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Notch signaling may negatively regulate neonatal rat cardiac fibroblast-myofibroblast transformation

Y-H Fan1, H Dong, Q Pan

  • 1Department of Cardiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, PR China.

Physiological Research
|August 5, 2011
PubMed

Insights

Inhibition of Notch signaling may promote cardiac fibroblast-myofibroblast transformation (CMT), a key process in myocardial fibrosis. Down-regulation of Notch receptors 1, 3, and 4 by TGF-beta1 appears to facilitate this transformation.

Area of Science:

  • Cardiovascular Biology
  • Cell Signaling
  • Fibrosis Research

Background:

  • Cardiac fibroblast-myofibroblast transformation (CMT) is central to myocardial fibrosis.
  • Notch signaling influences myofibroblast differentiation in various cell types.
  • The role of Notch signaling in CMT remains largely unexplored.

Purpose of the Study:

  • To investigate the expression of Notch receptors in cardiac fibroblasts (CFs).
  • To determine the effect of Notch signaling inhibition and TGF-beta1 on CMT.
  • To elucidate the involvement of Notch signaling in the CMT process.

Main Methods:

  • Examined Notch receptor expression in CFs.
  • Utilized a Notch signaling inhibitor (DAPT) and TGF-beta1.
  • Assessed CMT by measuring alpha-smooth muscle actin (α-SMA) expression and collagen synthesis.

Main Results:

  • Notch receptors 1, 2, 3, and 4 are expressed in CFs.
  • DAPT treatment promoted CMT in a time-dependent manner.
  • TGF-beta1-induced CMT involved down-regulation of Notch receptors 1, 3, and 4, correlating with increased α-SMA and collagen synthesis.

Conclusions:

  • Inhibiting Notch signaling may promote CMT.
  • Down-regulation of specific Notch receptors by TGF-beta1 could facilitate CMT.
  • Notch signaling inhibition represents a potential novel mechanism in myocardial fibrosis development.

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