Involvement of PI3K/Akt and p38 MAPK in the induction of COX-2 expression by bacterial lipopolysaccharide in murine adrenocortical cells

Mercau, María Elisa; Astort, Francisco; Giordanino, Elián F.; Calejman, Camila Martínez; Sánchez, Rocío; Caldareri, Lilian Julia; Repetto, Esteban Martín; Coso, Omar A.; Cymeryng, Cora

doi:10.1016/j.mce.2014.01.007

Cited by 30 publications

(20 citation statements)

References 59 publications

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“…Effect of TCA-induced ERK1/2 and Akt Activation on COX-2 Expression-It has been well documented that COX-2 expression is regulated by ERK1/2 and Akt in various cell types (8,(35)(36)(37)(38). To further delineate the role of S1PR2-mediated ERK1/2 and Akt activation in TCA-induced COX-2 expression in HuCCT1 cells, selective chemical inhibitors of MEK1/2 and Akt were used.…”

Section: Hucct1 Cells As Shown Inmentioning

confidence: 99%

Taurocholate Induces Cyclooxygenase-2 Expression via the Sphingosine 1-phosphate Receptor 2 in a Human Cholangiocarcinoma Cell Line

Liu

Xiao

et al. 2015

Journal of Biological Chemistry

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Background: Cyclooxygenase-2 (COX-2) and sphingosine 1-phosphate receptor 2 (S1PR2) are highly expressed in human cholangiocarcinoma (CCA) and taurocholate (TCA) promotes CCA cell growth via S1PR2. Results: TCA-mediated activation of S1PR2 contributed to COX-2 expression and CCA cell growth. Conclusion: S1PR2 plays a critical role in TCA-induced COX-2 expression and CCA growth. Significance: S1PR2 represents a novel therapeutic target for CCA.

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Section: Hucct1 Cells As Shown Inmentioning

confidence: 99%

Taurocholate Induces Cyclooxygenase-2 Expression via the Sphingosine 1-phosphate Receptor 2 in a Human Cholangiocarcinoma Cell Line

Liu

Xiao

et al. 2015

Journal of Biological Chemistry

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“…Mitogen‐activated protein kinase (MAPK) and its downstream target MAPK‐activated protein kinase 2 (MK2), regulate proinflammatory function after injury through the expression of the proinflammatory cytokine TNF‐α. Specifically, we studied Mitogen‐activated protein kinase 14, also called p38α‐MAPK14 (Gurgis et al, ; Mercau et al, ; Xu et al, ). The p38α‐MAPK14 is implicated in cell survival/apoptosis, proliferation, differentiation, migration, mRNA stability, and inflammatory response in diverse cell types through a variety of different target molecules (Young, ).…”

Section: Introductionmentioning

confidence: 99%

“…MK2 is one of the well‐studied downstream targets of p38α‐MAPK14 and together they have downstream targets with cAMP response element‐binding protein (CREB) and cyclooxygenase 2 (COX‐2), both of which have been implicated in the steroidal response to injury in the zebra finch brain (Klores et al, ; Mehos et al, ; Pedersen et al, ). The p38α‐MAPK14 activation also results in TNF‐α biosynthesis following activation of MAPKAPK‐2 (Gurgis et al, ; Martinez Calejman et al, ; Mercau et al, ). TNF‐α is downregulated following injury‐induced estrogen production.…”

Section: Introductionmentioning

confidence: 99%

“…The activated AKT phosphorylates target proteins involved in cell survival, cell cycling, angiogenesis, and metabolism for neuroprotection (Kitagishi and Matsuda, ; Li et al, ). These pathways also appear to interact, activating p38α‐MAPK14 and PI3K/Akt signaling pathways to converge in the modulation of NFκB transcriptional activity and increase transcription of COX‐2 (Mercau et al, ; Xu et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Exogenous progesterone is neuroprotective following injury to the male zebra finch brain

