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Ca^sub v^3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage
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Ca^sub v^3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage
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Ca^sub v^3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage
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Journal Article
Ca^sub v^3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage
2014
Overview
Intracellular Ca^sup 2+^ transient is crucial in initiating the differentiation of mesenchymal cells into chondrocytes, but whether voltage-gated Ca^sup 2+^ channels are involved remains uncertain. Here, we show that the T-type voltage-gated Ca^sup 2+^ channel Ca^sub v^3.2 is essential for tracheal chondrogenesis. Mice lacking this channel (Ca^sub v^3.2-/-) show congenital tracheal stenosis because of incomplete formation of cartilaginous tracheal support. Conversely, Ca^sub v^3.2 overexpression in ATDC5 cells enhances chondrogenesis, which could be blunted by both blocking T-type Ca^sup 2+^ channels and inhibiting calcineurin and suggests that Ca^sub v^3.2 is responsible for Ca^sup 2+^ influx during chondrogenesis. Finally, the expression of sex determination region of Y chromosome (SRY)-related high-mobility group-Box gene 9 (Sox9), one of the earliest markers of committed chondrogenic cells, is reduced in Ca^sub v^3.2-/- tracheas. Mechanistically, Ca^sup 2+^ influx via Ca^sub v^3.2 activates the calcineurin/nuclear factor of the activated T-cell (NFAT) signaling pathway, and a previously unidentified NFAT binding site is identified within the mouse Sox9 promoter using a luciferase reporter assay and gel shift and ChIP studies. Our findings define a previously unidentified mechanism that Ca^sup 2+^ influx via the Ca^sub v^3.2 T-type Ca^sup 2+^ channel regulates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis.
Publisher
National Academy of Sciences
Subject
