An analysis of the effects of stretch on IGF-I secretion from rat ventricular fibroblasts
Autor: | Betty S. Hu, Nakon Aroonsakool, Wayne R. Giles, Lee K. Landeen |
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Rok vydání: | 2007 |
Předmět: |
Male
medicine.medical_specialty Thapsigargin Physiology chemistry.chemical_element Calcium Biology Mechanotransduction Cellular Rats sprague dawley Rats Sprague-Dawley chemistry.chemical_compound Physiology (medical) Internal medicine medicine Animals Ventricular Function Secretion Insulin-Like Growth Factor I Fibroblast Cells Cultured Regulation of gene expression Fibroblasts Mechanical force Elasticity Rats Endocrinology medicine.anatomical_structure chemistry Circulatory system Stress Mechanical Cardiology and Cardiovascular Medicine |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 293:H677-H683 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.01413.2006 |
Popis: | Mechanical force can induce a number of fundamental short- and long-term responses in myocardium. These include alterations in ECM, activation of cell-signaling pathways, altered gene regulation, changes in cell proliferation and growth, and secretion of a number of peptides and growth factors. It is now known that a number of these autocrine/paracrine factors are secreted from both cardiomyocytes and ventricular cardiac fibroblasts (CFb) in response to stretch. One such substance is IGF-I. IGF-I is an important autocrine/paracrine factor that can regulate physiological or pathophysiological responses, such as hypertrophy. In this study, we addressed the possible effects of mechanical perturbation, biaxial strain, on IGF-I secretion from adult rat CFb. CFb were subjected to either static stretch (3–10%) or cyclic stretch (10%; 0.1–1 Hz) over a 24-h period. IGF-1 secretion from CFb in response to selected stretch paradigms was examined using ELISA to measure IGF-I concentrations in conditioned media. Static stretch did not result in any measurable modulation of IGF-I secretion from CFb. However, cyclic stretch significantly increased IGF-I secretion from CFb in a frequency- and time-dependent manner compared with nonstretched controls. This stretch-induced increase in secretion was relatively insensitive to changes in extracellular [Ca2+] or to block of L-type Ca2+ channels. In contrast, thapsigargin, an inhibitor of sarco(endo)plasmic reticulum Ca2+ ATPase, remarkably decreased stretch-induced IGF-I secretion from CFb. We further show that IGF-I can upregulate mRNA expression of atrial natriuretic peptide in myocytes. In summary, cyclic stretch can significantly increase IGF-I secretion from CFb, and this effect is dependent on a thapsigargin-sensitive pool of intracellular [Ca2+]. |
Databáze: | OpenAIRE |
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