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Canonical transient receptor potential 3 channels regulate mitochondrial calcium uptake.


ABSTRACT: Mitochondrial Ca(2+) homeostasis is fundamental to regulation of mitochondrial membrane potential, ATP production, and cellular Ca(2+) homeostasis. It has been known for decades that isolated mitochondria can take up Ca(2+) from the extramitochondrial solution, but the molecular identity of the Ca(2+) channels involved in this action is largely unknown. Here, we show that a fraction of canonical transient receptor potential 3 (TRPC3) channels is localized to mitochondria, a significant fraction of mitochondrial Ca(2+) uptake that relies on extramitochondrial Ca(2+) concentration is TRPC3-dependent, and the up- and down-regulation of TRPC3 expression in the cell influences the mitochondrial membrane potential. Our findings suggest that TRPC3 channels contribute to mitochondrial Ca(2+) uptake. We anticipate our observations may provide insights into the mechanisms of mitochondrial Ca(2+) uptake and advance understanding of the physiological role of TRPC3.

SUBMITTER: Feng S 

PROVIDER: S-EPMC3704010 | biostudies-literature | 2013 Jul

REPOSITORIES: biostudies-literature

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Canonical transient receptor potential 3 channels regulate mitochondrial calcium uptake.

Feng Shengjie S   Li Hongyu H   Tai Yilin Y   Huang Junbo J   Su Yujuan Y   Abramowitz Joel J   Zhu Michael X MX   Birnbaumer Lutz L   Wang Yizheng Y  

Proceedings of the National Academy of Sciences of the United States of America 20130617 27


Mitochondrial Ca(2+) homeostasis is fundamental to regulation of mitochondrial membrane potential, ATP production, and cellular Ca(2+) homeostasis. It has been known for decades that isolated mitochondria can take up Ca(2+) from the extramitochondrial solution, but the molecular identity of the Ca(2+) channels involved in this action is largely unknown. Here, we show that a fraction of canonical transient receptor potential 3 (TRPC3) channels is localized to mitochondria, a significant fraction  ...[more]

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