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April 16, 2018Journal of Cell ScienceOpen Access

Treatment with 8-Br-cAMP, PDE2 inhibition, and sAC overexpression intensified mitochondrial Ca2+ uptake, an effect reduced by Epac1 blockade, and sAC overexpression potentiated aldosterone production.

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Population

H295R adrenocortical cells and HeLa cells

Comparison

Modulation of mitochondrial cAMP via reduction… vs Control cells

Design

Preclinical

Authors

GSGergő SzandaÉWÉva WisniewskiARAnikó Rajki

Discussion

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Overview

Mitochondrial cAMP-Epac1 signaling may initiate steroidogenesis; hypothesis-generating for adrenal disorders pending human validation.

Structured PICO

P
Population
H295R adrenocortical cells and HeLa cells
I
Intervention
Modulation of mitochondrial cAMP (mt-cAMP) via reduction of formation, treatment with 8-Br-cAMP, inhibition of phosphodiesterase 2, or overexpression of soluble adenylyl cyclase (sAC)
C
Comparator
Control cells
O
Outcome
Mitochondrial Ca2+ accumulation and aldosterone productionsurrogate

Mitochondrial cAMP exerts a positive feedback on mitochondrial Ca2+ uptake via Epac1 recruitment, which may play a role in the rapid initiation of steroidogenesis.

Cite This Study

Szanda et al. (2018) studied this question.

synapsesocial.com/papers/6a8bd08a0c58d86fb4cadd7ehttps://doi.org/10.1242/jcs.215178
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