BCL2L1 (BCL-X) promotes survival of adult and developing retinal ganglion cells

Jeffrey M. Harder, Qian Ding, Kimberly A. Fernandes, Jonathan D. Cherry, Lin Gan, Richard T. Libby

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

The Bcl-2 family is responsible for regulating cell death pathways in neurons during development, after injury and in disease. The activation of the pro-death family member BAX is often the final step before cell death in neurons. Pro-survival family members such as BCL-X (BCL2L1) act to inhibit BAX activation. Overexpression studies have suggested that BCL-X could play an important physiological role in mediating neuronal viability. Loss-of-function studies performed in vivo have implicated BCL-X as a mediator of neuronal survival during the early stages of neurodevelopment. To assess whether BCL-X is needed to promote the survival of neurons in the central nervous system throughout life, Bcl-x was conditionally removed from the optic cup or throughout the adult mouse. During development BCL-X was required for the survival of differentiating retinal ganglion cells (RGCs) leading up to their normal window of developmental death. Despite its expression in adult RGCs, BCL-X was not required for maintaining RGC viability in adult retinas. However, the loss of BCL-X in adult RGCs did significantly increase the rate of death of RGCs after axonal injury. Thus, in developing and injured RGCs there appears to be an active cell survival program preventing neuronal death.

Original languageEnglish (US)
Pages (from-to)53-59
Number of pages7
JournalMolecular and Cellular Neuroscience
Volume51
Issue number1-2
DOIs
StatePublished - Aug 1 2012
Externally publishedYes

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Keywords

  • Axonal injury
  • Axotomy
  • Bcl-
  • Bcl2
  • Developmental cell death
  • Glaucoma
  • Neurodegeneration

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience
  • Cell Biology

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