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Publication : The acyl-CoA binding protein is required for normal epidermal barrier function in mice.

First Author  Bloksgaard M Year  2012
Journal  J Lipid Res Volume  53
Issue  10 Pages  2162-74
PubMed ID  22829653 Mgi Jnum  J:188040
Mgi Id  MGI:5439041 Doi  10.1194/jlr.M029553
Citation  Bloksgaard M, et al. (2012) The acyl-CoA binding protein is required for normal epidermal barrier function in mice. J Lipid Res 53(10):2162-74
abstractText  The acyl-CoA binding protein (ACBP) is a 10 kDa intracellular protein expressed in all eukaryotic species. Mice with targeted disruption of Acbp (ACBP(-/-) mice) are viable and fertile but present a visible skin and fur phenotype characterized by greasy fur and development of alopecia and scaling with age. Morphology and development of skin and appendages are normal in ACBP(-/-) mice; however, the stratum corneum display altered biophysical properties with reduced proton activity and decreased water content. Mass spectrometry analyses of lipids from epidermis and stratum corneum of ACBP(+/+) and ACBP(-/-) mice showed very similar composition, except for a significant and specific decrease in the very long chain free fatty acids (VLC-FFA) in stratum corneum of ACBP(-/-) mice. This finding indicates that ACBP is critically involved in the processes that lead to production of stratum corneum VLC-FFAs via complex phospholipids in the lamellar bodies. Importantly, we show that ACBP(-/-) mice display a approximately 50% increased transepidermal water loss compared with ACBP(+/+) mice. Furthermore, skin and fur sebum monoalkyl diacylglycerol (MADAG) levels are significantly increased, suggesting that ACBP limits MADAG synthesis in sebaceous glands. In summary, our study shows that ACBP is required for production of VLC-FFA for stratum corneum and for maintaining normal epidermal barrier function.
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