Key result
Orosomucoid (ORM) reduced hypoxia-induced apoptosis in cardiomyocytes through caspase-3 inhibition, suggesting a cardioprotective role for ORM in epicardial adipose tissue secretomes.
Why the study?
Does orosomucoid (ORM) from epicardial adipose tissue secretomes reduce hypoxia-induced apoptosis in cardiomyocytes?
Does orosomucoid (ORM) from epicardial adipose tissue secretomes reduce hypoxia-induced apoptosis in cardiomyocytes?
Orosomucoid released from epicardial adipose tissue demonstrates a cardioprotective role by reducing hypoxia-induced apoptosis in cardiomyocytes.
ORM effects on cardiomyocytes are hypothesis-generating; leaves open any clinical role for EAT-derived ORM.
Epicardial adipose tissue releases orosomucoid (ORM), an acute phase protein with multiple modulatory and protective properties. We aimed to identify the effect of EAT-supernatants according to their ORM levels on H9C2 cells. H9C2 were cultured with EAT-secretomes or ORM protein itself on a Real-Time Cell Analyser. Secretome proteins identification was performed by LC-mass spectrometry according to their ORM levels. Two of them were validated by ELISA in EAT-supernatants from 42 patients. ORM effect on H9C2 and neonatal rat cardiomyocytes apoptosis under hypoxia with or without fatty acid treatment was determined by Annexin-V flow cytometry measurement. Caspase-3 expression levels were determined by western blot in H9C2. Our results showed a differential effect of EAT-secretomes according their ORM levels. Although additional secreted proteins can contribute to their beneficial effects, ORM reduced hypoxia-induced apoptosis through caspase-3 inhibition. Our data showed the cardioprotective role of ORM and suggest that its quantification on EAT secretomes might help us to find new secreted factors with a cardioprotective role.
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Lage et al. (2015) studied Cardiovascular disease (n=42). Orosomucoid (ORM) and EAT-secretomes vs. Control (hypoxia without ORM / low ORM secretomes) was evaluated on Hypoxia-induced apoptosis. Orosomucoid (ORM) reduced hypoxia-induced apoptosis in cardiomyocytes through caspase-3 inhibition, suggesting a cardioprotective role for ORM in epicardial adipose tissue secretomes.
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