Stemness and differentiation potential-recovery effects of sinapic acid against ultraviolet-A-induced damage through the regulation of p38 MAPK and NF-κB

Abstract Background Epiregulin (EREG) is an important component of EGF, which was demonstrated to promote the osteo/dentinogenic differentiation of stem cells from SCAPs. Whether it could stimulate the osteo/dentinogenic differentiation of DPSCs in inflammatory environment is not clear. The purpose of the present study was to investigate the role of EREG on the DPSCs’ osteo/dentinogenic differentiation ability in inflammatory environment. Methods DPSCs were isolated from human third molars. Short hairpin RNAs (shRNAs) was used to knock down the EREG expression in DPSCs. Recombinant human EREG protein (rhEREG) was adopted in the rescue experiment. TNF-α was employed to mimic the inflammatory environment in vitro. Alkaline phosphatase (ALP) staining, Alizarin red staining, quantitative calcium analysis, and real time RT-PCR was used to detect the osteo/dentinogenic differentiation markers and related signaling pathways under normal and inflammatory environment. Results EREG depletion promoted ALP activity and mineralization ability of DPSCs. Expression of BSP, DMP-1, and DSPP were also enhanced. Besides, 50ng/ml rhEREG treatment weakened the osteo/dentinogenic differentiation potential. 10 ng/mL TNF-α treatment for 4h increased the expression of EREG in DPSCs. However, knockdown of EREG rescued the impaired osteo/dentinogenic differentiation ability caused by TNF-α treatment. Further mechanism study showed that, EREG depletion activated p38 MAPK and Erk signaling pathways in DPSCs under normal and inflammatory environment. Conclusions Our results demonstrated that EREG could inhibited the osteo/dentinogenic differentiation potential of DPSCs via p38 MAPK and Erk signaling pathways in normal and inflammatory environment.

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Ultraviolet A induced modulation of gap junctional intercellular communication by P38 MAPK activation in human keratinocytes

Experimental Dermatology ◽

10.1111/j.1600-0625.2007.00662.x ◽

2008 ◽

Vol 17 (2) ◽

pp. 115-124 ◽

Cited By ~ 18

Author(s):

Barbara Bellei ◽

Arianna Mastrofrancesco ◽

Stefania Briganti ◽

Nicaela Aspite ◽

Niloofar Ale-Agha ◽

...

Keyword(s):

P38 Mapk ◽

Intercellular Communication ◽

Human Keratinocytes ◽

Ultraviolet A ◽

Gap Junctional Intercellular Communication ◽

Mapk Activation ◽

Gap Junctional

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Depletion of EREG enhances the osteo/dentinogenic differentiation ability of dental pulp stem cells via the p38 MAPK and Erk pathways in an inflammatory microenvironment

BMC Oral Health ◽

10.1186/s12903-021-01675-0 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Ran Ran ◽

Haoqing Yang ◽

Yangyang Cao ◽

Wanhao Yan ◽

Luyuan Jin ◽

...

Keyword(s):

