Sox6 suppression induces RA-dependent apoptosis mediated by BMP-4 expression during neuronal differentiation in P19 cellsReportar como inadecuado




Sox6 suppression induces RA-dependent apoptosis mediated by BMP-4 expression during neuronal differentiation in P19 cells - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Molecular and Cellular Biochemistry

, Volume 412, Issue 1–2, pp 49–57

First Online: 20 November 2015Received: 03 September 2015Accepted: 14 November 2015DOI: 10.1007-s11010-015-2607-8

Cite this article as: Hamada-Kanazawa, M., Ogawa, D., Takano, M. et al. Mol Cell Biochem 2016 412: 49. doi:10.1007-s11010-015-2607-8

Abstract

Sox6 is a transcription factor that induces neuronal differentiation in P19 cells; its suppression not only inhibits neuronal differentiation but also induces retinoic acid RA-dependent apoptosis of P19 cells. In the present study, we found that Sox6 suppression-induced apoptosis was mediated by activation of caspase 9 and 3. Moreover, we noted a weak leakage of cytochrome c into the cytoplasm from the mitochondria, indicating that apoptosis occurs through a mitochondrial pathway in Sox6-suppressed P19 P19anti-Sox6 cells. Sox6 suppression in the presence of RA also induced the expression and secretion of bone morphogenetic protein 4 BMP-4. Addition of an anti-BMP-4 antibody for neutralization increased cell viability and led to RA-dependent death of P19anti-Sox6 cells. Our results indicate that Sox6 suppression induces RA-dependent cell death of P19 cells, mediated by BMP-4 expression and secretion. Normally, high Sox6 expression leads to RA-mediated neuronal differentiation in P19 cells; however, Sox6 deficiency induces production and secretion of BMP-4, which mediates selective cell death. Our findings suggest that Sox6 contributes to cell survival by suppressing BMP-4 transcription during neuronal differentiation.

KeywordsSox6 P19 BMP-4 Retinoic acid Apoptosis BMPRIB  Download fulltext PDF



Autor: Michiko Hamada-Kanazawa - Daisuke Ogawa - Masaoki Takano - Masaharu Miyake

Fuente: https://link.springer.com/







Documentos relacionados