Blackshear

Giessner

Hayden

et al. 2017

J of Neuroscience Research

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The use of progesterone following brain injury has a controversial history. On one hand, some lab-based models have showed progesterone as being neuroprotective, but on the other, clinical trials have showed quite the opposite. One of many complaints that arose from this discrepancy was the lack of a diverse pool of animal models and paradigms employed during the preclinical phase. However, over the past decade, the zebra finch has emerged as an optimal organism for the study of steroid-mediated neuroprotection. Following an injury, steroid hormones and receptors are upregulated, serving to decrease neuroinflammation and overall damage to the brain. As compared to other vertebrate models, zebra finches can upregulate expression of both estrogens and androgens at a faster and more robust response, suggesting that vertebrates differ in their neuroprotective mechanisms and timing following injury. Therefore, to expand the types organisms studied in pre-clinical trials, we chose to use zebra finches. While the majority of work in the zebra finch brain has focused on estrogens and androgens, we sought to clarify the role of progesterone following injury. Adult male zebra finches were given daily injections of progesterone following a penetrating injury and then were assessed for the size of injury and expression of various genes associated with neuroinflammation and cell survival. Treatment with progesterone decreased the injury size in zebra finches over controls and increased expression of various genes associated with cell survival and neuroinflammation. These data suggest that progesterone does mediate neuroprotection, most likely through the alteration of neuroinflammatory and cell survival pathways.

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“…Several signaling pathways have been demonstrated to play various roles in COX-2 or IL-8 regulation. NF-kB (Chen et al, 2012), mitogen-activated protein kinase (MAPK) p38 (Mercau et al, 2014), and c-Jun N-terminal kinase (JNK; Park et al, 2008) have all been shown to be involved in the regulation of COX-2 expression. In addition, the MAPK extracellular signal-regulated kinase (Erk1/2; Hong et al, 2010) and NF-kB (Nishio et al, 2014) have been demonstrated to be involved in the regulation of IL-8 expression.…”

mentioning

confidence: 99%

Inhibition of PKC‐Induced COX‐2 and IL‐8 Expression in Human Breast Cancer Cells by Glucosamine

Chou

Chuang

Sun

et al. 2015

Journal Cellular Physiology

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Breast cancer is a common cancer leading to many deaths among females. Cyclooxygenase-2 (COX-2) and interleukin-8 (IL-8) are two highly expressed inflammatory mediators to be induced by the protein kinase C (PKC) signaling via various inflammatory stimuli and both contribute significantly to cancer metastasis/progression. Glucosamine has been shown to act as an anti-inflammation molecule. The aim of this study was to clarify the role and acting mechanism of glucosamine during the PKC-regulation of COX-2/IL-8 expression and the associated impact on breast cancer. In MCF-7 breast cancer cells, glucosamine effectively suppresses the PKC induction of COX-2 and IL-8 promoter activity, mRNA and protein levels, as well as the production of prostaglandin E(2) (PGE(2)) and IL-8. Glucosamine is able to promote COX-2 protein degradation in a calpain-dependent manner and IL-8 protein degradation in calpain-dependent and proteasome-dependent manners. The MAPK and NF-κB pathways are involved in PKC-induced COX-2 expression, but only the NF-κB pathway is involved in PKC-induced IL-8 expression. Glucosamine attenuates PKC-mediated IκBα phosphorylation, nuclear NF-κB translocation, and NF-κB reporter activation. Both PGE(2) and IL-8 promote cell proliferation and IL-8 induces cell migration; thus, glucosamine appears to suppress PKC-induced cell proliferation and migration. Furthermore, glucosamine significantly inhibits the growth of breast cancer xenografts and this is accompanied by a reduction in COX-2 and IL-8 expression. In conclusion, glucosamine seems to attenuate the inflammatory response in vitro and in vivo and this occurs, at least in part by targeting to the NF-κB signaling pathway, resulting in an inhibition of breast cancer cell growth.

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Involvement of PI3K/Akt and p38 MAPK in the induction of COX-2 expression by bacterial lipopolysaccharide in murine adrenocortical cells

Cited by 30 publications

References 59 publications

Taurocholate Induces Cyclooxygenase-2 Expression via the Sphingosine 1-phosphate Receptor 2 in a Human Cholangiocarcinoma Cell Line

Taurocholate Induces Cyclooxygenase-2 Expression via the Sphingosine 1-phosphate Receptor 2 in a Human Cholangiocarcinoma Cell Line

Exogenous progesterone is neuroprotective following injury to the male zebra finch brain

Inhibition of PKC‐Induced COX‐2 and IL‐8 Expression in Human Breast Cancer Cells by Glucosamine

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