scholarly journals Arsenic acid inhibits proliferation of skin fibroblasts, and increases cellular senescence through ROS mediated MST1-FOXO signaling pathway

2016 ◽  
Vol 41 (1) ◽  
pp. 105-113 ◽  
Author(s):  
Yuya Yamaguchi ◽  
Harishkumar Madhyastha ◽  
Radha Madhyastha ◽  
Narantsog Choijookhuu ◽  
Yoshitaka Hishikawa ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cellular Senescence ◽  
Skin Fibroblasts ◽  
Arsenic Acid ◽  
Foxo Signaling Pathway

scholarly journals Gas6 Delays Senescence in Vascular Smooth Muscle Cells through the PI3K/ Akt/FoxO Signaling Pathway

2015 ◽  
Vol 35 (3) ◽  
pp. 1151-1166 ◽  
Author(s):  
Cheng-wei Jin ◽  
Hui Wang ◽  
Yan-qing Chen ◽  
Meng-xiong Tang ◽  
Guan-qi Fan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Vascular Smooth Muscle Cells ◽  
Cellular Senescence ◽  
Replicative Senescence ◽  
Muscle Cells ◽  
Specific Protein ◽  
Foxo Signaling Pathway

Background/Aims: Growth arrest-specific protein 6 (Gas6) is a cytokine that can be synthesized by a variety of cell types and secreted into the extracellular matrix. Previous studies have confirmed that Gas6 is involved in certain pathophysiological processes of the cardiovascular system through binding to its receptor, Axl. In the present study, we investigated the role of Gas6 in cellular senescence and explored the mechanisms underlying its activity. Methods: We used vascular smooth muscle cells (VSMCs) to create two cellular senescence models, one for replicative senescence (RS) and one for induced senescence (IS), to test the hypothesis that Gas6 delays senescence. Results: Gas6-treated cells appear relatively younger compared with non-Gas6-treated cells. In particular, Gas6-treated cells displayed decreased staining for SA-β-Gal, fewer G1 phase cells, and decreased levels of p16INK4a and p21Cip1 expression; conversely, Gas6-treated cells displayed more S phase cells and significantly increased proliferation indexes. Furthermore, in both the IS and RS models with Gas6 treatment, the levels of PI3K, p-Akt, and p-FoxO3a decreased following Axl inhibition by R428; similarly, the levels of p-Akt and p-FoxO3a also decreased following PI3K inhibition by LY294002. Conclusion: Gas6/Axl signaling is essential for delaying the cellular senescence process regulated by the PI3K/Akt/FoxO signaling pathway.

scholarly journals The Transplantation Resistance of Type II Diabetes Mellitus Adipose-Derived Stem Cells Is Due to G6PC and IGF1 Genes Related to the FoxO Signaling Pathway

2021 ◽  
Vol 22 (12) ◽  
pp. 6595
Author(s):  
Michiko Horiguchi ◽  
Yuya Turudome ◽  
Kentaro Ushijima
Keyword(s):  
Diabetes Mellitus ◽  
Stem Cells ◽  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Signaling Pathway ◽  
Cell Transplantation ◽  
Type Ii ◽  
Lower Performance ◽  
Foxo Signaling Pathway ◽  
Healthy Persons

In cases of patients with rapidly progressive diabetes mellitus (DM), autologous stem cell transplantation is considered as one of the regenerative treatments. However, whether the effects of autonomous stem cell transplantation on DM patients are equivalent to transplantation of stem cells derived from healthy persons is unclear. This study revealed that adipose-derived mesenchymal stem cells (ADSC) derived from type II DM patients had lower transplantation efficiency, proliferation potency, and stemness than those derived from healthy persons, leading to a tendency to induce apoptotic cell death. To address this issue, we conducted a cyclopedic mRNA analysis using a next-generation sequencer and identified G6PC3 and IGF1, genes related to the FoxO signaling pathway, as the genes responsible for lower performance. Moreover, it was demonstrated that the lower transplantation efficiency of ADSCs derived from type II DM patients might be improved by knocking down both G6PC3 and IGF1 genes. This study clarified the difference in transplantation efficiency between ADSCs derived from type II DM patients and those derived from healthy persons and the genes responsible for the lower performance of the former. These results can provide a new strategy for stabilizing the quality of stem cells and improving the therapeutic effects of regenerative treatments on autonomous stem cell transplantation in patients with DM.

scholarly journals Studies of the Anti-Diabetic Mechanism of Pueraria lobata Based on Metabolomics and Network Pharmacology

