Please use this identifier to cite or link to this item:
Title: Selective deletion of PPARβ/δ in fibroblasts causes dermal fibrosis by attenuated LRG1 expression
Authors: Sng, Ming Keat
Chan, Jeremy Soon Kiat
Teo, Ziqiang
Phua, Terri
Tan, Eddie Han Pin
Wee, Jonathan Wei Kiat
Koh, Nikki Jun Ning
Tan, Chek Kun
Chen, Jia Peng
Pal, Mintu
Tong, Benny Meng Kiat
Tnay, Ya Lin
Ng, Xuan Rui
Zhu, Pengcheng
Chiba, Shunsuke
Wang, Xiaomeng
Wahli, Walter
Tan, Nguan Soon
Keywords: Selective Deletion
Dermal Fibrosis
Issue Date: 2018
Source: Sng, M. K., Chan, J. S. K., Teo, Z., Phua, T., Tan, E. H. P., Wee, J. W. K., et al. (2018). Selective deletion of PPARβ/δ in fibroblasts causes dermal fibrosis by attenuated LRG1 expression. Cell Discovery, 4(1), 15-.
Series/Report no.: Cell Discovery
Abstract: Connective tissue diseases of the skin are characterized by excessive collagen deposition in the skin and internal organs. Fibroblasts play a pivotal role in the clinical presentation of these conditions. Nuclear receptor peroxisome-proliferator activated receptors (PPARs) are therapeutic targets for dermal fibrosis, but the contribution of the different PPAR subtypes are poorly understood. Particularly, the role of fibroblast PPARβ/δ in dermal fibrosis has not been elucidated. Thus, we generated a mouse strain with selective deletion of PPARβ/δ in the fibroblast (FSPCre-Pparb/d−/−) and interrogated its epidermal and dermal transcriptome profiles. We uncovered a downregulated gene, leucine-rich alpha-2-glycoprotein-1 (Lrg1), of previously unknown function in skin development and architecture. Our findings suggest that the regulation of Lrg1 by PPARβ/δ in fibroblasts is an important signaling conduit integrating PPARβ/δ and TGFβ1-signaling networks in skin health and disease. Thus, the FSPCre-Pparb/d−/− mouse model could serve as a novel tool in the current gunnery of animal models to better understand dermal fibrosis.
DOI: 10.1038/s41421-018-0014-5
Rights: © 2018 The Author(s). This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:LKCMedicine Journal Articles
SBS Journal Articles
SPMS Journal Articles

Google ScholarTM




Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.