Hair growth cycle is arrested in SCD1-deficiency by impaired Wnt3a-palmitoleoylation and retrieved by artificial lipid barrier.

Stoffel W, Schmidt-Soltau I, Jenke B et al.

Laboratory of Molecular Neurosciences, Institute of Biochemistry, University of Cologne, 50931 Cologne, Germany; CMMC (Center of Molecular Medicine), University of Cologne, 50931 Cologne, Germany; CECAD (Cluster of Excellence: Cellular Stress Responses in Aging-Associated Diseases), University of Cologne, 50931 Cologne, Germany. Electronic address:

The Journal of investigative dermatology. Mar 2017.

Stearoyl-CoA desaturase 1 (SCD1) is the dominant member of the SCD-isozyme family, regarded as a major regulator of lipid and energy metabolism in liver and adipose tissue. SCD1-deficiency impairs the desaturation of de novo-synthesized palmitoyl- and stearoyl-CoA to palmitoleoyl- and oleoyl- CoA. Scd1-/- mice develop metabolic waste syndrome and skin lesions: epidermal barrier disruption, alopecia and degeneration of sebaceous glands. The unifying molecular link between the two divergent traits remains incompletely understood. Here we show the absence of palmitoleic acid (9Z-16:1) in the lipidome of the scd1-null mouse, that prohibits posttranslational O-palmitoleoylation of Wnt3a-protein, essential for Wnt3a/ß-catenin signaling in stem cell lineage decision in development of the epidermal barrier, hair growth cycle, and sebaceous glands. Substitution of the disrupted epidermal lipid barrier by an inert hydrocarbon coat prevents excessive transepidermal water loss, normalizes thermogenesis and metabolic parameters, and surprisingly leads to the activation of hair bulge progenitor cells and reprograming of a regular hair growth cycle and development of a regular fur in scd1-/- mice. Progenitor sebocytes are not activated. Independent of age, application or removal of the artificial lipid barrier allows the reversible telogen-anagen reentry and exit of the hair growth cycle.


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