Dysregulated expression of sterol O-acyltransferase 1 (Soat1) in the hair shaft of Hoxc13 null mice

被引:5
|
作者
Potter, Christopher S. [1 ]
Kern, Michael J. [2 ]
Baybo, Mary Ann [2 ]
Pruett, Nathanael D. [1 ]
Godwin, Alan R. [3 ]
Sundberg, John P. [4 ]
Awgulewitsch, Alexander [1 ,2 ]
机构
[1] Med Univ S Carolina, Dept Med, Charleston, SC 29425 USA
[2] Med Univ S Carolina, Dept Regenerat Med & Cell Biol, Charleston, SC 29425 USA
[3] Colorado State Univ, Dept Microbiol Immunol & Pathol, Ft Collins, CO 80523 USA
[4] Jackson Lab, Bar Harbor, ME 04609 USA
基金
美国国家卫生研究院;
关键词
Hoxc13; Soat1; Hair follicle; Lipid metabolism; Hox regulatory target; GENE; DEFECTS; FOXQ1;
D O I
10.1016/j.yexmp.2015.08.016
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
The cholesterol-metabolizing enzyme sterol O-acetyltransferase (SOAT1) is implicated in an increasing number of biological and pathological processes in a number of organ systems, including the differentiation of the hair shaft While the functional and regulatory mechanisms underlying these diverse functional roles remain poorly understood, the compartment of the hair shaft known as medulla, affected by mutations in Soat1, may serve as a suitable model for defining some of these mechanisms. A comparative analysis of mRNA and protein expression patterns of Soat1/SOAT1 and the transcriptional regulator Hoxc13/HOXC13 in postnatal skin of FVB/NTac mice indicated co-expression in the most proximal cells of the differentiating medulla. This finding combined with the significant downregulation of Soat1 expression in postnatal skin of both Hoxc13 gene-targeted and transgenic mice based on previously reported DNA microarray results suggests a potential regulatory relationship between the two genes. Non-detectable SOAT1 expression in the defective hair follicle medulla of Hoxc13(tm1Mrc) mice and evidence for binding of HOXC13 to the Soat1 upstream control region obtained by ChIP assay suggests that Soat1 is a downstream regulatory target for HOXC13 during medulla differentiation. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:441 / 444
页数:4
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