Abstract
In a large scale screen for skin, hair, and nail abnormalities in null mice generated by The Jackson Laboratory’s KOMP center, homozygous mutant Far2tm2b(KOMP)Wtsi/2J (hereafter referrred to as Far2-/-) mice were found to develop focal areas of alopecia as they aged. As sebocytes matured in wildtype C57BL/NJ mice they became pale with fine, uniformly sized clear lipid containing vacuoles that were released when sebocytes disintegrated in the duct. By contrast, the Far2-/- null mice had sebocytes that were similar within the gland but become brightly eosinophilic when the cells entered the sebaceous gland duct. As sebocytes disintegrated, their contents did not readily dissipate. Scattered throughout the dermis, and often at the dermal hypodermal fat junction, were dystrophic hair follicles or ruptured follicles with a foreign body granulomatous reaction surrounding free hair shafts (trichogranuloma). The Meibomian and clitoral glands (modified sebaceous glands) of Far2-/- mice showed ducts dilated to various degrees that were associated with mild changes in the sebocytes as seen in the truncal skin. Skin surface lipidomic analysis revealed a lower level of wax esters, cholesterol esters, ceramides, and diacylglycerols compared to wildtype control mice. Similar changes were described in a number of other mouse mutations that affected the sebaceous glands resulting in primary cicatricial alopecia.
Highlights
Primary cicatricial alopecia (PCA) is a term that encompasses a group of human diseases historically believed to be due to an inflammatory or autoinflammatory skin disease process leading to follicle destruction, fibrosis, and loss of stem cells in the bulge region, resulting in follicular scars
We describe here abnormalities of the sebaceous glands and skin surface lipids associated with follicular dystrophy leading to follicular scarring without direct effects on the hair shafts in these mutant mice
fatty acyl coA reductase 2 (Far2)-/- mice developed hair loss consistently at 4 months of age initially on the ventral skin where it presented as a gradual thinning of hair
Summary
Primary cicatricial (scarring) alopecia (PCA) is a term that encompasses a group of human diseases historically believed to be due to an inflammatory or autoinflammatory skin disease process leading to follicle destruction, fibrosis, and loss of stem cells in the bulge region, resulting in follicular scars. These can be primary or secondary; the primary forms often are associated with damage to sebaceous glands [1]. Primary cicatricial alopecia in Far2-/- mice were supported in part by Basic Cancer Center Core Grant from the National Cancer Institute (CA034196). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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