Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice

Abstract The calcium sensing receptor (CaSR) is a G-protein coupled receptor that especially plays an important role in the sensing of extracellular calcium to maintain its homeostasis. Several in-vitro studies demonstrated that CaSR plays a role in adipose tissue metabolism and inflammation, result...

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Autores principales: Sai Sahana Sundararaman, Linsey J. F. Peters, Yvonne Jansen, Selin Gencer, Yi Yan, Sumra Nazir, Andrea Bonnin Marquez, Florian Kahles, Michael Lehrke, Erik A. L. Biessen, Joachim Jankowski, Christian Weber, Yvonne Döring, Emiel P. C. van der Vorst
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/87fd70aad42849868f01443f6ec9d2fe
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spelling oai:doaj.org-article:87fd70aad42849868f01443f6ec9d2fe2021-12-02T14:58:37ZAdipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice10.1038/s41598-021-89893-y2045-2322https://doaj.org/article/87fd70aad42849868f01443f6ec9d2fe2021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-89893-yhttps://doaj.org/toc/2045-2322Abstract The calcium sensing receptor (CaSR) is a G-protein coupled receptor that especially plays an important role in the sensing of extracellular calcium to maintain its homeostasis. Several in-vitro studies demonstrated that CaSR plays a role in adipose tissue metabolism and inflammation, resulting in systemic inflammation and contributing to atherosclerosis development. The aim of this study was to investigate whether adipocyte CaSR plays a role in adipose tissue inflammation in-vivo and atherosclerosis development. By using a newly established conditional mature adipocyte specific CaSR deficient mouse on a hyperlipidemic and atherosclerosis prone Apoe −/− background it could be shown that CaSR deficiency in adipocytes does neither contribute to initiation nor to progression of atherosclerotic plaques as judged by the unchanged lesion size or composition. Additionally, CaSR deficiency did not influence gonadal visceral adipose tissue (vAT) inflammation in-vivo, although a small decrease in gonadal visceral adipose cholesterol content could be observed. In conclusion, adipocyte CaSR seems not to be involved in vAT inflammation in-vivo and does not influence atherosclerosis development in hyperlipidemic Apoe−/− mice.Sai Sahana SundararamanLinsey J. F. PetersYvonne JansenSelin GencerYi YanSumra NazirAndrea Bonnin MarquezFlorian KahlesMichael LehrkeErik A. L. BiessenJoachim JankowskiChristian WeberYvonne DöringEmiel P. C. van der VorstNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Sai Sahana Sundararaman
Linsey J. F. Peters
Yvonne Jansen
Selin Gencer
Yi Yan
Sumra Nazir
Andrea Bonnin Marquez
Florian Kahles
Michael Lehrke
Erik A. L. Biessen
Joachim Jankowski
Christian Weber
Yvonne Döring
Emiel P. C. van der Vorst
Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice
description Abstract The calcium sensing receptor (CaSR) is a G-protein coupled receptor that especially plays an important role in the sensing of extracellular calcium to maintain its homeostasis. Several in-vitro studies demonstrated that CaSR plays a role in adipose tissue metabolism and inflammation, resulting in systemic inflammation and contributing to atherosclerosis development. The aim of this study was to investigate whether adipocyte CaSR plays a role in adipose tissue inflammation in-vivo and atherosclerosis development. By using a newly established conditional mature adipocyte specific CaSR deficient mouse on a hyperlipidemic and atherosclerosis prone Apoe −/− background it could be shown that CaSR deficiency in adipocytes does neither contribute to initiation nor to progression of atherosclerotic plaques as judged by the unchanged lesion size or composition. Additionally, CaSR deficiency did not influence gonadal visceral adipose tissue (vAT) inflammation in-vivo, although a small decrease in gonadal visceral adipose cholesterol content could be observed. In conclusion, adipocyte CaSR seems not to be involved in vAT inflammation in-vivo and does not influence atherosclerosis development in hyperlipidemic Apoe−/− mice.
format article
author Sai Sahana Sundararaman
Linsey J. F. Peters
Yvonne Jansen
Selin Gencer
Yi Yan
Sumra Nazir
Andrea Bonnin Marquez
Florian Kahles
Michael Lehrke
Erik A. L. Biessen
Joachim Jankowski
Christian Weber
Yvonne Döring
Emiel P. C. van der Vorst
author_facet Sai Sahana Sundararaman
Linsey J. F. Peters
Yvonne Jansen
Selin Gencer
Yi Yan
Sumra Nazir
Andrea Bonnin Marquez
Florian Kahles
Michael Lehrke
Erik A. L. Biessen
Joachim Jankowski
Christian Weber
Yvonne Döring
Emiel P. C. van der Vorst
author_sort Sai Sahana Sundararaman
title Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice
title_short Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice
title_full Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice
title_fullStr Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice
title_full_unstemmed Adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic Apoe −/− mice
title_sort adipocyte calcium sensing receptor is not involved in visceral adipose tissue inflammation or atherosclerosis development in hyperlipidemic apoe −/− mice
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/87fd70aad42849868f01443f6ec9d2fe
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