scholarly journals Cigarette Smoking Exposure Alters Pebp1 DNA Methylation and Protein Profile Involved in MAPK Signaling Pathway in Mice Testis1

2013 ◽  
Vol 89 (6) ◽  
Author(s):  
Wangjie Xu ◽  
Peng Fang ◽  
Zijue Zhu ◽  
Jingbo Dai ◽  
Dongsheng Nie ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cigarette Smoking ◽  
Signaling Pathway ◽  
Protein Profile ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Smoking Exposure ◽  
Cigarette Smoking Exposure

Characterization of Methylation Patterns in Diffuse Large B Cell Lymphoma By Genome-Wide Methylation Analysis

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 1243-1243
Author(s):  
Fengyi Zhao ◽  
Lei Zhang ◽  
Yan Qin ◽  
Ming-Zhe Han ◽  
Xiaohong Han ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Signaling Pathway ◽  
Methylation Level ◽  
Enrichment Analysis ◽  
B Cell Lymphoma ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Pathway Enrichment Analysis ◽  
Ffpe Tissues ◽  
Methylation Patterns

Background: Diffuse large B cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma worldwide. Although the reference standard for identifying of the cell types is considered of gene expression profiling (GEP). But immunohistochemistry (IHC) is the most common method commercially available. The purpose of this study was to characterize the circulating cell-free DNA (cfDNA) methylation profile in DLBCL and to compare this profile with methylation observed in formalin fixed paraffin-embedded (FFPE) tissues. Additional efforts were made to correlate the observed methylation patterns with prognostic analysis and selected clinical features. Methods: The cfDNA and DNA of FFPE were extracted from 72 patients and 39 patients respectively. We assessed DNA methylation from plasma samples obtained from 29 individuals with GCB DLBCL at the time before treatment along with 43 samples of non-GCB DLBCL as controls. DNA from FFPE tissues were extracted from 11 individuals of GCB DLBCL and 28 individuals with non-GCB DLBCL. DNA methylation was analyzed with the Infinium MethylationEPIC BeadChip that quantitatively measures the methylation levels of more than 850,000 CpG sites across the genome. M values were used for visualization and intuitive interpretation of the results. Moreover, pathway enrichment analysis was performed with the Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway Database. Results: We found a total of 207 significant differentional differentially methylated positions (DMPs) of cfDNA between the GCB and non-GCB groups, identified with a p value of 0.001 (Fig. 1A). Of these, 65 presented at least 10% (|Δbeta| > 0.1) difference in the methylation level between GCB and non-GCB. 29 (44.6%) were found hypermethylated in GCB DLBCL, while 36 (55.4%) appeared hypomethylated (Fig. 1B). The distribution of the DMPs identified according to their location relative to CpG islands (CGI) were represented in Fig. 1C. Unsupervised clustering performed on DNA methylation values for the 207 DMPs identified is presented in Fig. 1D. These results highlight the differences between GCB and non-GCB samples. There are 1549 significant DMPs of DNA from FFPE between the GCB and non-GCB groups, identified with a p value of 0.001 (Fig. 1E). Of these, 1512 presented at least 10% (|Δbeta| > 0.1) difference in the methylation level between GCB and non-GCB . 1370 (90.6%) were found hypermethylated in GCB DLBCL, while 142 (9.4%) appeared hypomethylated (Fig. 1F). The distribution of the DMPs identified according to their location relative to CpG islands (CGI) were represented in Fig. 1G. Unsupervised clustering performed on DNA methylation values for the 1549 DMPs identified is presented in Fig. 1H. These results highlight the differences between GCB and non-GCB in FFPE samples which according with that in serum. The KEGG pathway enrichment analysis of DNA from FFPE tissue methylation revealed that the process "PI3K/Akt, Ras, MAPK signaling pathway" and "Human papillomavirus infection" are likely major contributors to Hans pathological type. In addition, the enrichment analysis of cfDNA methylation revealed that the process "MAPK signaling pathway" is likely the most important factor. Furthermore, we also have analyzed the methylation level between refractory or relapsed (R/R) DLBCL patients and individuals with a good prognosis. The differential methylation patterns were also found both in serums and FFPE tissues. Conclusions: The DNA methylation differs in GCB and non-GCB DLBCL patients. MAPK signaling pathway plays an important role in it. The mechanism needs to be further explored. Figure 1 Disclosures No relevant conflicts of interest to declare.

