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Chloride intracellular channel 1 regulates osteoblast differentiation

 Jae-Yeon Yang  ;  Ju Yeon Jung  ;  Sun Wook Cho  ;  Hyung Jin Choi  ;  Sang Wan Kim  ;  Seong Yeon Kim  ;  Hee Joong Kim  ;  Chang Han Jang  ;  Min Goo Lee  ;  Jin Han  ;  Chan Soo Shin 
 BONE, Vol.45(6) : 1175-1185, 2009 
Journal Title
Issue Date
Adipogenesis ; Alkaline Phosphatase/antagonists & inhibitors ; Alkaline Phosphatase/metabolism ; Animals ; Cell Differentiation* ; Cell Line ; Cell Membrane/metabolism ; Chloride Channels/genetics ; Chloride Channels/metabolism* ; Culture Media ; Electrophoresis, Gel, Two-Dimensional ; Gene Expression Regulation ; Humans ; Membrane Potential, Mitochondrial ; Mice ; Osteoblasts/cytology* ; Osteoblasts/metabolism* ; Osteogenesis ; Protein Transport ; RNA, Small Interfering/metabolism ; Rats ; Retroviridae/genetics ; Signal Transduction ; Subcellular Fractions/metabolism ; Wnt Proteins/metabolism
Osteoblast ; Wnt ; Chloride intracellular channel ; Mitochondria ; Differentiation
We have identified chloride intracellular channel 1 (CLIC1) through proteomic approach, which was increased in response to canonical wnt signaling while being almost shut-off by adipogenic treatment in mouse mesenchymal C3H10T1/2 cells. We found that CLIC1 was expressed in mouse (MC3T3-E1), rat (ROS 17/2.8 and UMR-106) or human (MG63 and SaOS2) osteoblastic cell lines as well as primary culture of mouse calvarial cells by RT-PCR or Western blot analysis. The expression level of CLIC1 is increased upon treatment of osteogenic medium, whereas it almost disappeared in adipogenic condition, confirming the proteomic data. The expression of CLIC1 was localized mainly in nuclear membrane and vesiculo-cytoplasmic, the latter of which was colocalized with mitochondria. Retroviral overexpression of CLIC1 did not increase whole-cell current but induces hyperpolarization of mitochondrial membrane potential estimated using the fluorescent dye TMRE. Moreover, overexpression of CLIC1 resulted in increase in osteoblastic differentiation of C3H10T1/2 cells as measured by ALP activities or osteoblastic gene expression (osterix, ALP and osteocalcin), although it did not result in induction of Runx2 transcription activities at mouse osteocalcin (OG2) promoter. Finally, in vitro knock-down of CLIC1 using stable siRNA CLIC1 significantly suppressed osteoblastic differentiation. Taken together, these results suggest that CLIC1 may play a role in the regulation of osteoblastic differentiation from mesenchymal progenitors, although its physiologic role in osteoblasts remains to be determined
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1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
Yonsei Authors
Lee, Min Goo(이민구) ORCID logo https://orcid.org/0000-0001-7436-012X
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