Rosiglitazone ameliorates senescence-like phenotypes in a cellular photoaging model

Chen, Liang; Bi, Bo; Zeng, Jiping; Zhou, Yiqun; Yang, Ping; Guo, Yu; Zhu, Jingjing; Yang, Qingjian; Zhu, Nianyong; Liu, Tianyi

doi:10.1016/j.jdermsci.2015.01.007

Cited by 16 publications

(19 citation statements)

References 39 publications

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“…ADSC-EV treatment counteracted ROS production by increasing the expression of the antioxidant enzymes SOD-1 and CAT ( Fig. 7), consistent with previous reports [35,45].…”

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confidence: 91%

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Extracellular vesicles from adipose-derived stem cells ameliorate ultraviolet B-induced skin photoaging by attenuating reactive oxygen species production and inflammation

Zhang

et al. 2020

Stem Cell Res Ther

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Background: Large numbers of adipose-derived stem cells (ADSCs) are easily obtained and have been demonstrated to protect against ultraviolet B (UVB)-induced skin photoaging. Extracellular vesicles (EVs) exhibit some of the same effects as the cells from which they originate and have many advantages over stem cells. In particular, their application circumvents many safety concerns associated with cell therapy. Thus, as a cell-free agent, adipose-derived stem cell extracellular vesicles (ADSC-EVs) have anti-photoaging potential. However, the protective effects of ADSC-EVs in skin photoaging remain uncertain. Methods: To investigate the effect of ADSC-EVs on mice with UVB-induced photoaging, 150 μg and 300 μg ADSC-EVs were subcutaneously injected weekly into photoaging mice for 8 weeks. The protective effect was evaluated by gross assessment and hematoxylin and eosin, Masson's trichrome, and β-galactosidase staining. Proliferating cell nuclear antigen, CD68, and dihydroethidium staining were performed to evaluate cell proliferation, inflammation infiltration, and reactive oxygen species (ROS) production, respectively. In vitro, 100 μg/mL and 200 μg/mL ADSC-EVs were used to treat photoaging fibroblasts (FBs). β-galactosidase staining and collagen 1 and matrix metalloproteinase 3 (MMP-3) expression were analyzed to evaluate FB senescence. To explain the protective mechanism of ADSC-EVs, their role in regulating ROS production, antioxidant enzyme expression, cell cycle arrest, and inflammation was evaluated. Results: In vivo, we showed that ADSC-EVs decreased skin wrinkles in mice with UVB-induced photoaging, while promoting epidermal cell proliferation and attenuating macrophage infiltration and ROS production. In vitro, we showed that ADSC-EVs increased FB activity and protected FBs from UVB-induced senescence, attenuated raw 264.7 cell differentiation from M0 to M1 macrophages, reduced intracellular ROS production, promoted antioxidant enzyme expression, and rescued FBs from cell cycle arrest. Conclusion: The anti-photoaging effect of ADSC-EVs was attributed to their ability to attenuate ROS production and the inflammatory response, which are key factors in MMP activation and collagen degradation.

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“…ADSC-EV treatment counteracted ROS production by increasing the expression of the antioxidant enzymes SOD-1 and CAT ( Fig. 7), consistent with previous reports [35,45].…”

supporting

confidence: 91%

“…e, f The mRNA and protein expression of Col-1 and MMP-3 in four groups. *P < 0.05 indicated a significant difference of ADSC-EVs, which have been widely used to research skin photoaging [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicles from adipose-derived stem cells ameliorate ultraviolet B-induced skin photoaging by attenuating reactive oxygen species production and inflammation

Zhang

et al. 2020

Stem Cell Res Ther

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“…PPARγ, which belonged to a family of nuclear hormone receptors that regulated the function and expression of complex gene networks, especially involved in cell proliferation and differentiation, glucose metabolism and homeostasis, insulin sensitivity and lipid metabolism 43 . It was reported that after treatment with RSG observably attenuated GCI-induced elevation of the LC3-II and Beclin-1 hippocampus of brain, these observations suggested that RSG might exert its inhibitory effect by inactivating neuronal autophagy through decreasing Beclin-1 and LC3-II, and thus achieve a cerebral protective effect 44 .…”

Section: Discussionmentioning

confidence: 99%

Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway

Bai

Yao

Jiang

et al. 2016

Sci Rep

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Chronic exposures to arsenic had been associated with metabolism diseases. Peroxisome proliferator-activated receptor gamma (PPARγ) was found in the liver, regulated metabolism. Here, we found that the expression of PPARγ was decreased, the generation of reactive oxygen species (ROS) and autophagy were increased after treatment with As2O3 in offsprings’ livers. Taurine (Tau), a sulfur-containing β–amino acid could reverse As2O3-inhibited PPARγ. Tau also inhibit the generation of ROS and autophagy. We also found that As2O3 caused autophagic cell death and ROS accelerated in HepG2 cells. Before incubation with As2O3, the cells were pretreated with PPARγ activator Rosiglitazone (RGS), we found that autophagy and ROS was inhibited in HepG2 cells, suggesting that inhibition of PPARγ contributed to As2O3-induced autophagy and the generation of ROS. After pretreatment with Tau, the level of PPARγ was improved and the autophagy and ROS was inhibited in As2O3-treated cells, suggesting that Tau could protect hepatocytes against As2O3 through modulating PPARγ pathway.

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“…Our results demonstrated that UVA irradiation can reduce cell adhesion strength and that may be due to cell senescence. Typically, dermal fibroblasts undergo senescence rather than apoptosis after DNA damage or multiple rounds of cell division since the presence of senescent fibroblasts in the dermis of photoaged skin has been shown by β-galactosidase staining [ 24 ]. A recent study indicated an age-dependent decline in the expression of E-cadherin, the cell-cell adhesion molecule, in the germline stem cells of the Drosophila ovary and testis [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

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

Fang

Huang

Tsai

et al. 2016

IJMS

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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.

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Rosiglitazone ameliorates senescence-like phenotypes in a cellular photoaging model

Cited by 16 publications

References 39 publications

Extracellular vesicles from adipose-derived stem cells ameliorate ultraviolet B-induced skin photoaging by attenuating reactive oxygen species production and inflammation

Extracellular vesicles from adipose-derived stem cells ameliorate ultraviolet B-induced skin photoaging by attenuating reactive oxygen species production and inflammation

Taurine protects against As2O3-induced autophagy in livers of rat offsprings through PPARγ pathway

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

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