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Versican maintains the homeostasis of adipose tissues and regulates energy metabolism
Versican is a large chondroitin sulfate proteoglycan in the extracellular matrix. It plays a pivotal role in the formation of the provisional matrix. S100a4, previously known as fibroblast-specific protein, functions as a calcium channel-binding protein. To investigate the role of versican expressed...
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Published in: | Biochemical and biophysical research communications 2024-10, Vol.727, p.150309, Article 150309 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Versican is a large chondroitin sulfate proteoglycan in the extracellular matrix. It plays a pivotal role in the formation of the provisional matrix. S100a4, previously known as fibroblast-specific protein, functions as a calcium channel-binding protein. To investigate the role of versican expressed in fibroblasts, we generated conditional knockout mice in which versican expression is deleted in cells expressing S100a4. We found that S100a4 is expressed in adipose tissues, and these mice exhibit obesity under a normal diet, which becomes apparent as early as five months. The white adipose tissues of these mice exhibited decreased expression levels of S100a4 and versican and hypertrophy of adipocytes. qRT-PCR showed a reduced level of UCP1 in their white adipose tissues, indicating that the basic energy metabolism is diminished. These results suggest that versican in adipose tissues maintains the homeostasis of adipose tissues and regulates energy metabolism.
•Versican in adipose tissue maintains homeostasis and regulates energy metabolism.•Reduced versican and S100a4 expression causes fewer adipocytes and decreased UCP1 levels.•Lack of versican expression does not cause inflammation in adipose tissue.•Versican expression in S100a4-positive adipose tissue is necessary for maintaining physical activity and energy expenditure.•Versican is unlikely related to diabetic conditions. |
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ISSN: | 0006-291X 1090-2104 1090-2104 |
DOI: | 10.1016/j.bbrc.2024.150309 |