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Phosphorylation of Bcl-xL after spinal cord injury

Diana M Cittelly1, Olivera Nesic-Taylor, J Regino Perez-Polo

  • 1Neuroscience and Cell Biology Department, University of Texas Medical Branch, Galveston, Texas 77555-1072, USA.

Journal of Neuroscience Research
|June 7, 2007
PubMed

Insights

Spinal cord injury (SCI) decreases antiapoptotic Bcl-x(L) protein, leading to cell death. Phosphorylation of Bcl-x(L) in the cytosol correlates with neuronal apoptosis and may reduce its protective function in SCI.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Spinal cord injury (SCI) causes functional impairment partly due to secondary apoptosis.
  • Decreased levels of the antiapoptotic protein Bcl-x(L) are implicated in SCI-induced cell death.
  • The subcellular localization and posttranslational modification of Bcl-x(L) following SCI are not fully understood.

Purpose of the Study:

  • To investigate the role of Bcl-x(L) subcellular rerouting and posttranslational phosphorylation in SCI-induced decreases.
  • To determine the cellular localization and compartmentalization of Bcl-x(L) and its phosphorylated form (P-ser(62)-Bcl-x(L)) after SCI.
  • To explore the correlation between Bcl-x(L) phosphorylation and neuronal apoptosis in an in vitro model.

Main Methods:

  • Immunohistochemistry to detect Bcl-x(L) and P-ser(62)-Bcl-x(L) in rat spinal cord tissue.
  • Western blot analysis to quantify Bcl-x(L) and P-ser(62)-Bcl-x(L) levels in different subcellular fractions (mitochondria, ER, nuclei, cytosol).
  • In vitro neuronal culture model to assess the relationship between cytosolic P-ser(62)-Bcl-x(L) and apoptosis.

Main Results:

  • Bcl-x(L) was found in neurons and oligodendrocytes, while P-ser(62)-Bcl-x(L) was localized to neuronal organelles. Following SCI, Bcl-x(L) levels decreased in all cellular fractions within 24 hours.
  • SCI induced the appearance of P-ser(62)-Bcl-x(L) in the cytosol, correlating with increased neuronal apoptosis, suggesting a proapoptotic role for phosphorylation in neurons.
  • Activated microglia/macrophages expressed Bcl-x(L) and P-ser(62)-Bcl-x(L) post-SCI, indicating a potential role in modulating inflammatory responses.

Conclusions:

  • SCI alters Bcl-x(L) subcellular distribution and promotes its cytosolic phosphorylation in neurons, contributing to neuronal apoptosis.
  • Bcl-x(L) phosphorylation may have dual roles: promoting neuronal death while potentially inducing apoptosis in activated microglia/macrophages to limit inflammation.
  • Targeting Bcl-x(L) phosphorylation could offer a therapeutic strategy for managing SCI-induced neuronal loss and neuroinflammation.

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