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Intracellular Ca ²⁺ transient is crucial in initiating the differentiation of mesenchymal cells into chondrocytes, but whether voltage-gated Ca ²⁺ channels are involved remains uncertain. Here, we show that the T-type voltage-gated Ca ²⁺ channel Ca ᵥ3.2 is essential for tracheal chondrogenesis. Mice lacking this channel (Ca ᵥ3.2 ⁻/⁻) show congenital tracheal stenosis because of incomplete formation of cartilaginous tracheal support. Conversely, Ca ᵥ3.2 overexpression in ATDC5 cells enhances chondrogenesis, which could be blunted by both blocking T-type Ca ²⁺ channels and inhibiting calcineurin and suggests that Ca ᵥ3.2 is responsible for Ca 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 ᵥ3.2 ⁻/⁻ tracheas. Mechanistically, Ca ²⁺ influx via Ca ᵥ3.2 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 ²⁺ influx via the Ca ᵥ3.2 T-type Ca ²⁺ channel regulates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis.

Objective: It has been reported that antroquinonol extracted from Golden- Antrodia camphorate exerts protective effects on liver function both in vitro and in vivo . However, the protective effects of Golden- Antrodia camphorata on liver function have not been fully investigated in human clinical studies. Therefore, the present study aimed to evaluate the beneficial effects of Golden- Antrodia camphorata on hepatic function after alcohol consumption in human subjects. Methods: A total of 80 participants with increased γ-glutamyl transferase levels (60–180 U/L) were enrolled in the current study and were randomly divided into two groups. Participants in the first group were orally administrated with 300 mg/day Golden- Antrodia camphorata (tablets), while those in the second group received placebo tablets for 12 weeks. Biochemical routine blood tests were performed at 6 and 12 weeks following the first administration. Results: At 12 weeks post the first Golden- Antrodia camphorata administration, the serum levels of aspartate aminotransferase (AST; p < 0.0001), alanine aminotransferase (ALT; p = 0.0002) and triglyceride ( p = 0.0158) were notably declined in the Golden- Antrodia camphorata treatment group compared with the placebo group. No clinically significant differences were observed between the Golden- Antrodia camphorata treatment and placebo groups in terms of general safety parameters. Conclusion: A statistically significant difference was obtained in the serum levels of AST, ALT and triglycerides between the Golden- Antrodia camphorata and placebo groups. However, no clinical significance was observed in any of the safety parameters examined. Overall, these findings indicated that treatment with Golden- Antrodia camphorata exerted protective effects on liver function.

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.

The tracheal cartilage rings are important for protecting and maintaining the airway. However, the chondrogenesis of tracheal cartilage is not completely understood. We demonstrate that the Ca v 3.2 T-type calcium channel is required for normal tracheal cartilage ring formation. Calcium influx via Ca v 3.2 induces chondrogenesis and up-regulates a chondrogenic master gene, sex determination region of Y chromosome (SRY)-related high-mobility group-Box gene 9 (Sox9), via a calcium and calcineurin-dependent pathway. Ca v 3.2-dependent regulation of Sox9 is mediated by a newly identified nuclear factor of activated T-cell binding site on the Sox9 promoter. Our study provides novel insight into the roles of Ca v 3.2 T-type calcium channels in tracheal development. Moreover, CACNA1H , the human homolog of the mouse Ca v 3.2-encoding gene, may be a potential candidate gene involved in congenital tracheal stenosis in humans. Intracellular Ca 2+ transient is crucial in initiating the differentiation of mesenchymal cells into chondrocytes, but whether voltage-gated Ca 2+ channels are involved remains uncertain. Here, we show that the T-type voltage-gated Ca 2+ channel Ca v 3.2 is essential for tracheal chondrogenesis. Mice lacking this channel (Ca v 3.2 −/− ) show congenital tracheal stenosis because of incomplete formation of cartilaginous tracheal support. Conversely, Ca v 3.2 overexpression in ATDC5 cells enhances chondrogenesis, which could be blunted by both blocking T-type Ca 2+ channels and inhibiting calcineurin and suggests that Ca v 3.2 is responsible for Ca 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 v 3.2 −/− tracheas. Mechanistically, Ca 2+ influx via Ca 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 2+ influx via the Ca v 3.2 T-type Ca 2+ channel regulates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis.

Intracellular Ca super( 2+) transient is crucial in initiating the differentiation of mesenchymal cells into chondrocytes, but whether voltage-gated Ca super( 2+) channels are involved remains uncertain. Here, we show that the T-type voltage-gated Ca super( 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 super( 2+) channels and inhibiting calcineurin and suggests that Ca sub( v)3.2 is responsible for Ca super( 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 super( 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 super( 2+) influx via the Ca sub( v)3.2 T-type Ca super( 2+) channel regulates Sox9 expression through the calcineurin/NFAT signaling pathway during tracheal chondrogenesis.