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Angiopoietin-1 promotes cardiac and skeletal myocyte survival through integrins

Susan M Dallabrida1, Nesreen Ismail, Julianne R Oberle

  • 1Division of Vascular Biology, Children's Hospital, Boston, MA 02115, USA.

Circulation Research
|February 5, 2005
PubMed

Insights

Angiopoietin-1 directly protects cardiac myocytes from injury, independent of its known vascular effects. This novel mechanism involves integrin-mediated signaling, offering potential for treating heart failure by preserving myocyte viability.

Area of Science:

  • Cardiovascular Biology
  • Cellular and Molecular Medicine
  • Integrin Signaling

Background:

  • Cardiac myocyte loss leads to heart failure through compensatory remodeling.
  • Angiopoietin-1 (Ang-1) is known to limit ischemia-induced cardiac injury, primarily attributed to its vascular effects via the Tie2 receptor.
  • The direct role of Ang-1 on cardiac myocytes for cardioprotection remains underexplored.

Purpose of the Study:

  • To investigate the direct, non-Tie2 interactions of Ang-1 on cardiac myocytes.
  • To determine if Ang-1 confers a survival advantage to cardiac myocytes.
  • To elucidate the signaling pathways involved in Ang-1-mediated myocyte survival.

Main Methods:

  • Studied myocyte adhesion to Ang-1 and Ang-2 in mouse C2C12 skeletal myocytes, human skeletal myocytes (HSMs), and rat neonatal cardiac myocytes (NCMs).
  • Investigated the role of divalent cations, EDTA/EGTA, RGD peptides, and integrin antibodies in Ang-1-myocyte interactions.
  • Assessed myocyte survival using MTT and trypan blue assays under serum-starved and taxol-induced apoptosis conditions.
  • Analyzed the phosphorylation of Akt and MAPK signaling pathways in response to Ang-1 using Western blotting.

Main Results:

  • Cardiac myocytes lacking Tie2 adhered to Ang-1 and Ang-2 in a dose-dependent manner, mediated by divalent cations and blocked by RGD peptides and integrin antibodies.
  • Ang-1 significantly enhanced myocyte survival, exceeding the effects of common cell matrices.
  • Ang-1 promoted survival in serum-starved and prevented apoptosis in NCMs and C2C12 cells.
  • Ang-1 activated Akt and MAPK phosphorylation in myocytes, a response inhibited by EDTA, RGD peptides, and integrin antibodies.

Conclusions:

  • Angiopoietin-1 directly interacts with cardiac myocytes via integrin-dependent mechanisms, independent of Tie2.
  • This direct interaction confers a significant survival advantage to cardiac myocytes.
  • The findings suggest a novel role for Ang-1 in supporting myocyte viability, contributing to its cardioprotective effects beyond vascular actions and offering therapeutic potential in cardiac remodeling.

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