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• W2169132132 abstract "Osteoblasts support hematopoietic cell development, including B lymphopoiesis. We have previously shown that the nuclear factor of activated T cells (NFAT) negatively regulates osteoblast differentiation and bone formation. Interestingly, in smooth muscle, NFAT has been shown to regulate the expression of vascular cellular adhesion molecule-1 (VCAM-1), a mediator of cell adhesion and signaling during leukocyte development. To examine whether NFAT signaling in osteoblasts regulates hematopoietic development in vivo , we generated a mouse model expressing dominant-negative NFAT driven by the 2.3 kb fragment of the collagen-<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mrow><mml:mi>α</mml:mi></mml:mrow></mml:math>I promoter to disrupt NFAT activity in osteoblasts (dnNFAT OB ). Bone histomorphometry showed that dnNFAT OB mice have significant increases in bone volume (44%) and mineral apposition rate (131%) and decreased trabecular thickness (18%). In the bone microenvironment, dnNFAT OB mice displayed a significant increase (87%) in Lineage − cKit + Sca-1 + (LSK) cells and significant decreases in B220 + CD19 − IgM − pre-pro-B cells (41%) and B220 + CD19 + IgM + immature B cells (40%). Concurrent with these findings, LSK cell differentiation into B220 + cells was inhibited when cocultured on differentiated primary osteoblasts harvested from dnNFAT OB mice. Gene expression and protein levels of VCAM-1 in osteoblasts decreased in dnNFAT OB mice compared to controls. These data suggest that osteoblast-specific NFAT activity mediates early B lymphopoiesis, possibly by regulating VCAM-1 expression on osteoblasts." @default.
• W2169132132 created "2016-06-24" @default.
• W2169132132 creator A5039917099 @default.
• W2169132132 creator A5084467016 @default.
• W2169132132 date "2013-01-01" @default.
• W2169132132 modified "2023-10-16" @default.
• W2169132132 title "NFAT Signaling in Osteoblasts Regulates the Hematopoietic Niche in the Bone Microenvironment" @default.
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• W2169132132 doi "https://doi.org/10.1155/2013/107321" @default.
• W2169132132 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3654658" @default.
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