Fülöp, László and Rajki, Anikó and Katona, Dávid and Szanda, Gergő and Spät, András (2013) Extramitochondrial OPA1 and adrenocortical function. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 381 (1-2). pp. 70-79. ISSN 0303-7207
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Abstract
We have previously described that silencing of the mitochondrial protein OPA1 enhances mitochondrial Ca2+ 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), Ca2+ signaling and aldosterone secretion. In conclusion, OPA1 could be detected in the post-mitochondrial fractions, nevertheless, OPA1 did not interfere with the cAMP - PKA - HSL mediated activation of aldosterone secretion.
Item Type: | Article |
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Uncontrolled Keywords: | Optic Atrophy 1Aldosterone Perilipin Hormone sensitive lipase Mitochondria H295R cell |
Subjects: | R Medicine / orvostudomány > R1 Medicine (General) / orvostudomány általában |
SWORD Depositor: | MTMT SWORD |
Depositing User: | MTMT SWORD |
Date Deposited: | 28 Jan 2014 14:25 |
Last Modified: | 28 Jan 2014 14:25 |
URI: | http://real.mtak.hu/id/eprint/9315 |
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