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Int J Mol Sci. 2016 Jul 14;17(7). pii: E1129. doi: 10.3390/ijms17071129.

Dermal Lipogenesis Inhibits Adiponectin Production in Human Dermal Fibroblasts while Exogenous Adiponectin Administration Prevents against UVA-Induced Dermal Matrix Degradation in Human Skin.

Author information

1
Division of Plastic and Reconstructive Surgery, Department of Surgery, Ditmanson Medical Foundation Chia-Yi Christian Hospital, No. 539, Zhongxiao Rd., Chiayi City 60002, Taiwan. fangcl68@hotmail.com.
2
Department of Biochemical Science and Technology, National Chia Yi University, No. 300, Syuefu Rd., Chiayi City 60004, Taiwan. s102605@alumni.ncyu.edu.tw.
3
Department of Biochemical Science and Technology, National Chia Yi University, No. 300, Syuefu Rd., Chiayi City 60004, Taiwan. s1040681@mail.ncyu.edu.tw.
4
Department of Biochemical Science and Technology, National Chia Yi University, No. 300, Syuefu Rd., Chiayi City 60004, Taiwan. hchang@mail.ncyu.edu.tw.

Abstract

Adiponectin is one of the most abundant adipokines from the subcutaneous fat, and regulates multiple activities through endocrine, paracrine, or autocrine mechanisms. However, its expression in adipogenic induced fibroblasts, and the potential role in photoaging has not been determined. Here, human dermal fibroblasts, Hs68, were presented as a cell model of dermal lipogenesis through stimulation of adipogenic differentiation medium (ADM). Similar to other studies in murine pre-adipocyte models (i.e., 3T3-L1), Hs68 fibroblasts showed a tendency to lipogenesis based on lipid accumulation, triglyceride formation, and the expressions of PPAR-γ, lipoprotein lipase (LPL), and FABP4 mRNA. As expected, ADM-treated fibroblasts displayed a reduction on adiponectin expression. Next, we emphasized the photoprotective effects of adiponectin against UVA-induced damage in Hs68 fibroblasts. UVA radiation can downregulate cell adhesion strength and elastic modulus of Hs68 fibroblasts. Moreover, UVA radiation could induce the mRNA expressions of epidermal growth factor receptor (EGFR), adiponectin receptor 1 (AdipoR1), matrix metalloproteinase-1 (MMP-1), MMP-3, and cyclooxygenase-2 (COX-2), but downregulate the mRNA expressions of type I and type III collagen. On the other hand, post-treatment of adiponectin can partially overcome UVA-induced reduction in the cell adhesion strength of Hs68 fibroblasts through the activation of AdipoR1 and the suppression of EGF-R. In addition, post-treatment of adiponectin indicated the increase of type III collagen and elastin mRNA expression and the decrease of MMP-1 and MMP-3 mRNA expression, but a limited degree of recovery of elastic modulus on UVA-irradiated Hs68 fibroblasts. Overall, these results suggest that dermal lipogenesis may inhibit the expression of adiponectin while exogenous adiponectin administration prevents against UVA-induced dermal matrix degradation in Hs68 fibroblasts.

KEYWORDS:

adipogenic differentiation medium; adiponectin; human dermal fibroblast; lipogenesis; photoaging

PMID:
27428951
PMCID:
PMC4964503
DOI:
10.3390/ijms17071129
[Indexed for MEDLINE]
Free PMC Article

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