| First Author | Tano JY | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 410 |
| Issue | 3 | Pages | 643-7 |
| PubMed ID | 21684255 | Mgi Jnum | J:174948 |
| Mgi Id | MGI:5141551 | Doi | 10.1016/j.bbrc.2011.06.045 |
| Citation | Tano JY, et al. (2011) Impairment of survival signaling and efferocytosis in TRPC3-deficient macrophages. Biochem Biophys Res Commun 410(3):643-7 |
| abstractText | We 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 TNFalpha induced time-dependent phosphorylation of IkappaBalpha, 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. |
