ArticleMolecular and cellular biochemistry2010
Osteogenic role of endosomal chloride channels in MC3T3-E1 cells.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Age-related decline in bone mineral transport and bone matrix proteins in osteoblasts from stromal stem cells.American journal of physiology. Cell physiology · 2023Article
- Novel variants in theFrontiers in neurology · 2023Article
- The role of the Smad2/3/4 signaling pathway in osteogenic differentiation regulation by ClC-3 chloride channels in MC3T3-E1 cells.Journal of orthopaedic surgery and research · 2022Article
- Carbonic Anhydrase 12 Protects Endplate Cartilage From Degeneration Regulated by IGF-1/PI3K/CREB Signaling Pathway.Frontiers in cell and developmental biology · 2020Article
- ClC-3 chloride channel mediates the role of parathyroid hormone [1-34] on osteogenic differentiation of osteoblasts.PloS one · 2017Article
- Chloride-hydrogen antiporters ClC-3 and ClC-5 drive osteoblast mineralization and regulate fine-structure bone patterning in vitro.Physiological reports · 2015Article
- Chitosan nanofiber scaffold improves bone healing via stimulating trabecular bone production due to upregulation of the Runx2/osteocalcin/alkaline phosphatase signaling pathway.International journal of nanomedicine · 2015Article
- Improving effects of chitosan nanofiber scaffolds on osteoblast proliferation and maturation.International journal of nanomedicine · 2014Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ClC-3, ClC-4, and ClC-5 belong to the voltage gated chloride channels (ClCs) and facilitate the endosomal acidification. The mutations of these endosomal chloride channel genes cause different genetic diseases with various bone disorders. We hypothesized that these endosomal ClCs might be involved in the bone development or osteoblast differentiation. Here we used MC3T3-E1 osteoprogenitor cell line and primarily cultured mouse osteoblasts and detected the expression of Clcn3, Clcn4, and Clcn5 in these cells. We analyzed the relationships between three endosomal ClCs and the osteogenic phenotype using osteoinductive treatment, overexpressing of ClCs and RNAi of ClCs. We found the increased mRNA levels of osteogenic markers [alkaline phosphatase (Alp), osteocalcin (Oc), bone sialoprotein (Bsp), and runt-related transcription factor 2 (Runx2)] were in parallel to that of Clcn3, Clcn4 and Clcn5 with osteoinductive treatment and overexpressed ClCs. Overexpressed ClCs were localized in intracellular periphery and also promoted the mineralization of cells in vitro. While RNAi mediated gene silencing of ClC-3, ClC-4, and ClC-5 down regulated the expression of the four osteogenic markers. The positive relationship between endosomal ClCs and the osteogenic markers suggested a new function of endosomal ClCs in osteogenic differentiation.
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