Ceramide Generated by Sphingomyelin Hydrolysis and the Salvage Pathway Is Involved in Hypoxia/Reoxygenation-induced Bax Redistribution to Mitochondria in NT-2 Cells*

By Junfei Jin, Q. Hou, T. Mullen, Y. Zeidan, J. Bielawski, J. Kraveka, A. Bielawska, LM Obeid, Yusuf A. Hannun, Y. Hsu. 2008

82 citations recorded by the source corpus.

Ceramide functions as an important second messenger in apoptosis signaling pathways. In this report, we show that treatment of NT-2 neuronal precursor cells with hypoxia/reoxygenation (H/R) resulted in ceramide up-regulation. This elevation in ceramide was primarily due to the actions of acid sphingomyelinase and ceramide synthase LASS 5, demonstrating the action of the salvage pathway. Hypoxia/reoxygenation treatment led to Bax translocation from the cytoplasm to mitochondria and cytochrome c release from mitochondria. Down-regulation of either acid sphingomyelinase or LASS 5-attenuated ceramide accumulation and H/R-induced Bax translocation to mitochondria. Overall, we have demonstrated that ceramide up-regulation following H/R is pertinent to Bax activation to promote cell death.

Subfields: Molecular Biology

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Citations in the corpus

Mammalian Ceramide Synthases (2010, background): “On knocking down acid-sphingomyelinase and CerS5 activities in NT-2 cells, Bax localization to mitochondria was attenuated (73).”