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Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte

Endostatin, a fragment of collagen XVIII, is known as an endogenous angiogenesis inhibitor, and its serum concentration increases in various cardiovascular diseases. T-type Ca(2+) channel, low voltage-activated Ca(2+) channel, is not expressed in adult ventricular myocytes. Re-expression of T-type C...

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Autores principales: YASUDA, Jumpei, OKADA, Muneyoshi, YAMAWAKI, Hideyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japanese Society of Veterinary Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638298/
https://www.ncbi.nlm.nih.gov/pubmed/25947888
http://dx.doi.org/10.1292/jvms.14-0551
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author YASUDA, Jumpei
OKADA, Muneyoshi
YAMAWAKI, Hideyuki
author_facet YASUDA, Jumpei
OKADA, Muneyoshi
YAMAWAKI, Hideyuki
author_sort YASUDA, Jumpei
collection PubMed
description Endostatin, a fragment of collagen XVIII, is known as an endogenous angiogenesis inhibitor, and its serum concentration increases in various cardiovascular diseases. T-type Ca(2+) channel, low voltage-activated Ca(2+) channel, is not expressed in adult ventricular myocytes. Re-expression of T-type Ca(2+) channels in cardiac myocytes is thought to be involved in the development of cardiac hypertrophy. We examined the effects of endostatin on T-type Ca(2+) channel current by whole-cell patch clamp technique in freshly isolated adult guinea pig ventricular myocytes, which exceptionally express T-type Ca(2+) channels. Although endostatin 300 ng/ml had no effect on L-type Ca(2+) current, it significantly inhibited T-type Ca(2+) current. These data indicate that endostatin can be an endogenous inhibitor of T-type Ca(2+) channels in the cardiac myocytes.
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spelling pubmed-46382982015-11-10 Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte YASUDA, Jumpei OKADA, Muneyoshi YAMAWAKI, Hideyuki J Vet Med Sci Pharmacology Endostatin, a fragment of collagen XVIII, is known as an endogenous angiogenesis inhibitor, and its serum concentration increases in various cardiovascular diseases. T-type Ca(2+) channel, low voltage-activated Ca(2+) channel, is not expressed in adult ventricular myocytes. Re-expression of T-type Ca(2+) channels in cardiac myocytes is thought to be involved in the development of cardiac hypertrophy. We examined the effects of endostatin on T-type Ca(2+) channel current by whole-cell patch clamp technique in freshly isolated adult guinea pig ventricular myocytes, which exceptionally express T-type Ca(2+) channels. Although endostatin 300 ng/ml had no effect on L-type Ca(2+) current, it significantly inhibited T-type Ca(2+) current. These data indicate that endostatin can be an endogenous inhibitor of T-type Ca(2+) channels in the cardiac myocytes. The Japanese Society of Veterinary Science 2015-05-04 2015-10 /pmc/articles/PMC4638298/ /pubmed/25947888 http://dx.doi.org/10.1292/jvms.14-0551 Text en ©2015 The Japanese Society of Veterinary Science http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License.
spellingShingle Pharmacology
YASUDA, Jumpei
OKADA, Muneyoshi
YAMAWAKI, Hideyuki
Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte
title Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte
title_full Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte
title_fullStr Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte
title_full_unstemmed Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte
title_short Endostatin inhibits T-type Ca(2+) channel current in guinea pig ventricular myocyte
title_sort endostatin inhibits t-type ca(2+) channel current in guinea pig ventricular myocyte
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638298/
https://www.ncbi.nlm.nih.gov/pubmed/25947888
http://dx.doi.org/10.1292/jvms.14-0551
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