 01/2018, Vol.17(1), pp.209-215
Main Author: Guo, Ruimin
Other Authors: Han, Min , Song, Juan , Liu, Jun , Sun, Yanni
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2017.7878
Link: http://www.spandidos-publications.com/molecular medicine reports/17/1/209
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recordid: spandido10.3892/mmr.2017.7878
title: Adiponectin and its receptors are involved in hypertensive vascular injury
format: Article
creator:
  • Guo, Ruimin
  • Han, Min
  • Song, Juan
  • Liu, Jun
  • Sun, Yanni
subjects:
  • Adiponectin
  • Adiponectin Receptors
  • Hypertension
  • Vascular Injury
ispartof: Molecular Medicine Reports, 01/2018, Vol.17(1), pp.209-215
description: Adipocyte-derived adiponectin (APN) is involved in the protection against cardiovascular disease, but the endogenous APN and its receptor expression in the perivascular adipocytes and their role in hypertensive vascular injury remain unclear. The present study aimed to detect endogenous APN and its receptor expression and their protective effects against hypertensive vascular injury. APN was mainly expressed in the perivascular adipocytes, while its receptors AdipoR1 and AdipoR2 were ubiquitously expressed in the blood vessels. Angiotensin II (Ang II)-induced hypertension resulted in a significant decrease of APN and AdipoR1 and AdipoR2 in the perivascular adipocytes and vascular cells. The migration assay used demonstrated that APN attenuated Ang II-induced vascular smooth muscle cells migration and p38 phosphorylation Furthermore, the in vivo study demonstrated that APN receptor agonist AdipoRon attenuated Ang II-induced hypertensive vascular hypertrophy and fibrosis. Taken together, the present study indicated that perivascular adipocytes-derived APN attenuated hypertensive vascular injury possibly via its receptor-mediated inhibition of p38 signaling pathway.
language: eng
source:
identifier: ISSN: 1791-2997 ; E-ISSN: 1791-3004 ; DOI: 10.3892/mmr.2017.7878
fulltext: fulltext
issn:
  • 1791-2997
  • 17912997
  • 1791-3004
  • 17913004
url: Link


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descriptionAdipocyte-derived adiponectin (APN) is involved in the protection against cardiovascular disease, but the endogenous APN and its receptor expression in the perivascular adipocytes and their role in hypertensive vascular injury remain unclear. The present study aimed to detect endogenous APN and its receptor expression and their protective effects against hypertensive vascular injury. APN was mainly expressed in the perivascular adipocytes, while its receptors AdipoR1 and AdipoR2 were ubiquitously expressed in the blood vessels. Angiotensin II (Ang II)-induced hypertension resulted in a significant decrease of APN and AdipoR1 and AdipoR2 in the perivascular adipocytes and vascular cells. The migration assay used demonstrated that APN attenuated Ang II-induced vascular smooth muscle cells migration and p38 phosphorylation Furthermore, the in vivo study demonstrated that APN receptor agonist AdipoRon attenuated Ang II-induced hypertensive vascular hypertrophy and fibrosis. Taken together, the present study indicated that perivascular adipocytes-derived APN attenuated hypertensive vascular injury possibly via its receptor-mediated inhibition of p38 signaling pathway.
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descriptionAdipocyte-derived adiponectin (APN) is involved in the protection against cardiovascular disease, but the endogenous APN and its receptor expression in the perivascular adipocytes and their role in hypertensive vascular injury remain unclear. The present study aimed to detect endogenous APN and its receptor expression and their protective effects against hypertensive vascular injury. APN was mainly expressed in the perivascular adipocytes, while its receptors AdipoR1 and AdipoR2 were ubiquitously expressed in the blood vessels. Angiotensin II (Ang II)-induced hypertension resulted in a significant decrease of APN and AdipoR1 and AdipoR2 in the perivascular adipocytes and vascular cells. The migration assay used demonstrated that APN attenuated Ang II-induced vascular smooth muscle cells migration and p38 phosphorylation Furthermore, the in vivo study demonstrated that APN receptor agonist AdipoRon attenuated Ang II-induced hypertensive vascular hypertrophy and fibrosis. Taken together, the present study indicated that perivascular adipocytes-derived APN attenuated hypertensive vascular injury possibly via its receptor-mediated inhibition of p38 signaling pathway.
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abstractAdipocyte-derived adiponectin (APN) is involved in the protection against cardiovascular disease, but the endogenous APN and its receptor expression in the perivascular adipocytes and their role in hypertensive vascular injury remain unclear. The present study aimed to detect endogenous APN and its receptor expression and their protective effects against hypertensive vascular injury. APN was mainly expressed in the perivascular adipocytes, while its receptors AdipoR1 and AdipoR2 were ubiquitously expressed in the blood vessels. Angiotensin II (Ang II)-induced hypertension resulted in a significant decrease of APN and AdipoR1 and AdipoR2 in the perivascular adipocytes and vascular cells. The migration assay used demonstrated that APN attenuated Ang II-induced vascular smooth muscle cells migration and p38 phosphorylation Furthermore, the in vivo study demonstrated that APN receptor agonist AdipoRon attenuated Ang II-induced hypertensive vascular hypertrophy and fibrosis. Taken together, the present study indicated that perivascular adipocytes-derived APN attenuated hypertensive vascular injury possibly via its receptor-mediated inhibition of p38 signaling pathway.
pubD.A. Spandidos
doi10.3892/mmr.2017.7878
date2018-01