| First Author | Fülöp L | Year | 2013 |
| Journal | Mol Cell Endocrinol | Volume | 381 |
| Issue | 1-2 | Pages | 70-9 |
| PubMed ID | 23906536 | Mgi Jnum | J:211383 |
| Mgi Id | MGI:5574569 | Doi | 10.1016/j.mce.2013.07.021 |
| Citation | Fulop L, et al. (2013) Extramitochondrial OPA1 and adrenocortical function. Mol Cell Endocrinol 381(1-2):70-9 |
| abstractText | We have previously described that silencing of the mitochondrial protein OPA1 enhances mitochondrial Ca(2+) signaling and aldosterone production in H295R adrenocortical cells. Since extramitochondrial OPA1 (emOPA1) was reported to facilitate cAMP-induced lipolysis, we hypothesized that emOPA1, via the enhanced hydrolysis of cholesterol esters, augments aldosterone production in H295R cells. A few OPA1 immunopositive spots were detected in approximately 40% of the cells. In cell fractionation studies OPA1/COX IV (mitochondrial marker) ratio in the post-mitochondrial fractions was an order of magnitude higher than that in the mitochondrial fraction. The ratio of long to short OPA1 isoforms was lower in post-mitochondrial than in mitochondrial fractions. Knockdown of OPA1 failed to reduce db-cAMP-induced phosphorylation of hormone-sensitive lipase (HSL), Ca(2+) signaling and aldosterone secretion. In conclusion, OPA1 could be detected in the post-mitochondrial fractions, nevertheless, OPA1 did not interfere with the cAMP |
