Inhibition of p38 mitogen activated protein kinase increases lipopolysaccharide induced inhibition of apoptosis in neutrophils by activating extracellular signal-regulated kinase

Sheth, Ketan; Friel, John C.; Nolan, Brian; Bankey, Paul E.

doi:10.1067/msy.2001.115902

Cited by 53 publications

(45 citation statements)

References 20 publications

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“…3A). A similar augmentation of ERK activity by SB203580 has been reported (44) in human neutrophils stimulated with lipopolysaccharide. Likewise, SB203580 has been shown to potentiate the induction of c-fos and c-jun by both EGF and TPA (45).…”

Section: Discussionsupporting

confidence: 54%

Tumor Promoter Arsenite Stimulates Histone H3 Phosphoacetylation of Proto-oncogenes c-fos and c-jun Chromatin in Human Diploid Fibroblasts

Gorospe

Barnes

et al. 2003

Journal of Biological Chemistry

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Although epidemiological studies have long established that inorganic arsenic is a potent human carcinogen, the underlying mechanisms are still poorly understood. Recent studies suggest that inorganic arsenic may act as a tumor promoter by perturbing key signaling transduction pathways. We have shown previously that arsenite can potently activate the mitogen-activated protein kinase cascades and induce the expression of proliferation-associated genes, including protooncogenes c-jun and c-fos. In order to elucidate further the molecular mechanisms underlying its tumor-promoting properties, we investigated the signaling events involved in arsenite-mediated induction of c-fos and cjun. We found that induction of both c-fos and c-jun by arsenite can be substantially inhibited by the MEKselective inhibitor U0126, suggesting that the ERK pathway is critically involved in their up-regulation. Interestingly, arsenite dramatically induced the phosphorylation and acetylation of histone H3 preceding the induction of mRNAs encoding c-fos and c-jun. Finally, chromatin immunoprecipitation assays revealed that arsenite treatment markedly induced the phosphorylation/acetylation of histone H3 associated with the c-fos and c-jun genes through an ERK-dependent pathway. Our results strongly suggest that arsenic-triggered alterations in chromatin structure perturb specific gene transcription, including that of proto-oncogenes c-jun and c-fos, and may thereby contribute to the carcinogenic process.

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Section: Discussionsupporting

confidence: 54%

Tumor Promoter Arsenite Stimulates Histone H3 Phosphoacetylation of Proto-oncogenes c-fos and c-jun Chromatin in Human Diploid Fibroblasts

Gorospe

Barnes

et al. 2003

Journal of Biological Chemistry

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“…ERK and P38 have been recently reported to be involved in cancer cell death induced by anti-cancer reagents [23]. Once activated, ERK plays an important role in anti-apoptotic activity, while JNK and p38 are important for pro-apoptotic activity [24]. Our results showed that didymin treatment decreased the phosphorylations of MEK and ERK, but increased the phosphorylations of JNK and p38, suggesting that the MAPK signaling pathway is involved in didymin-induced apoptosis.…”

Section: Discussionsupporting

confidence: 31%

Didymin Alleviates Hepatic Fibrosis Through Inhibiting ERK and PI3K/Akt Pathways via Regulation of Raf Kinase Inhibitor Protein

