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Fas signaling and cardiac hypertrophy

Stimulation of Fas, the founding member of a family of dedicated cell surface "death receptors," activates one of the best studied routes to apoptosis. Evidence for Fas activation in cardiac myocytes subjected to pressure overload is therefore not surprising, but Badorff et al. have found that this protein subserves an unexpected role in these cells. As has been noted before, cardiac overexpression of the Fas ligand (FasL) does not kill myocytes but rather leads to a metabolic and morphological transition reminiscent of the adaptive hypertrophy. Working with cultured neonatal myocytes, Badorff and colleagues show that FasL treatment activates Akt, a protein kinase that has been extensively implicated in the hypertrophic response in the heart and elsewhere. Hypothesizing that Fas participates in the adaptive hypertrophy that allows the heart to compensate for pressure overload, the authors tested the effects of aortic banding in lpr mice, which are deficient in Fas. As predicted, these mice failed to compensate and often died within a week of the operation. Interestingly, mice lacking FasL showed no such defect, indicating that, although FasL can induce this response, Fas can be activated by other means during adaptive hypertrophy.


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Contact: John Ashkenas
scied@the-jci.org
416-946-7593
Journal of Clinical Investigation
30-Jan-2002


Page: 1

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