Key result
Short-term cyclic stretch of neonatal rat ventricular cardiomyocytes and cardiofibroblasts induced growth responses indicative of hypertrophy through direct, autocrine, and paracrine effects.
Cyclic stretch induces hypertrophic growth responses in neonatal rat ventricular cells through direct mechanical effects as well as autocrine and paracrine signaling.
No immediate clinical implications; leaves open translation of neonatal rat stretch responses to human hypertrophy.
Several studies have demonstrated that static stretch of cardiomyocytes induces cardiomyocyte hypertrophy. We investigated the effects of cyclic stretch, a more physiological stimulus, on protein synthesis and DNA synthesis of rat ventricular cardiomyocytes and cardiofibroblasts. Further-more, we investigated whether these effects are caused by autocrine mechanisms. In addition, we studied the paracrine influences of stretched cardiofibroblasts on cardiomyocyte growth. Short-term cyclic stretch (0-24 h) of cardiomyocytes induced a growth response indicative of cardiomyocyte hypertrophy, given the fact that increased rates of protein synthesis and DNA synthesis were accompanied by an elevated release of atrial natriuretic peptide into the culture medium. In cardiofibroblasts, short-term cyclic stretch also induced a growth response as indicated by an increased rate of protein synthesis and DNA synthesis. Furthermore, incubation of stationary cardiofibroblasts with conditioned medium derived from stretched cardiofibroblasts revealed an autocrine effect of stretch as illustrated by an increased rate of protein synthesis in stationary cardiofibroblasts. In analogy, there was an autocrine effect of stretch on stationary cardiomyocytes incubated with conditioned medium derived from stretched cardiomyocytes. Moreover, we observed a paracrine effect of the conditioned medium derived from stretched cardiofibroblasts on stationary cardiomyocytes. Thus, short-term cyclic stretch of cardiomyocytes and cardiofibroblasts induces growth responses that are the result of direct, autocrine, and paracrine effects. These autocrine/paracrine effects of stretch are most probably due to release of factors from stretched cells.
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Ruwhof et al. (2001) studied Cardiomyocyte hypertrophy. Short-term cyclic stretch vs. Stationary cells was evaluated on Protein synthesis and DNA synthesis. Short-term cyclic stretch of neonatal rat ventricular cardiomyocytes and cardiofibroblasts induced growth responses indicative of hypertrophy through direct, autocrine, and paracrine effects.
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