Distribution patterns of the Na+-Ca2+ exchanger and caveolin-3 in developing rabbit cardiomyocytes.

In adult cardiac cells the established mechanism of excitation-contraction coupling is by calcium-induced calcium release (CICR) mediated by L-type Ca(2+) channels. However, in neonate cardiomyocytes, a CICR modality involving reverse mode Na(+)-Ca(2+) exchanger (NCX) activity predominates. This has been hypothesized to be due, in part, to the high expression levels of NCX in the neonate heart which drop several fold during ontogeny.

Granzyme B induces smooth muscle cell apoptosis in the absence of perforin: involvement of extracellular matrix degradation.

Objective: T cell-induced cytotoxicity, of which granzyme B is a key mediator, is believed to contribute to the pathogenesis of inflammatory vascular diseases. In this report, we investigate the mechanism of granzyme B-induced smooth muscle cell (SMC) death.

Methods And Results: The addition of purified granzyme B alone to cultured SMCs caused a significant reduction in cell viability.

Granzyme B in atherosclerosis and transplant vascular disease: association with cell death and atherosclerotic disease severity.

Apoptosis of intimal cells is an important contributor to the pathogenesis of atherosclerosis and transplant vascular disease (TVD). Since the activated immune response may be a key regulator of apoptosis in these lesions, we used immunohistochemistry to characterize the presence and localization of granzyme B, a major mediator of the cytotoxic immune response, in advanced atherosclerosis and TVD. Formalin-fixed, paraffin-embedded transverse sections from human left anterior descending coronary arteries were cut serially and stained with antibodies specific for granzyme B, smooth muscle alpha-actin, CD68, and CD3.