Type XVII Collagen Coordinates Proliferation in the Interfollicular Epidermis
July 2017
in “
eLife
”
Studysummary This study found that COL17 deficiency in neonatal mice causes abnormal skin cell proliferation due to disrupted Wnt signaling, while replenishing or overexpressing COL17 can reverse this effect in both neonatal and aged skin.
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The study identified Type XVII collagen (COL17) as a crucial regulator of epidermal cell proliferation in the interfollicular epidermis (IFE) of both neonatal and aged mice. In neonatal mice, the absence of COL17 led to transient hyperproliferation due to disrupted Wnt signaling, which was reversible by replenishing COL17. In aged skin, loss of COL17 caused by inactive atypical protein kinase C signaling resulted in hyperproliferation, which could be suppressed by overexpressing human COL17. The research highlighted COL17's role in maintaining skin homeostasis and suggested its potential as a target for anti-aging treatments. However, the study faced limitations, including discrepancies between in vitro and in vivo results and a small sample size of patients with COL17A1 mutations, indicating a need for further investigation.
