Researchers from the Institute of Neurology, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences, and NIH in the United States published an article entitled "Canonical transient receptor potential 3 channels regulated mitochondrial calcium uptake" and found that transient receptor potential C (TRPC) channel protein is involved in regulating mitochondrial uptake Ca2 + reveals a new mechanism of mitochondrial uptake of Ca2 +. The research results were published in the online edition of the journal Proceedings of the National Academy of Sciences (PNAS).
Corresponding authors of the article are researcher Wang Yizheng of the Institute of Neurology, Shanghai Academy of Sciences, and Lutz Birnbaumer of the American Institute of Health.
The transient receptor potential C (TRPC) channel protein constitutes a non-selective cation channel on the cell membrane. These channels exist in various cells of mammals and bear various physiological functions. The members TRPC3 and TRPC6 play an important role in neuron survival. Mitochondrial Ca2 + uptake is involved in regulating cell energy metabolism and intracellular Ca2 + homeostasis. In response to stimuli, mitochondria can rapidly change the Ca2 + concentration in the matrix to affect cell metabolism and survival. Mitochondrial Ca2 + homeostasis is the basis for regulating its own membrane potential, ATP synthesis, and Ca2 + levels in the cytoplasm. However, it has not been known which Ca2 + channel on the mitochondria mediates the above process.
In this article, the researchers found that TRPC3 localizes on the cell membrane and mitochondrial inner membrane, can respond to changes in mitochondrial Ca2 +, and participates in the process of mitochondrial uptake of Ca2 + in the cytoplasm. Up-regulating or down-regulating TRPC3 protein expression can change the mitochondrial membrane potential. This reveals a new mechanism of mitochondrial Ca2 + uptake, and provides new ideas for understanding the physiological and pathological functions of TRPC3 channels.
Regarding TRPC, Wang Yizheng's research group had previously discovered the important role of TRPC6 in glioma cell proliferation and cell cycle, which illustrates the possibility of a non-selective cation channel as a target molecule for the treatment of glioma.
The researchers found that the expression of TRPC6 in human glioma tissue is significantly higher than that in normal brain tissue. Specifically blocking the TRPC6 channel can block the glioma cell cycle in the G2 phase and inhibit its proliferation. Blocking the TRPC6 channel reduces intracranial tumor volume and can significantly improve the survival rate of nude mice. In addition, blocking the TRPC6 channel can increase the sensitivity of glioma cells to radiation. This study proposed the possibility of TRPC6 channel as a new target molecule for the treatment of glioma. Wang Yizheng's research team has obtained many results in the study of TRPC channels. In 2005, Nature published the research results of Chinese scientists on the discovery of new mechanisms that guide the direction of nerve growth. This achievement was led by Wang Yizheng and Yuan Xiaobing. This achievement was first discovered in the world: a type of cation channel called "transient receptor potential channel" (TRPC) starts on the cell membrane of the frontmost growth cone of nerve fibers. It plays a key role in transmitting the "direction instruction" of nerve fiber growth.
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