MAPK: A Key Player in the Development and Progression of Stroke

2020 ◽  
Vol 19 (4) ◽  
pp. 248-256
Author(s):  
Yangmin Zheng ◽  
Ziping Han ◽  
Haiping Zhao ◽  
Yumin Luo
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Complex Disease ◽  
Therapeutic Targets ◽  
Cell Types ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Effective Prevention ◽  
Prevention And Treatment ◽  
Different Cell Types

Conclusion: Stroke is a complex disease caused by genetic and environmental factors, and its etiological mechanism has not been fully clarified yet, which brings great challenges to its effective prevention and treatment. MAPK signaling pathway regulates gene expression of eukaryotic cells and basic cellular processes such as cell proliferation, differentiation, migration, metabolism and apoptosis, which are considered as therapeutic targets for many diseases. Up to now, mounting evidence has shown that MAPK signaling pathway is involved in the pathogenesis and development of ischemic stroke. However, the upstream kinase and downstream kinase of MAPK signaling pathway are complex and the influencing factors are numerous, the exact role of MAPK signaling pathway in the pathogenesis of ischemic stroke has not been fully elucidated. MAPK signaling molecules in different cell types in the brain respond variously after stroke injury, therefore, the present review article is committed to summarizing the pathological process of different cell types participating in stroke, discussed the mechanism of MAPK participating in stroke. We further elucidated that MAPK signaling pathway molecules can be used as therapeutic targets for stroke, thus promoting the prevention and treatment of stroke.

scholarly journals STAMBP promotes lung adenocarcinoma metastasis by regulating the EGFR/MAPK signaling pathway

Neoplasia ◽  
2021 ◽  
Vol 23 (6) ◽  
pp. 607-623
Author(s):  
Hui Xu ◽  
Xiaomei Yang ◽  
Xiaofeng Xuan ◽  
Di Wu ◽  
Jieru Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway

Caffeine suppresses the progression of human glioblastoma via cathepsin B and MAPK signaling pathway

2016 ◽  
Vol 33 ◽  
pp. 63-72 ◽  
Author(s):  
Yu-Chen Cheng ◽  
You-Ming Ding ◽  
Dueng-Yuan Hueng ◽  
Jang-Yi Chen ◽  
Ying Chen
Keyword(s):  
Signaling Pathway ◽  
Cathepsin B ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Human Glioblastoma

Involvement of the p38 MAPK signaling pathway in S-phase cell-cycle arrest induced by Furazolidone in human hepatoma G2 cells

2012 ◽  
Vol 33 (12) ◽  
pp. 1500-1505 ◽  
Author(s):  
Yu Sun ◽  
Shusheng Tang ◽  
Xi Jin ◽  
Chaoming Zhang ◽  
Wenxia Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
S Phase ◽  
Mapk Signaling Pathway ◽  
Phase Cell ◽  
Human Hepatoma ◽  
Cycle Arrest

scholarly journals EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mian Wang ◽  
Hua Zhong ◽  
Xian Zhang ◽  
Xin Huang ◽  
Jing Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Weight Ratio ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Protective Mechanism ◽  
High Morbidity ◽  
Inflammatory Factor ◽  
Egcg Treatment

AbstractAcute lung injury (ALI), which could be induced by multiple factors such as lipopolysaccharide (LPS), refer to clinical symptoms of acute respiratory failure, commonly with high morbidity and mortality. Reportedly, active ingredients from green tea have anti-inflammatory and anticancer properties, including epigallocatechin-3-gallate (EGCG). In the present study, protein kinase C alpha (PRKCA) is involved in EGCG protection against LPS-induced inflammation and ALI. EGCG treatment attenuated LPS-stimulated ALI in mice as manifested as improved lung injury scores, decreased total cell amounts, neutrophil amounts and macrophage amounts, inhibited the activity of MPO, decreased wet-to-dry weight ratio of lung tissues, and inhibited release of inflammatory cytokines TNF-α, IL-1β, and IL-6. PRKCA mRNA and protein expression showed to be dramatically decreased by LPS treatment while reversed by EGCG treatment. Within LPS-stimulated ALI mice, PRKCA silencing further aggravated, while PRKCA overexpression attenuated LPS-stimulated inflammation and ALI through MAPK signaling pathway. PRKCA silencing attenuated EGCG protection. Within LPS-induced RAW 264.7 macrophages, EGCG could induce PRKCA expression. Single EGCG treatment or Lv-PRKCA infection attenuated LPS-induced increases in inflammatory factors; PRKCA silencing could reverse the suppressive effects of EGCG upon LPS-stimulated inflammatory factor release. In conclusion, EGCG pretreatment inhibits LPS-induced ALI in mice. The protective mechanism might be associated with the inhibitory effects of PRKCA on proinflammatory cytokine release via macrophages and MAPK signaling pathway.

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