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Multiple death pathways in retina-derived 661W cells following growth factor deprivation: crosstalk between caspases

V Gómez-Vicente1, M Donovan, T G Cotter

  • 1Cell Development and Disease Laboratory, Department of Biochemistry, Biosciences Research Institute, University College Cork, Cork, Ireland.

Cell Death and Differentiation
|April 23, 2005
PubMed

Insights

Retinal cone photoreceptors undergo apoptosis when deprived of growth factors, involving caspases and m-calpain. These pathways interact, suggesting a complex cell death mechanism crucial for retinal function.

Area of Science:

  • Cell Biology
  • Neuroscience
  • Ophthalmology

Background:

  • Neuronal survival and apoptosis are critical for retinal development and function.
  • Growth factors regulate cell survival and death pathways in the retina.
  • Understanding cone photoreceptor apoptosis is vital for preserving vision.

Purpose of the Study:

  • To investigate the apoptotic mechanisms in 661W cone photoreceptor cells upon growth factor deprivation.
  • To identify the specific molecular players involved in this cell death process.
  • To explore the interplay between different cell death pathways.

Main Methods:

  • Serum starvation of 661W cells to induce growth factor deprivation.
  • Assay of caspase activation (caspase-9, -3, -12).
  • Assessment of m-calpain activation and its role in apoptosis.
  • Inhibition studies using caspase inhibitors.

Main Results:

  • Growth factor deprivation triggered apoptosis in 661W cone photoreceptors.
  • Caspase-9, -3, and -12 were activated during apoptosis.
  • Caspase inhibition only delayed, but did not prevent, cell death.
  • m-Calpain activation occurred in parallel with caspases.
  • Crosstalk between caspase and calpain pathways was observed.

Conclusions:

  • Cone photoreceptors possess multiple apoptotic execution pathways, including both caspase-dependent and m-calpain-dependent routes.
  • The interaction between caspase and calpain pathways may amplify the apoptotic cascade.
  • These findings provide insights into the complex regulation of cell death in retinal neurons.

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