Plikus · Proceedings of the National Academy of Sciences of the United States of America 2013 · controlled laboratory animal experiment · n=?

Local circadian clock gates cell cycle progression of transient amplifying cells during regenerative hair cycling.

Cited 158 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal and laboratory mechanistic study

PubMed 23690597 · doi:10.1073/pnas.1215935110 · record verified 2026-08-30

What was done

Researchers investigated the role of peripheral circadian clocks in actively proliferating transient amplifying cells during anagen hair follicle regeneration in mice. They examined clock activity in the epithelial matrix and mesenchymal dermal papilla, measured hair growth rates across time points, and evaluated hair loss severity after administering equivalent doses of gamma-radiation in the morning versus evening in wild-type and circadian-mutant mice.

What was found

The abstract reports no exact numerical figures or statistical values. Peripheral clocks in epithelial matrix cells generated daily mitotic rhythms, causing hairs to grow faster in the morning than in the evening in mice. Morning gamma-radiation delivered during the mitotic peak caused substantial hair loss in wild-type mice, whereas evening administration resulted in minimal hair loss. This diurnal radioprotective variation was lost in circadian-mutant mice, mechanistically linked to the synchronization of the Cdc2/Cyclin B-mediated G2/M checkpoint.

Why it matters

The study shows that peripheral tissue clocks regulate cell cycle progression in rapidly dividing progenitor cells. This offers a mechanistic basis for chronotherapeutic scheduling of radiation or cytotoxic treatments to reduce normal tissue damage like alopecia.

Limits

The study was conducted exclusively in mice, and sample sizes, exact radiation doses, and quantitative effect sizes are not reported in the abstract. Because mice are nocturnal, circadian phase timing and susceptibility cannot be directly extrapolated to human patients without clinical validation.

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