Stem Cells ◽

P38 Mapk ◽

Dental Pulp ◽

Dental Pulp Stem Cells ◽

Signalling Pathways ◽

Alizarin Red ◽

Differentiation Potential ◽

Inflammatory Conditions ◽

Tnf Α ◽

Dentinogenic Differentiation

Abstract Background Epiregulin (EREG) is an important component of EGF and was demonstrated to promote the osteo/dentinogenic differentiation of stem cells from dental apical papilla (SCAPs). Whether EREG can stimulate the osteo/dentinogenic differentiation of dental pulp stem cells (DPSCs) in inflammatory environment is not clear. The purpose of the present study is to investigate the role of EREG on the osteo/dentinogenic differentiation ability of DPSCs in inflammatory environment. Methods DPSCs were isolated from human third molars. Short hairpin RNAs (shRNAs) were used to knock down EREG expression in DPSCs. Recombinant human EREG (rhEREG) protein was used in the rescue experiment. TNF-α was employed to mimic the inflammatory environment in vitro. Alkaline phosphatase (ALP) staining, Alizarin red staining, quantitative calcium analysis, and real-time RT-PCR were performed to detect osteo/dentinogenic differentiation markers and related signalling pathways under normal and inflammatory conditions. Results EREG depletion promoted the ALP activity and mineralization ability of DPSCs. The expression of BSP, DMP-1, and DSPP was also enhanced. Moreover, 50 ng/mL rhEREG treatment decreased the osteo/dentinogenic differentiation potential of DPSCs, while treatment with 10 ng/mL TNF-α for 4 h increased the expression of EREG in DPSCs. Conversely, EREG knockdown rescued the impaired osteo/dentinogenic differentiation ability caused by TNF-α treatment. Further mechanistic studies showed that EREG depletion activated the p38 MAPK and Erk signalling pathways in DPSCs under normal and inflammatory conditions. Conclusions Our results demonstrated that EREG could inhibit the osteo/dentinogenic differentiation potential of DPSCs via the p38 MAPK and Erk signalling pathways. Under inflammatory environment, EREG depletion enhanced osteo/dentinogenic differentiation potential of DPSCs by improving the expression of p-p38 MAPK and p-Erk.

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Sinapic Acid Promotes Browning of 3T3-L1 Adipocytes via p38 MAPK/CREB Pathway

BioMed Research International ◽

10.1155/2020/5753623 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

In-Seon Bae ◽

Sang Hoon Kim

Keyword(s):

Oxidative Phosphorylation ◽

P38 Mapk ◽

Mitochondrial Biogenesis ◽

Uncoupling Protein ◽

Sinapic Acid ◽

Mitogen Activated Protein Kinase ◽

Marker Genes ◽

Peroxisome Proliferator ◽

High Concentration ◽

Beige Adipocytes

Sinapic acid is a plant-derived phenolic compound, which acts as an antioxidant, anticancer, and anti-inflammatory agent. Although sinapic acid is valuable in a variety of therapeutic applications, its role in the improvement of obesity-related metabolic disease is relatively unexplored. Brown-like adipocytes (beige adipocytes) are characterized by a high concentration of mitochondria and high expression of uncoupling protein 1 (UCP1), which has specific functions in energy expenditure and thermogenesis. This study assessed the browning effects of sinapic acid in 3T3-L1 adipocytes. We investigated the expression of beige marker genes in 3T3-L1 adipocytes treated with sinapic acid. Sinapic acid increased the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and UCP1. Sinapic acid also promoted mitochondrial biogenesis by dose-dependently upregulating the oxygen consumption rate and enhancing the expression of representative subunits of oxidative phosphorylation complexes. In addition, treatment with p38 mitogen-activated protein kinase (MAPK) inhibitor and cAMP response element binding (CREB) inhibitor decreased the expressions of genes associated with thermogenesis, mitochondrial biogenesis, and oxidative phosphorylation. In summary, sinapic acid initiates browning 3T3-L1 adipocytes via the p38 MAPK/CREB signaling pathway. Thus, sinapic acid may have potential therapeutic implication in obesity.

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Ultrastructural changes in murine lymphoma cells exposed to ultraviolet-A radiation

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s042482010008482x ◽

1991 ◽

Vol 49 ◽

pp. 104-105

Author(s):

Delma P. Thomas ◽

Dianne E. Godar

Keyword(s):

Medical Devices ◽

Blood Cells ◽

White Blood Cells ◽

Consumer Products ◽

Ultrastructural Changes ◽

Ultraviolet A ◽

Uv Spectrum ◽

Lymphoma Cells ◽

Murine Lymphoma ◽

Transmission Electron

Ultraviolet radiation (UVR) from all three waveband regions of the UV spectrum, UVA (320-400 nm), UVB (290-320 nm), and UVC (200-290 nm), can be emitted by some medical devices and consumer products. Sunlamps can expose the blood to a considerable amount of UVR, particularly UVA and/or UVB. The percent transmission of each waveband through the epidermis to the dermis, which contains blood, increases in the order of increasing wavelength: UVC (10%) < UVB (20%) < UVA (30%). To investigate the effects of UVR on white blood cells, we chose transmission electron microscopy to examine the ultrastructure changes in L5178Y-R murine lymphoma cells.

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