Lin

Bai

Nie

et al. 2016

Cell Physiol Biochem

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Background: Didymin has been reported to have anti-cancer potential. However, the effect of didymin on liver fibrosis remains illdefined. Methods: Hepatic fibrosis was induced by CCl₄ in rats. The effects of didymin on liver pathology and collagen accumulation were observed by hematoxylin-eosin and Masson's trichrome staining, respectively. Serum transaminases activities and collagen-related indicators levels were determined by commercially available kits. Moreover, the effects of didymin on hepatic stellate cell apoptosis and cell cycle were analyzed by flow cytometry. Mitochondrial membrane potential was detected by using rhodamine-123 dye. The expression of Raf kinase inhibitor protein (RKIP) and the phosphorylation of the ERK/MAPK and PI3K/Akt pathways were assessed by Western blot. Results: Didymin significantly ameliorated chronic liver injury and collagen deposition. It strongly inhibited hepatic stellate cells proliferation, induced apoptosis and caused cell cycle arrest in G2/M phase. Moreover, didymin notably attenuated mitochondrial membrane potential, accompanied by release of cytochrome C. Didymin significantly inhibited the ERK/MAPK and PI3K/Akt pathways. The effects of didymin on the collagen accumulation in rats and on the biological behaviors of hepatic stellate cells were largely abolished by the specific RKIP inhibitor locostatin. Conclusion: Didymin alleviates hepatic fibrosis by inhibiting ERK/MAPK and PI3K/Akt pathways via regulation of RKIP expression.

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“…Another pathway that emerges after tyrosine phosphorylation of the IGF1R involves the activation of MAPK3 and MAPK1, through the recruitment of Grb2 and subsequent activation of ras, raf, and MEK. Although it has been established that the PI3K is an important player in regulating neutrophil apoptosis (Cowburn et al 2002, Yang et al 2003, the MEK-MAPK1 pathway has also been implicated in this process (Klein et al 2001, Sheth et al 2001, Gardai et al 2004, Kooijman 2006. We therefore established the effects of IGF1 in the presence of the MEK inhibitor U0126 and the PI3K inhibitor wortmannin.…”

Section: Discussionmentioning

confidence: 99%

Insulin-like growth factor-1 delays Fas-mediated apoptosis in human neutrophils through the phosphatidylinositol-3 kinase pathway

Himpe

Degaillier²,

Coppens³

et al. 2008

Journal of Endocrinology

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Apoptosis of human neutrophils is a crucial mechanism for the resolution of inflammation. We previously showed that insulinlike growth factor-1 (IGF1) delays spontaneous neutrophil apoptosis without influencing the secretion of cytokines by these cells. In the present study, we further addressed the role of IGF1 in regulating neutrophil survival in the presence of other factors present during inflammation, and the mechanism involved in delaying apoptosis. We show that IGF1 delays neutrophil apoptosis triggered by the agonistic anti-Fas antibody CH11 and that the effect of IGF1 is comparable in magnitude to that of the acknowledged anti-apoptotic cytokines interferon-g (IFNG) and granulocyte-macrophage colony-stimulating factor (GM-CSF; now known as CSF2). Furthermore, IGF1 exerted additional effects on cell survival in the presence of these cytokines. IGF1 did not affect Fas expression or activation by anti-Fas of caspase-8, but inhibited the depolarization of the mitochondrial membrane. Inhibitor studies indicate that the phosphatidylinositol-3 kinase (PI3K) pathway, but not the MEK-ERK pathway, mediates the effects of IGF1. However, in contrast to CSF2, IGF1 did not induce phosphorylation and translocation to the membrane of AKT, the canonical downstream target of PI3K. We therefore speculate that other downstream targets of PI3K are involved in the delay of neutrophil apoptosis by IGF1, possibly through stabilization of the mitochondrial membrane.

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Inhibition of p38 mitogen activated protein kinase increases lipopolysaccharide induced inhibition of apoptosis in neutrophils by activating extracellular signal-regulated kinase

Cited by 53 publications

References 20 publications

Tumor Promoter Arsenite Stimulates Histone H3 Phosphoacetylation of Proto-oncogenes c-fos and c-jun Chromatin in Human Diploid Fibroblasts

Tumor Promoter Arsenite Stimulates Histone H3 Phosphoacetylation of Proto-oncogenes c-fos and c-jun Chromatin in Human Diploid Fibroblasts

Didymin Alleviates Hepatic Fibrosis Through Inhibiting ERK and PI3K/Akt Pathways via Regulation of Raf Kinase Inhibitor Protein

Insulin-like growth factor-1 delays Fas-mediated apoptosis in human neutrophils through the phosphatidylinositol-3 kinase pathway

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