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논문 기본 정보

자료유형
학술저널
저자정보
Jae-Kyung Kwon (Neuroscience Graduate Program Department of Biomedical Sciences Ajou University School of Medicine) Dong-Joo Choi (Department of Pharmacology Ajou University School of Medicine Suwon 16499 KoreaChronic Inflammatory) Haijie Yang (Neuroscience Graduate Program Department of Biomedical Sciences Ajou University School of Medicine) Dong Wan Ko (Neuroscience Graduate Program Department of Biomedical Sciences Ajou University School of Medicine) Ilo Jou (Neuroscience Graduate Program Department of Biomedical Sciences Ajou University School of Medicine) Sang Myun Park (Neuroscience Graduate Program Department of Biomedical Sciences Ajou University School of Medicine) Eun-Hye Joe (Neuroscience Graduate Program Department of Biomedical Sciences Ajou University School of Medicine)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제25권 제6호
발행연도
2021.10
수록면
565 - 574 (10page)
DOI
10.4196/kjpp.2021.25.6.565

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Astrocytes are activated in response to brain damage. Here, we found that expression of Kir4.1, a major potassium channel in astrocytes, is increased in activated astrocytes in the injured brain together with upregulation of the neural stem cell markers, Sox2 and Nestin. Expression of Kir4.1 was also increased together with that of Nestin and Sox2 in neurospheres formed from dissociated P7 mouse brains. Using the Kir4.1 blocker BaCl2 to determine whether Kir4.1 is involved in acquisition of stemness, we found that inhibition of Kir4.1 activity caused a concentration-dependent increase in sphere size and Sox2 levels, but had little effect on Nestin levels. Moreover, induction of differentiation of cultured neural stem cells by withdrawing epidermal growth factor and fibroblast growth factor from the culture medium caused a sharp initial increase in Kir4.1 expression followed by a decrease, whereas Sox2 and Nestin levels continuously decreased. Inhibition of Kir4.1 had no effect on expression levels of Sox2 or Nestin, or the astrocyte and neuron markers glial fibrillary acidic protein and β-tubulin III, respectively. Taken together, these results indicate that Kir4.1 may control gain of stemness but not differentiation of stem cells.

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