Syndecan-1 Is Required to Maintain Intradermal Fat and Prevent Cold Stress

• DOI: 10.1371/journal.pgen.1004514
• Publication Date: 2014-08-07T18:06:55Z
• Authors: Ildiko Kasza; Yewseok Suh; Damian Wollny; Rod J. Clark; Avtar Roopra; Ricki J. Colman; Ormond A. MacDougald; Timothy A. Shedd; David W. Nelson; Mei-I Yen; Chi-Liang Eric Yen; Caroline M. Alexa...
• Keywords: Torpor

Homeostatic temperature regulation is fundamental to mammalian physiology and controlled by acute chronic responses of local, endocrine nervous regulators. Here, we report that loss the heparan sulfate proteoglycan, syndecan-1, causes a profoundly depleted intradermal fat layer, which provides crucial thermogenic insulation for mammals. Mice without syndecan-1 enter torpor upon fasting show multiple indicators cold stress, including activation stress checkpoint p38α in brown adipose tissue, liver lung. The metabolic phenotype mutant mice, reduced glycogen, rescued housing at thermoneutrality, suggesting cool temperatures underlies observed phenotypes. We find functions as facultative lipoprotein uptake receptor, required adipocyte differentiation vitro. Intradermal shows highly dynamic differentiation, continuously expanding involuting response hair cycle ambient temperature. This probably confers unique role Sdc1 this sub-type. PPARγ agonist rosiglitazone rescues Sdc1-/- placing downstream triggering differentiation. Our study indicates disruption tissue development results complex pathology.