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pubmed-article:21684255pubmed:abstractTextWe have recently shown that in macrophages proper operation of the survival pathways phosphatidylinositol-3-kinase (PI3K)/AKT and nuclear factor kappa B (NFkB) has an obligatory requirement for constitutive, non-regulated Ca(2+) influx. In the present work we examined if Transient Receptor Potential Canonical 3 (TRPC3), a member of the TRPC family of Ca(2+)-permeable cation channels, contributes to the constitutive Ca(2+) influx that supports macrophage survival. We used bone marrow-derived macrophages obtained from TRPC3(-/-) mice to determine the activation status of survival signaling pathways, apoptosis and their efferocytic properties. Treatment of TRPC3(+/+) macrophages with the pro-apoptotic cytokine TNF? induced time-dependent phosphorylation of I?B?, AKT and BAD, and this was drastically reduced in TRPC3(-/-) macrophages. Compared to TRPC3(+/+) cells TRPC3(-/-) macrophages exhibited reduced constitutive cation influx, increased apoptosis and impaired efferocytosis. The present findings suggest that macrophage TRPC3, presumably through its constitutive function, contributes to survival signaling and efferocytic properties.lld:pubmed
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pubmed-article:21684255pubmed:copyrightInfoCopyright © 2011 Elsevier Inc. All rights reserved.lld:pubmed
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pubmed-article:21684255pubmed:year2011lld:pubmed
pubmed-article:21684255pubmed:articleTitleImpairment of survival signaling and efferocytosis in TRPC3-deficient macrophages.lld:pubmed
pubmed-article:21684255pubmed:affiliationDepartment of Physiology and Pharmacology and the Center for Diabetes and Endocrine Research, University of Toledo College of Medicine, Health Science Campus, 3000 Arlington Av, Toledo, OH 43614, USA.lld:pubmed
pubmed-article:21684255pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21684255pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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