Extramitochondrial OPA1 and adrenocortical function

L. Fülöp, Anikó Rajki, Dávid Katona, G. Szanda, A. Spät

Research output: Contribution to journalArticle

6 Citations (Scopus)

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 ~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.

Original languageEnglish
Pages (from-to)70-79
Number of pages10
JournalMolecular and Cellular Endocrinology
Volume381
Issue number1-2
DOIs
Publication statusPublished - Dec 5 2013

Fingerprint

Aldosterone
Sterol Esterase
Cell Fractionation
Phosphorylation
Cholesterol Esters
Lipolysis
Mitochondrial Proteins
Fractionation
Hydrolysis
Protein Isoforms
Chemical activation

Keywords

  • AKAP
  • Aldosterone
  • H295R cell
  • Hormone sensitive lipase
  • Mitochondria
  • Optic Atrophy 1

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Biochemistry

Cite this

Extramitochondrial OPA1 and adrenocortical function. / Fülöp, L.; Rajki, Anikó; Katona, Dávid; Szanda, G.; Spät, A.

In: Molecular and Cellular Endocrinology, Vol. 381, No. 1-2, 05.12.2013, p. 70-79.

Research output: Contribution to journalArticle

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