scholarly journals Poly-L-Lactic Acid Increases Collagen Gene Expression and Synthesis in Cultured Dermal Fibroblast (Hs68) Through the p38 MAPK Pathway

2019 ◽  
Vol 31 (1) ◽  
pp. 97 ◽  
Author(s):  
Sung-Ae Kim ◽  
Hyo-Seon Kim ◽  
Jin-Woong Jung ◽  
Sung-Il Suh ◽  
Young-Wook Ryoo
Keyword(s):  
Gene Expression ◽  
Lactic Acid ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Dermal Fibroblast ◽  
Collagen Gene ◽  
Collagen Gene Expression ◽  
P38 Mapk Pathway

scholarly journals Activin Inhibits the Human Pit-1 Gene Promoter through the p38 Kinase Pathway in a Smad-Independent Manner

Endocrinology ◽  
2006 ◽  
Vol 147 (9) ◽  
pp. 4351-4362 ◽  
Author(s):  
Chantal de Guise ◽  
Annie Lacerte ◽  
Shahrzad Rafiei ◽  
Rachel Reynaud ◽  
Melanie Roy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pituitary Gland ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Critical Role ◽  
Gene Promoter ◽  
Negative Regulator ◽  
P38 Kinase ◽  
P38 Mapk Pathway ◽  
Lactotrope Cells

The pituitary transcription factor Pit-1 regulates hormonal production from the anterior pituitary gland. However, the mechanisms by which Pit-1 gene expression is regulated in humans are poorly understood. Activin, a member of the TGFβ superfamily, acts as a negative regulator of cell growth and prolactin gene expression in lactotrope cells. In this study, we show that activin negatively regulates the human Pit-1 gene promoter. We defined a 117-bp element within the Pit-1 promoter that is sufficient to relay these inhibitory effects. We further investigated the signaling pathways that mediate activin-induced inhibition of Pit-1 gene promoter in pituitary lactotrope cells. We found that the activin effects on Pit-1 gene regulation are Smad independent and require the p38 MAPK pathway. Specifically, blocking p38 kinase activity reverses activin-mediated inhibition of the Pit-1 gene promoter. Together, our results highlight the p38 MAPK pathway as a key regulator of activin function in pituitary lactotrope cells and further emphasizes the critical role played by activin in regulating hormonal production in the pituitary gland.

Irisin recovers osteoarthritic chondrocytes: a muscle-cartilage cross-talk boosted by physical activity

2020 ◽  
Author(s):  
Gianluca Vadalà ◽  
Giuseppina Di Giacomo ◽  
Luca Ambrosio ◽  
Francesca Cannata ◽  
Claudia Cicione ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Western Blot ◽  
P38 Mapk ◽  
Collagen Gene ◽  
Type Ii ◽  
Protein Levels ◽  
Collagen Gene Expression ◽  
Osteoarthritic Chondrocytes

Abstract Background Physical exercise favors weight loss and ameliorates both articular pain and function in patients suffering from osteoarthritis (OA). Irisin, a myokine released by skeletal muscles upon muscle contraction, has demonstrated to yield anabolic effects on different cell types. The study aimed to investigate the effect of irisin on human osteoarthritic chondrocytes (hOAC) in vitro . The hypothesis of this study was that irisin would improve hOAC metabolism and proliferation. Methods hOAC were isolated from osteochondral tissues of 5 patients undergoing total knee joint replacement. Cells were cultured in growing media and then exposed to either phosphate-buffered saline (control group) or human recombinant irisin (experimental group). Cell proliferation (Picogreen assay), glycosaminoglycan content (dimethylmethylene blue), type II/X collagen gene expression (Real-Time polymerase chain reaction) and quantification (Western blot and densitometric analysis), p38/ERK MAPK and Akt involvement (Western blot and densitometric analysis) were evaluated in both groups. Results Irisin increased hOAC proliferation ( p < 0.001) and both type II collagen gene expression ( p < 0.001) and protein levels ( p < 0.01), while decreased type X collagen gene expression ( p < 0.05) and protein levels ( p < 0.001). These effects seemed to be mediated by the inactivation of the p38 MAPK and PI3K-Akt intracellular pathways, as irisin reduced phosphorylated p38 (p-p38), ( p < 0.01) and phosphorylated Akt (p-Akt) ( p < 0.001) protein levels. Conclusion Irisin stimulated cell proliferation and anabolism in hOAC through p38 MAPK and PI3K-Akt inactivation in vitro , demonstrating for the first time the existence of a cross-talk between muscle and cartilage.

scholarly journals Aquaporin-3 Attenuates Oxidative Stress-Induced Nucleus Pulposus Cell Apoptosis Through Regulating the P38 MAPK Pathway

2018 ◽  
Vol 50 (5) ◽  
pp. 1687-1697 ◽  
Author(s):  
Yichun Xu ◽  
Hui Yao ◽  
Qiyou Wang ◽  
Wenbin Xu ◽  
Kaihua Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Oxidative Damage ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Aquaporin 3 ◽  
P38 Mapk Pathway ◽  
Intracellular Ros ◽  
Cellular Apoptosis

