Diabetes alters intracellular calcium transients in cardiac endothelial cells.

Diabetic cardiomyopathy (DCM) is a diabetic complication, which results in myocardial dysfunction independent of other etiological factors. Abnormal intracellular calcium ([Ca(2+)](i)) homeostasis has been implicated in DCM and may precede clinical manifestation. Studies in cardiomyocytes have shown...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Abdul Q Sheikh, Jennifer R Hurley, Wei Huang, Toloo Taghian, Andrei Kogan, Hongkwan Cho, Yigang Wang, Daria A Narmoneva
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b1df6052fb4446c88a61bed77e0fd405
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:b1df6052fb4446c88a61bed77e0fd405
record_format	dspace
spelling	oai:doaj.org-article:b1df6052fb4446c88a61bed77e0fd4052021-11-18T07:19:14ZDiabetes alters intracellular calcium transients in cardiac endothelial cells.1932-620310.1371/journal.pone.0036840https://doaj.org/article/b1df6052fb4446c88a61bed77e0fd4052012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22590623/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Diabetic cardiomyopathy (DCM) is a diabetic complication, which results in myocardial dysfunction independent of other etiological factors. Abnormal intracellular calcium ([Ca(2+)](i)) homeostasis has been implicated in DCM and may precede clinical manifestation. Studies in cardiomyocytes have shown that diabetes results in impaired [Ca(2+)](i) homeostasis due to altered sarcoplasmic reticulum Ca(2+) ATPase (SERCA) and sodium-calcium exchanger (NCX) activity. Importantly, altered calcium homeostasis may also be involved in diabetes-associated endothelial dysfunction, including impaired endothelium-dependent relaxation and a diminished capacity to generate nitric oxide (NO), elevated cell adhesion molecules, and decreased angiogenic growth factors. However, the effect of diabetes on Ca(2+) regulatory mechanisms in cardiac endothelial cells (CECs) remains unknown. The objective of this study was to determine the effect of diabetes on [Ca(2+)](i) homeostasis in CECs in the rat model (streptozotocin-induced) of DCM. DCM-associated cardiac fibrosis was confirmed using picrosirius red staining of the myocardium. CECs isolated from the myocardium of diabetic and wild-type rats were loaded with Fura-2, and UTP-evoked [Ca(2+)](i) transients were compared under various combinations of SERCA, sarcoplasmic reticulum Ca(2+) ATPase (PMCA) and NCX inhibitors. Diabetes resulted in significant alterations in SERCA and NCX activities in CECs during [Ca(2+)](i) sequestration and efflux, respectively, while no difference in PMCA activity between diabetic and wild-type cells was observed. These results improve our understanding of how diabetes affects calcium regulation in CECs, and may contribute to the development of new therapies for DCM treatment.Abdul Q SheikhJennifer R HurleyWei HuangToloo TaghianAndrei KoganHongkwan ChoYigang WangDaria A NarmonevaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 5, p e36840 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Abdul Q Sheikh Jennifer R Hurley Wei Huang Toloo Taghian Andrei Kogan Hongkwan Cho Yigang Wang Daria A Narmoneva Diabetes alters intracellular calcium transients in cardiac endothelial cells.
description	Diabetic cardiomyopathy (DCM) is a diabetic complication, which results in myocardial dysfunction independent of other etiological factors. Abnormal intracellular calcium ([Ca(2+)](i)) homeostasis has been implicated in DCM and may precede clinical manifestation. Studies in cardiomyocytes have shown that diabetes results in impaired [Ca(2+)](i) homeostasis due to altered sarcoplasmic reticulum Ca(2+) ATPase (SERCA) and sodium-calcium exchanger (NCX) activity. Importantly, altered calcium homeostasis may also be involved in diabetes-associated endothelial dysfunction, including impaired endothelium-dependent relaxation and a diminished capacity to generate nitric oxide (NO), elevated cell adhesion molecules, and decreased angiogenic growth factors. However, the effect of diabetes on Ca(2+) regulatory mechanisms in cardiac endothelial cells (CECs) remains unknown. The objective of this study was to determine the effect of diabetes on [Ca(2+)](i) homeostasis in CECs in the rat model (streptozotocin-induced) of DCM. DCM-associated cardiac fibrosis was confirmed using picrosirius red staining of the myocardium. CECs isolated from the myocardium of diabetic and wild-type rats were loaded with Fura-2, and UTP-evoked [Ca(2+)](i) transients were compared under various combinations of SERCA, sarcoplasmic reticulum Ca(2+) ATPase (PMCA) and NCX inhibitors. Diabetes resulted in significant alterations in SERCA and NCX activities in CECs during [Ca(2+)](i) sequestration and efflux, respectively, while no difference in PMCA activity between diabetic and wild-type cells was observed. These results improve our understanding of how diabetes affects calcium regulation in CECs, and may contribute to the development of new therapies for DCM treatment.
format	article
author	Abdul Q Sheikh Jennifer R Hurley Wei Huang Toloo Taghian Andrei Kogan Hongkwan Cho Yigang Wang Daria A Narmoneva
author_facet	Abdul Q Sheikh Jennifer R Hurley Wei Huang Toloo Taghian Andrei Kogan Hongkwan Cho Yigang Wang Daria A Narmoneva
author_sort	Abdul Q Sheikh
title	Diabetes alters intracellular calcium transients in cardiac endothelial cells.
title_short	Diabetes alters intracellular calcium transients in cardiac endothelial cells.
title_full	Diabetes alters intracellular calcium transients in cardiac endothelial cells.
title_fullStr	Diabetes alters intracellular calcium transients in cardiac endothelial cells.
title_full_unstemmed	Diabetes alters intracellular calcium transients in cardiac endothelial cells.
title_sort	diabetes alters intracellular calcium transients in cardiac endothelial cells.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/b1df6052fb4446c88a61bed77e0fd405
work_keys_str_mv	AT abdulqsheikh diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT jenniferrhurley diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT weihuang diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT tolootaghian diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT andreikogan diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT hongkwancho diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT yigangwang diabetesaltersintracellularcalciumtransientsincardiacendothelialcells AT dariaanarmoneva diabetesaltersintracellularcalciumtransientsincardiacendothelialcells
_version_	1718423619641540608

Diabetes alters intracellular calcium transients in cardiac endothelial cells.

Ejemplares similares