Hair Growth Cycle Is Arrested in SCD1 Deficiency by Impaired Wnt3a-Palmitoleoylation and Retrieved by the Artificial Lipid Barrier.
Stoffel W., Schmidt-Soltau I., Jenke B., Binczek E., Hammels I.
Animal Study on Hair Loss, published in J Invest Dermatol (2017) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- J Invest Dermatol (2017)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 28259688
- DOI
- 10.1016/j.jid.2017.02.973
Abstract (original English)
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, which 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.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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