Background/Aims: Previous studies have shown that oxidative damage is a main contributor to disc nucleus pulposus (NP) cell apoptosis. Aquaporin-3 (AQP-3) facilitates reactive oxygen species (ROS) scavenging and thus alleviates oxidative injury in other cells. This study aims to investigate the role and mechanism of AQP-3 in regulating NP cell apoptosis under oxidative damage. Methods: Rat NP cells were treated with H2O2 for 48 hours, while control NP cells were free of H2O2. Recombinant AQP-3 lentiviral vectors were used to investigate the effect of enhanced AQP-3 expression levels in NP cells. NP cell apoptosis was assessed by flow cytometry, caspase-3 activity, gene expression of apoptosis-related molecules (Bax, Bcl-2 and caspase-3), and protein expression of cellular apoptosis markers (cleaved PARP and cleaved caspase-3). Additionally, intracellular ROS content and activity of the p38 MAPK pathway were evaluated. Results: Compared with the control NP cells, oxidative damage in the treatment cells significantly increased cell apoptosis ratios and caspase-3 activity, upregulated gene expression of Bax and caspase-3, downregulated gene expression of Bcl-2, and increased protein expression of cleaved PARP and cleaved caspase-3, as well as increased intracellular ROS content and activity of the p38 MAPK pathway. However, AQP-3 overexpression partly alleviated cell apoptosis, decreased intracellular ROS content, and inhibited the p38 MAPK pathway in NP cells under oxidative damage. Conclusion: Oxidative damage can significantly downregulate AQP-3 expression. Enhancing AQP-3 expression in NP cells partly attenuates cellular apoptosis through regulating the p38 MAPK pathway under oxidative damage.

scholarly journals Polyunsaturated fatty acids and p38-MAPK link metabolic reprogramming to cytoprotective gene expression during dietary restriction

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Manish Chamoli ◽  
Anita Goyala ◽  
Syed Shamsh Tabrez ◽  
Atif Ahmed Siddiqui ◽  
Anupama Singh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Life Span ◽  
P38 Mapk ◽  
Dietary Restriction ◽  
Mapk Pathway ◽  
Metabolic Reprogramming ◽  
Metabolic State ◽  
P38 Mapk Pathway

Abstract The metabolic state of an organism instructs gene expression modalities, leading to changes in complex life history traits, such as longevity. Dietary restriction (DR), which positively affects health and life span across species, leads to metabolic reprogramming that enhances utilisation of fatty acids for energy generation. One direct consequence of this metabolic shift is the upregulation of cytoprotective (CyTP) genes categorized in the Gene Ontology (GO) term of “Xenobiotic Detoxification Program” (XDP). How an organism senses metabolic changes during nutritional stress to alter gene expression programs is less known. Here, using a genetic model of DR, we show that the levels of polyunsaturated fatty acids (PUFAs), especially linoleic acid (LA) and eicosapentaenoic acid (EPA), are increased following DR and these PUFAs are able to activate the CyTP genes. This activation of CyTP genes is mediated by the conserved p38 mitogen-activated protein kinase (p38-MAPK) pathway. Consequently, genes of the PUFA biosynthesis and p38-MAPK pathway are required for multiple paradigms of DR-mediated longevity, suggesting conservation of mechanism. Thus, our study shows that PUFAs and p38-MAPK pathway function downstream of DR to help communicate the metabolic state of an organism to regulate expression of CyTP genes, ensuring extended life span.

scholarly journals Research on Roles of Mongolian Medical Warm Acupuncture in Inhibiting p38 MAPK Activation and Apoptosis of Nucleus Pulposus Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Sha Li ◽  
Lidao Bao ◽  
Lengge Si ◽  
Xiaohui Wang ◽  
Agula Bo
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Nucleus Pulposus ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Active Oxygen ◽  
Nucleus Pulposus Cells ◽  
P38 Mapk Pathway

Background. Mongolian medical warm acupuncture has a desirable therapeutic effect on sciatica. Apoptosis of the nucleus pulposus cells is considered to play an important role in sciatica. Evidence has demonstrated that oxidative stress and its induced activation of the signaling pathways play important roles in sciatica. However, further research is expected to reveal whether Mongolian medical warm acupuncture can inhibit the apoptosis of nucleus pulposus cells and oxidative stress. Objective. To study the effect of the p38 MAPK pathway activated by the generated ROS on apoptosis and the expression of the genes related to the balance of the extracellular matrix metabolism during treatment of sciatica with Mongolian medical warm acupuncture. Method. The volume of the active oxygen generated in the nucleus pulposus cells was detected following intervention of Mongolian medical warm acupuncture. The p38 MAPK phosphorylation level was detected with Western blot. The genes are related to the metabolism of the nucleus pulposus extracellular matrix. Result. Mongolian medical warm acupuncture reduced the active oxygen within the nucleus pulposus cells and inhibited the activation of the p38 MAPK pathway (P=0.013). Meanwhile, it upregulated the gene expression of Type II collagen, aggrecan, Sox-9, and tissue matrix metalloproteinase reagent 1 (P-0.015; P=0.025; P=0.031; P=0.045) and downregulated the gene expression of matrix metalloproteinase 3 (P=0.015). Conclusion. Mongolian medical warm acupuncture may inhibit apoptosis of nucleus pulposus cells and activation of the extracellular matrix decomposition metabolism pathway and promote its anabolism. This process may rely on the oxidative stress matrix of the p38 MAPK pathway.

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