Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 189, Issue 5, Pages 1041-1052Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2019.01.012
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Funding
- Ministry of Science and Technology of China [2015BA108B02]
- Natural Science Foundation of Jiangsu Province [BK20181260]
- National Natural Science Foundation of China [31772550, 31301217, 31500944]
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Missense mutations in the gasdermin-A3 (Gsdma3) gene are associated with skin inflammation and hair loss in mice. However, the physiological function of Gsdma3 remains unclear. Herein, we reported that mice carrying the Gsdma3 Y344H mutation that encodes a presumptive activated form of Gsdma3 show increased heat production along with lower body fat percentages. Detailed analysis indicated that this metabolic phenotype is mediated by serum IL-6-induced up-regulation of thermogenesis in brown adipose tissue. The mutant form of Gsdma3 promotes the expression of IL-6 in the epidermis in a c-Jun N-terminal kinase (JNK) signaling-dependent manner. The higher whole-body heat production in alopecia and excoriation mice could be suppressed by an IL-6 receptor/GP130 inhibitor. Our results uncovered Gsdma3/IL-6-dependent cross talk between the skin and brown adipose tissue.
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