Linked Life Data

20506205

Source:http://linkedlifedata.com/resource/pubmed/id/20506205

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-8-30
pubmed:abstractText
ClC-3 chloride channel has been speculated to contribute to the acidification of synaptic vesicles and endosomes. However, the biological function of ClC-3 in osteogenesis remains to be determined. In this study, we first analyzed ClC-3 expression in MC3T3-E1 cells and primary mouse osteoblasts and then performed the osteoinductive procedure to determine the effects on gene expression. Subsequently, we transiently transfected ClC-3 cDNA or ClC-3-siRNA into MC3T3-E1 cells to determine the changed phenotype and gene expression. Lastly, we assessed the underlying mechanism responsible for ClC-3-induced osteodifferentiation. We found that ClC-3 mRNA was expressed in primary mouse osteoblasts and MC3T3-E1 cells and induced by using an osteoinductive procedure. We also found that overexpression of ClC-3 contributed to osteodifferentiation, such as increase in the expression of osteogenic markers [alkaline phosphatase (Alp), osteocalcin (Oc), bone sialoprotein (Bsp), osterix (Osx), and runt-related transcription factor 2 (Runx2)], morphological changes, and mineralized nodules in MC3T3-E1 cells. ClC-3 gene silencing suppressed gene expression of these osteogenic markers. Moreover, overexpressed ClC-3 protein co-localized with TGF-beta1 in intracellular organelles, inhibited TGF-beta1 protein expression and induced endosomal acidification. Nevertheless, knockdown of Runx2 expression antagonized the effects of ClC-3 in osteodifferentiation and expression of osteogenic markers. The data from the current study suggest that the function of ClC-3 in osteodifferentiation may be through the Runx2 pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1097-4644
pubmed:author
pubmed:copyrightInfo
(c) 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
49-58
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Chloride channel ClC-3 promotion of osteogenic differentiation through Runx2.
pubmed:affiliation
Department of Orthodontics, School of Stomatology, Fourth Military Medical University, Xi'an 710032, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't