JNK Pathway Signaling: A Novel and Smarter Therapeutic Target for Various Biological Diseases

Kumar, Ankit; Singh, Umesh Kumar; Kini, Suvarna G.; Garg, Vikas; Agrawal, Sanjay; Tomar, Praveen Kumar; Pathak, Prateek; Chaudhary, Anurag; Gupta, Pratibha; Malik, Amrita

doi:10.4155/fmc.15.132

Cited by 163 publications

(114 citation statements)

References 72 publications

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“…There is no evidence for a role of JNK in adipocyte differentiation, although it is clear that JNK1 decreases insulin sensitivity of the cells by phosphorylation of insulin receptor substrate (IRS)-1 [66]. However, the increased activation of JNK1/2 in mature adipocytes, as defined in this study, might be a marker of the elevated inflammatory response of the cells, as JNK1/2 regulates inflammatory processes and is associated with a variety of inflammatory diseases [67]. …”

Section: Discussionmentioning

confidence: 91%

Anti-Inflammatory Effects of Rosiglitazone in Obesity-Impaired Wound Healing Depend on Adipocyte Differentiation

et al. 2016

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Combined diabetes-obesity syndromes severely impair regeneration of acute skin wounds in mouse models. This study assessed the contribution of subcutaneous adipose tissue to exacerbated wound inflammatory conditions. Genetically obese (ob/ob) mice showed an increased expression of positive transcriptional effectors of adipocyte differentiation such as Krüppel-like factor (KLF)-5 and peroxisome proliferator-activated receptor (PPAR)-γ and an associated expression of leptin and fatty acid-binding protein (FABP)-4, but also CXCL2 in isolated subcutaneous fat. This observation in obese mice is in keeping with differentially elevated levels of KLF-5, PPAR-γ, leptin, FABP-4 and CXCL2 in in vitro-differentiated 3T3-L1 adipocytes. Notably, CXCL2 expression restrictively appeared upon cytokine (IL-1β/TNF-α) stimulation only in mature, but not immature 3T3-L1 adipocytes. Of importance, the critical regulator of adipocyte maturation, PPAR-γ, was merely expressed in the final phase of in-vitro induced adipocyte differentiation from 3T3-L1 pre-adipocytes. Consistently, the PPAR-γ agonist rosiglitazone suppressed cytokine-induced CXCL2 release from mature adipocytes, but not from early 3T3-L1 adipocyte stages. The inhibitory effect of PPAR-γ activation on CXCL2 release appeared to be a general anti-inflammatory effect in mature adipocytes, as cytokine-induced cyclooxygenase (Cox)-2 was simultaneously repressed by rosiglitazone. In accordance with these findings, oral administration of rosiglitazone to wounded obese mice significantly changed subcutaneous adipocyte morphology, reduced wound CXCL2 and Cox-2 expression and improved tissue regeneration. Thus, our data suggest that PPAR-γ might provide a target to suppress inflammatory signals from mature adipocytes, which add to the prolonged wound inflammation observed in diabetes-obesity conditions.

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Section: Discussionmentioning

confidence: 91%

Anti-Inflammatory Effects of Rosiglitazone in Obesity-Impaired Wound Healing Depend on Adipocyte Differentiation

et al. 2016

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“…34,35 Deregulation of JNK and p38MAPK is associated with various human diseases, including IHD. 34,35 Deregulation of JNK and p38MAPK is associated with various human diseases, including IHD.…”

Section: Discussionmentioning

confidence: 99%

Retracted: LncRNA‐LET relieves hypoxia‐induced injury in H9c2 cells through regulation of miR‐138

Zhang

et al. 2019

J of Cellular Biochemistry

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Ischemic heart disease (IHD) is a common cardiovascular disease, occurs when coronary artery blood circularity cannot match with the heart's need. The present work attempted to study the effects of long noncoding RNA (lncRNA) low expression in tumor (LET) on the progression of IHD. H9c2 cells were injured by hypoxia to mimic a cell model of IHD. The effects of lncRNA‐LET on hypoxia‐injured H9c2 cells were tested by using cell counting kit‐8 assay, flow cytometry, and Western blot analysis. MicroRNA‐138 (miR‐138) expression was tested by a quantitative real‐time polymerase chain reaction, and the expression of c‐Jun N‐terminal kinase (JNK) and p38MAPK (p38–mitogen‐activated protein kinase) proteins was measured by Western blot analysis. We found that hypoxia exposure significantly repressed the viability of H9c2 cells, and induced apoptosis. Meanwhile, phosphorylation of JNK and p38MAPK was enhanced by hypoxia. The expression of lncRNA‐LET was repressed by hypoxia. Overexpression of lncRNA‐LET attenuated hypoxia‐induced injury in H9c2 cells. Moreover, miR‐138 was a downstream effector of lncRNA‐LET, that miR‐138 was highly expressed in lncRNA‐LET‐overexpressed cell. The cardioprotective effects of lncRNA‐LET were abolished when miR‐138 was silenced. In conclusion, this study revealed the cardioprotective function of lncRNA‐LET. lncRNA‐LET conferred its cardioprotective effects possibly via upregulation of miR‐138 and thus repressing the JNK and p38MAPK pathways.

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“…Recent studies have suggested JNK signaling pathway plays important roles in many cellular events, such as regulating cell cycle, cell apoptosis and autophagy (19,20). To further elucidate the effect of Andro on JNK signal pathway, we measured the expression of JNK an p-P38 genes.…”

Section: Andro Induces Apoptosis In Melanoma Cell Linesmentioning

confidence: 99%

“…Inhibition of cell proliferation by Andro was detected using the 3-(4,5-dimethylthiazole-2-yl)-2,5-biphenyl tetrazolium bromide (MTT) assay. Briefly, cells were trypsinized and plated into 96-well plate at a density of 5x10 3 cells/well and incubated overnight at 37˚C in a humidified incubator, then treated with fresh medium containing various concentration of Andro (5,10,20,40, and 80 µM). And the cells were incubated for 24, 48 h. Subsequently, final concentration of 0.5 mg/ml MTT was added directly to and incubated for 4 h at 37˚C.…”

Section: Cells and Reagentsmentioning

confidence: 99%

Andrographolide inhibits proliferation and induces cell cycle arrest and apoptosis in human melanoma cells

Chu

2018

Oncol Lett

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JNK Pathway Signaling: A Novel and Smarter Therapeutic Target for Various Biological Diseases

Cited by 163 publications

References 72 publications

Anti-Inflammatory Effects of Rosiglitazone in Obesity-Impaired Wound Healing Depend on Adipocyte Differentiation

Anti-Inflammatory Effects of Rosiglitazone in Obesity-Impaired Wound Healing Depend on Adipocyte Differentiation

Retracted: LncRNA‐LET relieves hypoxia‐induced injury in H9c2 cells through regulation of miR‐138

Andrographolide inhibits proliferation and induces cell cycle arrest and apoptosis in human melanoma cells

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