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

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.

Liposome-Encapsulated Baicalein Suppressed Lipogenesis and Extracellular Matrix Formation in Hs68 Human Dermal Fibroblasts

“…However, in skin wound healing, the role of lipogenesis in dermal fibroblasts were under investigated and the mechanisms has yet to be defined. Our previous study confirmed that adipogenic differentiation medium (ADM) can stimulate the differentiation of Hs68 human dermal fibroblasts to adipocyte-like cells through the lipid accumulation and mRNA expressions of PPAR-γ, LPL and FABP4 ( Fang et al, 2016 ). In the present study, we aim to further investigate the impact of lipogenesis on the inflammation responses and ECM formation in Hs68 fibroblasts.…”

Chemical Constituents from Leaves of <i>Hydrangea serrata</i> and Their Anti-photoaging Effects on UVB-Irradiated Human Fibroblasts

“…The dermis is composed of fibrous structural collagen-rich extracellular matrix (ECM) which is essentially responsible for the skin's tensile strength and mechanical properties, together with elastin and hyaluronic acid. 1,2) Upon exposure to solar UV, especially UVB, degradation of ECM is being processed through activation of matrix metalloproteinases (MMPs) with decreased pro-collagen synthesis, resulting in wrinkle formation and sagging skin (skin photoaging). 3) A great number of plant extracts and phytochemicals including polyphenols (flavonoids and non-flavonoids) and non-phenolic derivatives possess anti-oxidant and anti-inflammatory properties.…”

Melatonin attenuates the detrimental effects of UVA irradiation in human dermal fibroblasts by suppressing oxidative damage and MAPK/AP‐1 signal pathway in vitro

“…8,10 UVA-induced activation of EGFR has been reported by previous in vivo and in vitro studies 13,17 . Fang et al 35 found that 2.808 J/cm 2 UVA irradiation leads to increases in EGFR expression in Hs68 fibroblast cells.…”

“…The level of collagen in the normal skin is maintained by the balance between synthesis in dermal fibroblasts and enzymatic degradation by MMPs and tissue inhibitors of metalloproteinases (TIMPs) which can be induced by UV irradiation. 8,10,35 MMPs are a family of zinc-and calcium-dependent endoproteinases, which are capable of degrading collagen, elastin, and other components of the ECM of the skin. It has been reported that MMP-1, interstitial collagenase, and MMP-3, stromelysin-1, are both responsible for the degradation of dermal collagen and their activities are regulated by their interactions with TIMPs.…”