Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.

The question of whether the distinct isoforms of the family of enzymes phosphoinositide 3-kinases (PI3Ks) play redundant roles within a cell or whether they control distinct cellular processes or distinct steps within the same cellular process has gained considerable importance in the recent years d...

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Autores principales:	Gianpaolo Tibolla, Roberto Piñeiro, Daniela Chiozzotto, Ioanna Mavrommati, Ann P Wheeler, Giuseppe Danilo Norata, Alberico Luigi Catapano, Tania Maffucci, Marco Falasca
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a1570001acab419d946f7496865e7b2b
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spelling	oai:doaj.org-article:a1570001acab419d946f7496865e7b2b2021-11-18T08:02:17ZClass II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.1932-620310.1371/journal.pone.0053808https://doaj.org/article/a1570001acab419d946f7496865e7b2b2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23320105/?tool=EBIhttps://doaj.org/toc/1932-6203The question of whether the distinct isoforms of the family of enzymes phosphoinositide 3-kinases (PI3Ks) play redundant roles within a cell or whether they control distinct cellular processes or distinct steps within the same cellular process has gained considerable importance in the recent years due to the development of inhibitors able to selectively target individual isoforms. It is important to understand whether inhibition of one PI3K can result in compensatory effect from other isoform(s) and therefore whether strategies aimed at simultaneously blocking more than one PI3K may be needed. In this study we investigated the relative contribution of distinct PI3K isoforms to endothelial cells (EC) functions specifically regulated by the sphingolipid sphingosine-1-phosphate (S1P) and by high density lipoproteins (HDL), the major carrier of S1P in human plasma. Here we show that a co-ordinated action of different PI3Ks is required to tightly regulate remodelling of EC on Matrigel, a process dependent on cell proliferation, apoptosis and migration. The contribution of each isoform to this process appears to be distinct, with the class II enzyme PI3K-C2β and the class IB isoform p110γ mainly regulating the S1P- and HDL-dependent EC migration and PI3K-C2α primarily controlling EC survival. Data further indicate that PI3K-C2β and p110γ control distinct steps involved in cell migration supporting the hypothesis that different PI3Ks regulate distinct cellular processes.Gianpaolo TibollaRoberto PiñeiroDaniela ChiozzottoIoanna MavrommatiAnn P WheelerGiuseppe Danilo NorataAlberico Luigi CatapanoTania MaffucciMarco FalascaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 1, p e53808 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Gianpaolo Tibolla Roberto Piñeiro Daniela Chiozzotto Ioanna Mavrommati Ann P Wheeler Giuseppe Danilo Norata Alberico Luigi Catapano Tania Maffucci Marco Falasca Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
description	The question of whether the distinct isoforms of the family of enzymes phosphoinositide 3-kinases (PI3Ks) play redundant roles within a cell or whether they control distinct cellular processes or distinct steps within the same cellular process has gained considerable importance in the recent years due to the development of inhibitors able to selectively target individual isoforms. It is important to understand whether inhibition of one PI3K can result in compensatory effect from other isoform(s) and therefore whether strategies aimed at simultaneously blocking more than one PI3K may be needed. In this study we investigated the relative contribution of distinct PI3K isoforms to endothelial cells (EC) functions specifically regulated by the sphingolipid sphingosine-1-phosphate (S1P) and by high density lipoproteins (HDL), the major carrier of S1P in human plasma. Here we show that a co-ordinated action of different PI3Ks is required to tightly regulate remodelling of EC on Matrigel, a process dependent on cell proliferation, apoptosis and migration. The contribution of each isoform to this process appears to be distinct, with the class II enzyme PI3K-C2β and the class IB isoform p110γ mainly regulating the S1P- and HDL-dependent EC migration and PI3K-C2α primarily controlling EC survival. Data further indicate that PI3K-C2β and p110γ control distinct steps involved in cell migration supporting the hypothesis that different PI3Ks regulate distinct cellular processes.
format	article
author	Gianpaolo Tibolla Roberto Piñeiro Daniela Chiozzotto Ioanna Mavrommati Ann P Wheeler Giuseppe Danilo Norata Alberico Luigi Catapano Tania Maffucci Marco Falasca
author_facet	Gianpaolo Tibolla Roberto Piñeiro Daniela Chiozzotto Ioanna Mavrommati Ann P Wheeler Giuseppe Danilo Norata Alberico Luigi Catapano Tania Maffucci Marco Falasca
author_sort	Gianpaolo Tibolla
title	Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
title_short	Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
title_full	Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
title_fullStr	Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
title_full_unstemmed	Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
title_sort	class ii phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/a1570001acab419d946f7496865e7b2b
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Class II phosphoinositide 3-kinases contribute to endothelial cells morphogenesis.

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