Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 110, Issue 27, Pages 11011-11016Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1309531110
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Funding
- National Neural Science Foundation of China (NNSF) [81130081]
- 973 program [2011CBA00400]
- National Institutes of Health (NIH) [Z01-ES-101684, R01 GM081658]
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Mitochondrial Ca2+ homeostasis is fundamental to regulation of mitochondrial membrane potential, ATP production, and cellular Ca2+ homeostasis. It has been known for decades that isolated mitochondria can take up Ca2+ from the extramitochondrial solution, but the molecular identity of the Ca2+ 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 Ca2+ uptake that relies on extramitochondrial Ca2+ 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 Ca2+ uptake. We anticipate our observations may provide insights into the mechanisms of mitochondrial Ca2+ uptake and advance understanding of the physiological role of TRPC3.
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