Processes ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 1245
Author(s):  
Shu Zhang ◽  
Qi Ge ◽  
Liang Chen ◽  
Keping Chen
Keyword(s):  
Signaling Pathway ◽  
Diabetes Complications ◽  
Mapk Signaling ◽  
Network Pharmacology ◽  
Pueraria Lobata ◽  
Insulin Deficiency ◽  
Active Ingredients ◽  
Foxo Signaling Pathway ◽  
Anti Inflammation

Diabetes mellitus (DM), as a chronic disease caused by insulin deficiency or using obstacles, is gradually becoming a principal worldwide health problem. Pueraria lobata is one of the traditional Chinese medicinal and edible plants, playing roles in improving the cardiovascular system, lowering blood sugar, anti-inflammation, anti-oxidation, and so on. Studies on the hypoglycemic effects of Pueraria lobata were also frequently reported. To determine the active ingredients and related targets of Pueraria lobata for DM, 256 metabolites were identified by LC/MS non targeted metabonomics, and 19 active ingredients interacting with 51 DM-related targets were screened. The results showed that puerarin, quercetin, genistein, daidzein, and other active ingredients in Pueraria lobata could participate in the AGE-RAGE signaling pathway, insulin resistance, HIF-1 signaling pathway, FoxO signaling pathway, and MAPK signaling pathway by acting on VEGFA, INS, INSR, IL-6, TNF and AKT1, and may regulate type 2 diabetes, inflammation, atherosis and diabetes complications, such as diabetic retinopathy, diabetic nephropathy, and diabetic cardiomyopathy.

scholarly journals Cellular senescence and senescence‐associated secretory phenotype via the cGAS‐STING signaling pathway in cancer

2019 ◽  
Vol 111 (2) ◽  
pp. 304-311 ◽  
Author(s):  
Tze Mun Loo ◽  
Kenichi Miyata ◽  
Yoko Tanaka ◽  
Akiko Takahashi
Keyword(s):  
Signaling Pathway ◽  
Cellular Senescence ◽  
Secretory Phenotype

Japanese encephalitis virus induces apoptosis by inhibiting Foxo signaling pathway

2018 ◽  
Vol 220 ◽  
pp. 73-82 ◽  
Author(s):  
Fenglin Guo ◽  
Xilan Yu ◽  
Ahui Xu ◽  
Jing Xu ◽  
Qianruo Wang ◽  
...  
Keyword(s):  
Japanese Encephalitis Virus ◽  
Signaling Pathway ◽  
Japanese Encephalitis ◽  
Encephalitis Virus ◽  
Foxo Signaling Pathway

Assessment of transcriptional activity genes associated with the IL‐17 signaling pathway in skin fibroblasts under the influence of adalimumab

2019 ◽  
Vol 32 (6) ◽  
Author(s):  
Beniamin Oskar Grabarek ◽  
Dominika Wcisło‐Dziadecka ◽  
Kinga Bednarek ◽  
Celina Kruszniewska‐Rajs ◽  
Joanna Gola
Keyword(s):  
Signaling Pathway ◽  
Transcriptional Activity ◽  
Skin Fibroblasts

scholarly journals Protective Effect of Pyropia yezoensis Peptide on Dexamethasone-Induced Myotube Atrophy in C2C12 Myotubes

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 284 ◽  
Author(s):  
Min-Kyeong Lee ◽  
Jeong-Wook Choi ◽  
Youn Hee Choi ◽  
Taek-Jeong Nam
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
C2c12 Myotubes ◽  
Protective Effects ◽  
Factor I ◽  
Igf I ◽  
Foxo Signaling Pathway

Dexamethasone (DEX), a synthetic glucocorticoid, causes skeletal muscle atrophy. This study examined the protective effects of Pyropia yezoensis peptide (PYP15) against DEX-induced myotube atrophy and its association with insulin-like growth factor-I (IGF-I) and the Akt/mammalian target of rapamycin (mTOR)-forkhead box O (FoxO) signaling pathway. To elucidate the molecular mechanisms underlying the effects of PYP15 on DEX-induced myotube atrophy, C2C12 myotubes were treated for 24 h with 100 μM DEX in the presence or absence of 500 ng/mL PYP15. Cell viability assays revealed no PYP15 toxicity in C2C12 myotubes. PYP15 activated the insulin-like growth factor-I receptor (IGF-IR) and Akt-mTORC1 signaling pathway in DEX-induced myotube atrophy. In addition, PYP15 markedly downregulated the nuclear translocation of transcription factors FoxO1 and FoxO3a, and inhibited 20S proteasome activity. Furthermore, PYP15 inhibited the autophagy-lysosomal pathway in DEX-stimulated myotube atrophy. Our findings suggest that PYP15 treatment protected against myotube atrophy by regulating IGF-I and the Akt-mTORC1-FoxO signaling pathway in skeletal muscle. Therefore, PYP15 treatment appears to exert protective effects against skeletal muscle atrophy.

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