β‐carotene attenuates weaning‐induced apoptosis via inhibition of PERK‐CHOP and IRE1‐JNK/p38 MAPK signalling pathways in piglet jejunum

2019 ◽  
Vol 104 (1) ◽  
pp. 280-290 ◽  
Author(s):  
Ruonan Li ◽  
Yu Yang ◽  
Pan Hong ◽  
Ziqi Zhang ◽  
Lingqian Li ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Signalling Pathways ◽  
Mapk Signalling ◽  
Induced Apoptosis ◽  
Β Carotene

scholarly journals Autophagy Plays a Protective Role in Advanced Glycation End Product-Induced Apoptosis in Cardiomyocytes

2015 ◽  
Vol 37 (2) ◽  
pp. 697-706 ◽  
Author(s):  
Pengfei Hu ◽  
Hui Zhou ◽  
Ming Lu ◽  
Liping Dou ◽  
Gang Bo ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Treated Group ◽  
Protective Role ◽  
Signalling Pathways ◽  
Control Group ◽  
Advanced Glycation ◽  
Rat Cardiomyocytes ◽  
Advanced Glycation End Product ◽  
Mapk Signalling ◽  
Induced Apoptosis

Background/Aims: To investigate the effect of advanced glycation endproduct-induced autophagy in rat cardiomyocytes and to identify the role of autophagy in advanced glycation end product-induced cell apoptosis. Methods: After cultured rat cardiomyocytes were treated with advanced glycation end products (AGEs), protein expression was detected by western blotting, autophagosomes were observed by electron microscopy, the cell apoptotic rate was determined by flow cytometry, and cell variability was quantified by the MTT assay. Results: After cultured cardiomyocytes were treated with AGEs, the level of autophagy-associated protein LC3-II was up-regulated and SQSTM1/p62 was down-regulated; the number of autophagosomes was increased. Compared with the control group, the apoptotic rate of cardiomyocytes increased, and the cardiomyocyte viability was decreased in the AGE-treated group. Furthermore, pretreating cells with3-MA, an autophagy inhibitor, could enhance these effects. Treatment with AGEs activated phospho-ERK, phospho-JNK, and phospho-p38/MAPK but inhibited phospho-Akt and phospho-mTOR. Pretreatment with an ERK inhibitor and an Akt activator could inhibit AGE-induced autophagy, demonstrating that AGEs induce autophagy in cardiomyocytes through the ERK and Akt signalling pathways. Conclusion: AGEs can induce autophagy through the PI3K/AKT/mTOR and ERK signalling pathways and induce apoptosis through the PI3K/AKT/mTOR and p38/MAPK signalling pathways in rat cardiomyocytes. Autophagy plays a protective role in AGE-induced apoptosis in cardiomyocytes.

scholarly journals trans-Cinnamic acid, but not p-coumaric acid or methyl cinnamate, induces fibroblast migration through PKA- and p38-MAPK signalling pathways

2021 ◽  
Author(s):  
Fernanda Lima Torres de Aquino ◽  
Juliane Pereira da Silva ◽  
Jamylle Nunes de Souza Ferro ◽  
Vincent Lagente ◽  
Emiliano Barreto
Keyword(s):  
P38 Mapk ◽  
Cinnamic Acid ◽  
Signalling Pathways ◽  
Coumaric Acid ◽  
Methyl Cinnamate ◽  
Fibroblast Migration ◽  
Mapk Signalling

scholarly journals The mechanism of TDP‐43 gene expression on inflammatory factors and the JNK and p38 MAPK signalling pathways in ischaemic hypoxic stress dependence

2019 ◽  
Vol 16 (3) ◽  
pp. 724-729 ◽  
Author(s):  
He Huang ◽  
Zhao‐Fei Zhang ◽  
Feng‐Wei Qin ◽  
Wang Tang ◽  
Dong‐Hua Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
P38 Mapk ◽  
Inflammatory Factors ◽  
Signalling Pathways ◽  
Hypoxic Stress ◽  
Stress Dependence ◽  
Mapk Signalling

Antagonistic roles of the ERK and p38 MAPK signalling pathways in globin expression, haem biosynthesis and iron uptake1

2010 ◽  
Vol 432 (1) ◽  
pp. 145-151 ◽  
Author(s):  
Louay Mardini ◽  
Jadwiga Gasiorek ◽  
Anna Derjuga ◽  
Lucie Carrière ◽  
Matthias Schranzhofer ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Iron Uptake ◽  
Mapk Pathway ◽  
Globin Gene ◽  
Erythroid Differentiation ◽  
Mitogen Activated Protein Kinase ◽  
Signalling Pathways ◽  
Erythroid Cells ◽  
Mapk Signalling ◽  
Haem Biosynthesis

Late-stage erythroid cells synthesize large quantities of haemoglobin, a process requiring the co-ordinated regulation of globin and haem synthesis as well as iron uptake. In the present study, we investigated the role of the ERK (extracellular-signal-regulated kinase) and p38 MAPK (mitogen-activated protein kinase) signalling pathways in MEL (mouse erythroleukaemia) cell differentiation. We found that treatment of HMBA (hexamethylene bisacetamide)-induced MEL cells with the ERK pathway inhibitor UO126 results in an increase in intracellular haem and haemoglobin levels. The transcript levels of the genes coding for βmajor-globin, the haem biosynthesis enzyme 5-aminolevulinate synthase 2 and the mitochondrial iron transporter mitoferrin 1 are up-regulated. We also showed enhanced expression of globin and transferrin receptor 1 proteins upon UO126 treatment. With respect to iron uptake, we found that ERK inhibitor treatment led to an increase in both haem-bound and total iron. In contrast, treatment of MEL cells with the p38 MAPK pathway inhibitor SB202190 had the opposite effect, resulting in decreased globin expression, haem synthesis and iron uptake. Reporter assays showed that globin promoter and HS2 enhancer-mediated transcription was under the control of MAPKs, as inhibition of the ERK and p38 MAPK pathways led to increased and decreased gene activity respectively. Our present results suggest that the ERK1/2 and p38α/β MAPKs play antagonistic roles in HMBA-induced globin gene expression and erythroid differentiation. These results provide a novel link between MAPK signalling and the regulation of haem biosynthesis and iron uptake in erythroid cells.

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