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Circulating Growth Differentiation Factor 11/8 Levels Decline With Age.

Tommaso Poggioli1, Ana Vujic1, Peiguo Yang1

  • 1From the Department of Stem Cell and Regenerative Biology, Harvard Stem Cell Institute, Harvard University, Cambridge, MA (T.P., A.V., P.Y., C.M.-T., A.U., F.S.L., J.R.P., M.C., J.G., R.M.T., E.G., A.J.W., Y.W.F., R.T.L.); Brigham Regenerative Medicine Center and Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (T.P., A.V., P.Y., C.M.-T., A.U., F.S.L., J.R.P., R.M.T., E.G., Y.W.F., R.T.L.); Department of Molecular Genetics, College of Medicine, University of Cincinnati, OH (R.G.W., T.B.T.); and Howard Hughes Medical Institute, Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, Boston, MA (M.C., J.G., A.J.W.).

Circulation Research
|October 23, 2015
PubMed
Summary

Circulating Growth Differentiation Factor 11 (GDF11) levels decline with age across species. Exogenous GDF11 reduces cardiac mass by activating SMAD signaling, offering insights into age-related heart conditions.

Keywords:
Gdf11 protein, mouseMstn protein, mouseagingintercellular signaling peptides and proteinstransforming growth factor-β

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Area of Science:

  • Aging research
  • Cardiovascular biology
  • Molecular signaling

Background:

  • Growth Differentiation Factor 11 (GDF11) and GDF8 are highly homologous TGF-β superfamily members.
  • Previous studies showed conflicting results regarding age-related changes in circulating GDF11 levels.

Purpose of the Study:

  • Clarify the age-dependent changes in circulating GDF11/8 levels.
  • Investigate the impact of GDF11 administration on the murine heart.

Main Methods:

  • Validated age-dependent GDF11/8 decline in mice, rats, horses, and sheep.
  • Utilized Western analysis to identify antibody cross-reactivity issues.
  • Administered GDF11 to mice and assessed SMAD signaling and cardiac mass.

Main Results:

  • Confirmed age-dependent decline of GDF11/8 in multiple species.
  • Identified immunoglobulin cross-reactivity as a cause for reported age-related increases.
  • GDF11 administration activated SMAD2/3 signaling and reduced cardiac mass in a dose-dependent manner.

Conclusions:

  • Serum GDF11/8 levels decrease with age across mammals.
  • Exogenous GDF11 activates SMAD signaling and reduces cardiomyocyte size.
  • Understanding GDF11 decline may reveal mechanisms of age-related cardiac pathologies.