Pannexin 1, a large-pore membrane channel, contributes to hypotonicity-induced ATP release in Schwann cells
Autor: | Gang Chen, Wen-Feng Su, Dai Yujuan, Hui-Lin Qu, Ya-Yu Zhao, Zhongya Wei, Wei-Xing Shen, Zhuo-Min Ling, Qian Wang |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Small interfering RNA RHOA injury atp cytoskeleton neuron pannexin 1 peripheral nerve ras homolog family member a schwann cells lcsh:RC346-429 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Developmental Neuroscience medicine Schwann cells Cytoskeleton lcsh:Neurology. Diseases of the nervous system Cytochalasin D biology Pannexin Ras homolog family member A Cell biology ATP Nocodazole 030104 developmental biology medicine.anatomical_structure chemistry biology.protein Membrane channel Neuron 030217 neurology & neurosurgery Research Article |
Zdroj: | Neural Regeneration Research Neural Regeneration Research, Vol 16, Iss 5, Pp 899-904 (2021) |
ISSN: | 1673-5374 |
DOI: | 10.4103/1673-5374.290911 |
Popis: | Pannexin 1 (Panx 1), as a large-pore membrane channel, is highly permeable to ATP and other signaling molecules. Previous studies have demonstrated the expression of Panx 1 in the nervous system, including astrocytes, microglia, and neurons. However, the distribution and function of Panx 1 in the peripheral nervous system are not clear. Blocking the function of Panx 1 pharmacologically (carbenoxolone and probenecid) or with small interfering RNA targeting pannexins can greatly reduce hypotonicity-induced ATP release. Treatment of Schwann cells with a Ras homolog family member (Rho) GTPase inhibitor and small interfering RNA targeting Rho or cytoskeleton disrupting agents, such as nocodazole or cytochalasin D, revealed that hypotonicity-induced ATP release depended on intracellular RhoA and the cytoskeleton. These findings suggest that Panx 1 participates in ATP release in Schwann cells by regulating RhoA and the cytoskeleton arrangement. This study was approved by the Animal Ethics Committee of Nantong University, China (No. S20180806-002) on August 5, 2018. |
Databáze: | OpenAIRE |
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