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Static mechanical stretch increases IGF‐1 secretion by cardiac fibroblasts
Author(s) -
Hu Betty S,
Landeen Lee K,
Aroonsakool Nakon,
Giles Wayne R,
Omens Jeff H
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1414-a
Insulin‐like growth factor 1 (IGF‐1), is a 70‐amino acid peptide, can play significant roles in cell proliferation and differentiation. In the neonatal heart, IGF‐1 is secreted by cardiac fibroblasts (CFb) and acts by paracrine/autocrine mechanisms. IGF‐1 can stimulate myocyte growth and CFb collagen synthesis. IGF‐1 can also attenuate myocyte apoptosis and improve cardiac function following myocardial infarction, through its ability to regulate tissue remodeling. In models of adult rat ventricular hypertrophy, an increase in IGF‐1 has been detected. We hypothesize that mechanical stimulation of rat CFb can modulate IGF‐1 secretion. A cell stretching device imposed a constant ~4% equibiaxial (~10% uniaxial) strain on either adult or neonatal rat CFb. IGF‐1 protein levels in serum free conditioned media were determined by enzyme immunoassay and normalized to numbers of CFb. Preliminary results show that adult CFb respond to strain by markedly increasing IGF‐1 secretion, by a mean of 73% pmol /10 6 CFb vs. unstretched. Between 12h and 24h, secretion increased by 35% pmol /10 6 CFb in stretched CFb. In neonatal CFb, an identical strain also increased IGF‐1 secretion.These results demonstrate that CFb release IGF‐1 in a time‐dependent manner when subjected to stretch. IGF‐1 secreted by CFb may function as a modulator of remodeling in both myocytes and fibroblasts.