The selective cyclooxygenase-2 inhibitor celecoxib modulates the formation of vasoconstrictor eicosanoids and activates PPARγ. Influence of albumin

López-Parra, Marta; Clària, Joan; Titos, Esther; Planagumà, Anna; Párrizas, Marcelina; Masferrer, Jaime L.; Jiménez, Wladimiro; Arroyo, Vicente; Rivera, Francisca; Rodés, Joan

doi:10.1016/j.jhep.2004.09.011

Cited by 16 publications

(16 citation statements)

References 42 publications

(45 reference statements)

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“…Furthermore, there are reports demonstrating several NSAIDs to elicit direct activation of PPAR ␥ ( 49,50 ). In the case of celecoxib, direct activation of PPAR ␥ was observed in rat mesangial cells ( 42 ). On the other hand, celecoxib failed to elicit such effect in rheumatoid synovial fi broblasts ( 51 ), which is in line with our data from lung cancer cells that did not reveal a direct, COX-2-independent PPAR ␥ activation by celecoxib within a 2 h time frame.…”

Section: Impact Of Exogenous Pgs On Nuclear and Total Levels Of Ppar ␥supporting

confidence: 91%

Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib

Ramer

Walther

Borchert

et al. 2013

Journal of Lipid Research

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Section: Impact Of Exogenous Pgs On Nuclear and Total Levels Of Ppar ␥supporting

confidence: 91%

Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib

Ramer

Walther

Borchert

et al. 2013

Journal of Lipid Research

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“…Therefore, it seems that NSAIDs upregulate ER chaperones as a part of their general mechanism of action. Concentrations of NSAIDs required for induction of GRP78 in vitro (60-100 mM) are relatively higher than clinical available concentrations of celecoxib (1-10 mM) (Lopez-Parra et al, 2005;Patel et al, 2005). It was reported that oral administration of celecoxib (100-200 mg/kg/day, similar conditions to our experiments in Figure 3) caused serum concentrations of 8.6-11.3 mM (Kulp et al, 2004).…”

Section: Discussionmentioning

confidence: 98%

Celecoxib upregulates endoplasmic reticulum chaperones that inhibit celecoxib-induced apoptosis in human gastric cells

et al. 2005

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Nonsteroidal anti-inflammatory drugs (NSAIDs) induce apoptosis in cancer cells and this effect is involved in their antitumor activity. We recently demonstrated that NSAIDs upregulate GRP78, an endoplasmic reticulum (ER) chaperone, in gastric mucosal cells in primary culture. In the present study, induction of ER chaperones by NSAIDs and the effect of those chaperones on NSAID-induced apoptosis were examined in human gastric carcinoma cells. Celecoxib, an NSAID, upregulated ER chaperones (GRP78 and its cochaperones ERdj3 and ERdj4) but also C/EBP homologous transcription factor (CHOP), a transcription factor involved in apoptosis. Celecoxib also upregulated GRP78 in xenograft tumors, accompanying with the suppression of tumor growth in nude mice. Celecoxib caused phosphorylation of eukaryotic translation initiation factor 2 kinase (PERK) and eukaryotic initiation factor-2a (eIF2a) and production of activating transcription factor (ATF)4 mRNA. Suppression of ATF4 expression by small interfering RNA (siRNA) partially inhibited the celecoxib-dependent upregulation of GRP78. Celecoxib increased the intracellular Ca 2 þ concentration, while 1,2-bis(2-aminophenoxy) ethane-N,N,N 0 N 0 -tetraacetic acid, an intracellular Ca 2 þ chelator, inhibited the upregulation of GRP78 and ATF4. These results suggest that the Ca 2 þ -dependent activation of the PERK-eIF2a-ATF4 pathway is involved in the upregulation of ER chaperones by celecoxib. Overexpression of GRP78 partially suppressed the apoptosis and induction of CHOP in the presence of celecoxib and this suppression was stimulated by coexpression of either ERdj3 or ERdj4. On the other hand, suppression of GRP78 expression by siRNA drastically stimulated cellular apoptosis and production of CHOP in the presence of celecoxib. These results show that upregulation of ER chaperones by celecoxib protects cancer cells from celecoxib-induced apoptosis, thus may decrease the potential antitumor activity of celecoxib.

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“…Although, NSAIDs appear to be useful in preventing the development of experimental liver fibrosis, cirrhosis and hepatic focal lesions caused by a choline-deficient diet [149], unfortunately, these drugs are not recommended in patients with liver disease because of renal side effects [42]. Since selective COX-2 inhibitors have been shown to spare the renal function in cirrhosis [43,44,150], these compounds represent a novel therapeutic strategy to dampen liver inflammation. In our laboratory, we have been able to prevent liver fibrogenesis by administering SC-236, a selective COX-2 inhibitor, to CCl 4 -treated rats [151].…”

Section: Kupffer Cells Are Key Targets For the Modulation Of Liver Inmentioning

confidence: 99%

“…In our laboratory, we have been able to prevent liver fibrogenesis by administering SC-236, a selective COX-2 inhibitor, to CCl 4 -treated rats [151]. The mechanisms by which SC-236 exerts antifibrotic effects are not well defined, but include the inhibiton of proinflammatory PGs, the induction of apoptosis in Kupffer cells and HSCs as well as COX-inde-pendent pathways such as activation of PPAR [143,150]. PPAR is a ligand-activated transcription factor with a DNA binding domain that recognizes response elements in the promoter region of specific target genes linked to inflammation, cell proliferation, apoptosis and differentiation [152][153][154][155].…”

Section: Kupffer Cells Are Key Targets For the Modulation Of Liver Inmentioning

confidence: 99%

New Insights into the Regulation of Liver Inflammation and Oxidative Stress

Ferré¹,

Clariá

2006

MRMC

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Pro-inflammatory lipid mediators (i.e. eicosanoids), cytokines (i.e. TNF-alpha) and reactive oxygen species are targets of interest in the regulation of liver inflammation and oxidative stress. In the current review, we summarize recent advances in the pharmacological modulation of these pathways with especial emphasis on the participation of Kupffer cells, the liver resident macrophages and the cell type most directly related to the production of inflammatory mediators in this organ.

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The selective cyclooxygenase-2 inhibitor celecoxib modulates the formation of vasoconstrictor eicosanoids and activates PPARγ. Influence of albumin

Cited by 16 publications

References 42 publications

Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib

Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib

Celecoxib upregulates endoplasmic reticulum chaperones that inhibit celecoxib-induced apoptosis in human gastric cells

New Insights into the Regulation of Liver Inflammation and Oxidative Stress

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