Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response

In this study, the ER stressor thapsigargin (TG), which depletes ER calcium, induced death of cultured neonatal rat ventricular myocytes (NRVMs) in high media volume but fostered protection in low media volume. In contrast, another ER stressor, tunicamycin (TM), a protein glycosylation inhibitor, induced NRVM death in all media volumes, suggesting that protective proteins were secreted in response to TG but not TM.
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Source Type: research