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Kir4.1 is coexpressed with stemness markers in activated astrocytes in the injured brain and a Kir4.1 inhibitor BaCl2 negatively regulates neurosphere formation in culture.
Kwon, Jae-Kyung; Choi, Dong-Joo; Yang, Haijie; Ko, Dong Wan; Jou, Ilo; Park, Sang Myun; Joe, Eun-Hye.
Afiliación
  • Kwon JK; Neuroscience Graduate Program, Department of Biomedical Sciences, Ajou University School of Medicine, Suwon 16499, Korea.
  • Choi DJ; Department of Pharmacology, Ajou University School of Medicine, Suwon 16499, Korea.
  • Yang H; Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon 16499, Korea.
  • Ko DW; Neuroscience Graduate Program, Department of Biomedical Sciences, Ajou University School of Medicine, Suwon 16499, Korea.
  • Jou I; Department of Pharmacology, Ajou University School of Medicine, Suwon 16499, Korea.
  • Park SM; Center for Convergence Research of Neurological Disorders, Ajou University School of Medicine, Suwon 16499, Korea.
  • Joe EH; Neuroscience Graduate Program, Department of Biomedical Sciences, Ajou University School of Medicine, Suwon 16499, Korea.
Korean J Physiol Pharmacol ; 25(6): 565-574, 2021 Nov 01.
Article en En | MEDLINE | ID: mdl-34697267
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 ß-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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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Korean J Physiol Pharmacol Año: 2021 Tipo del documento: Article Pais de publicación: Corea del Sur

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Korean J Physiol Pharmacol Año: 2021 Tipo del documento: Article Pais de publicación: Corea del Sur