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TL;DR
This preclinical, in vivo study used a loss-of-function approach with BMAL1 knockout mice and a contraction-resistance wound healing protocol to map histone acetylation (H3 and H4) in epithelial cells during skin injury.
Experimental dermatology · 5 authors, 4 centres
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This preclinical, in vivo study used a loss-of-function approach with BMAL1 knockout mice and a contraction-resistance wound healing protocol to map histone acetylation (H3 and H4) in epithelial cells during skin injury.
This preclinical, in vivo study used a loss-of-function approach with BMAL1 knockout mice and a contraction-resistance wound healing protocol to map histone acetylation (H3 and H4) in epithelial cells during skin injury. The authors found significant differences in histone acetylation levels in both homeostatic and injured skin with deregulated BMAL1. In intact BMAL1 knockout skin, varied acetylation levels were observed, including hyperacetylation of H3K9. The most pronounced changes occurred at the repair site, with notable alterations in histone H4 acetylation patterns, specifically increased H4K5 acetylation in the recovering epidermis and H4K16 acetylation in the wound margin, alongside deacetylation of H3K9 at the wound margin. The study identifies a link between circadian clock gene function and epigenetic modifications crucial for tissue regeneration. The authors note the small sample size as a limitation, which may affect statistical power, and suggest that therapeutic modulation of BMAL1 and its epigenetic events could be harnessed to improve skin regeneration.