Regulation of Expression and Potential Carcinogenic Role of Cyclooxygenase-2

Streptococcus suis is a common pathogen colonising the respiratory tract of pigs. It can cause meningitis, sepsis and pneumonia leading to economic losses in the pig industry worldwide. Cyclooxygenase-2 (COX-2) and its metabolites play an important regulatory role in different biological processes like inflammation modulation and immune activation. In this report we analysed the induction of COX-2 and the production of its metabolite prostaglandin E2 (PGE2) in a porcine precision-cut lung slice (PCLS) model. Using Western blot analysis, we found a time-dependent induction of COX-2 in the infected tissue resulting in increased PGE2 levels. Immunohistological analysis revealed a strong COX-2 expression in the proximity of the bronchioles between the ciliated epithelial cells and the adjacent alveolar tissue. The morphology, location and vimentin staining suggested that these cells are subepithelial bronchial fibroblasts. Furthermore, we showed that COX-2 expression as well as PGE2 production was detected following infection with two prevalent S. suis serotypes and that the pore-forming toxin suilysin played an important role in this process. Therefore, this study provides new insights in the response of porcine lung cells to S. suis infections and serves as a basis for further studies to define the role of COX-2 and its metabolites in the inflammatory response in porcine lung tissue during infections with S. suis.

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Radiation Induced Inflammatory Changes in the Mouse Bladder: The Role of Cyclooxygenase-2

The Journal of Urology ◽

10.1016/s0022-5347(05)00658-0 ◽

2006 ◽

Vol 175 (4) ◽

pp. 1529-1533 ◽

Cited By ~ 26

Author(s):

Jana Jaal ◽

Wolfgang Dörr

Keyword(s):

Cyclooxygenase 2 ◽

Radiation Induced ◽

Inflammatory Changes

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One of the tightly clustered genes of the mouse surfeit locus is a highly expressed member of a multigene family whose other members are predominantly processed pseudogenes.

Molecular and Cellular Biology ◽

10.1128/mcb.8.9.3898 ◽

1988 ◽

Vol 8 (9) ◽

pp. 3898-3905 ◽

Cited By ~ 21

Author(s):

C Huxley ◽

T Williams ◽

M Fried

Keyword(s):

Multigene Family ◽

Open Reading Frame ◽

The Other ◽

Base Pairs ◽

Regulation Of Expression ◽

Reading Frame ◽

Processed Pseudogenes ◽

Dna Fragment ◽

Basic Polypeptide

The mouse surfeit locus is unusual in that it contains a number of closely clustered genes (Surf-1, -2, and -4) that alternate in their direction of transcription (T. Williams, J. Yon, C. Huxley, and M. Fried, Proc. Natl. Acad. Sci. USA 85:3527-3530, 1988). The heterogeneous 5' ends of Surf-1 and Surf-2 are separated by 15 to 73 base pairs (bp), and the 3' ends of Surf-2 and Surf-4 overlap by 133 bp (T. Williams and M. Fried, Mol. Cell. Biol. 6:4558-4569, 1986; T. Williams and M. Fried, Nature (London) 322:275-279, 1986). A fourth gene in this locus, Surf-3, which is a member of a multigene family, has been identified. The poly(A) addition site of Surf-3 lies only 70 bp from the poly(A) addition site of Surf-1. Transcription of Surf-3 has been studied in the absence of the other members of its multigene family after transfection of a cloned genomic mouse DNA fragment, containing the Surf-3 gene, into heterologous monkey cells. Surf-3 specifies a highly expressed 1.0-kilobase mRNA that contains a long open reading frame of 266 amino acids, which would encode a highly basic polypeptide (23% Arg plus Lys). The other members of the Surf-3 multigene family are predominantly, if not entirely, intronless pseudogenes with the hallmarks of being generated by reverse transcription. The role of the very tight clustering on regulation of expression of the genes in the surfeit locus is discussed.

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The role of cyclooxygenase-2 on endurance exercise training in female LDL-receptor knockout ovariectomized mice

Anais da Academia Brasileira de Ciências ◽

10.1590/s0001-37652013005000046 ◽

2013 ◽

Vol 85 (3) ◽

pp. 1157-1164 ◽

Cited By ~ 3

Author(s):

FLAVIA DE OLIVEIRA ◽

LAURA B.M. MAIFRINO ◽

GUSTAVO P.P. DE JESUS ◽

JULIANA G. CARVALHO ◽

CLAUDIA MARCHON ◽

...

Keyword(s):

Cardiovascular Risk ◽

Exercise Training ◽

Ldl Receptor ◽

Density Lipoprotein ◽

Cyclooxygenase 2 ◽

Sedentary Control ◽

Down Regulation ◽

Ovariectomized Mice ◽

Cox 2

Estrogen deprivation in postmenopausal women increases cardiovascular risk. Cardiovascular risk as a result of atherosclerosis is able to induce an inflammatory disease as far as cyclooxygenase-2 ( COX-2) expression. The purpose of the study was to investigate the role of COX-2 on exercise training in female mice low-density lipoprotein receptor knockout ( LDL-KO) with or without ovariectomy. A total of 15 female C57BL/6 mice and 15 female LDL-KO mice were distributed into 6 groups: sedentary control, sedentary control ovariectomized, trained control ovariectomized, LDL-KO sedentary, LDL-KO sedentary ovariectomized and LDL-KO trained ovariectomized. The ascending part of the aorta was stained with H&E and COX-2 expression was assessed by immunohistochemistry. Results revealed that ovariectomy as well as exercise training were not able to induce histopathological changes in mouse aorta for all groups investigated. LDL-KO mice demonstrated plaque containing cholesterol clefts, foamy histiocytes and mild inflammatory process for all groups indistinctly. Ovariectomy induced a strong immunoexpression in atherosclerosis lesion of LDL-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDL-KO sedentary. Our results are consistent with the notion that exercise training is able to modulate COX-2 expression in LDL-KO mice as a result of COX-2 down-regulation.

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Role of nuclear factor-κB in gastric ulcer healing in rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.280.6.g1296 ◽

2001 ◽

Vol 280 (6) ◽

pp. G1296-G1304 ◽

Cited By ~ 15

Author(s):

Satoru Takahashi ◽

Takuya Fujita ◽

Akira Yamamoto

Keyword(s):

Gastric Ulcer ◽

Mrna Expression ◽

Ulcer Healing ◽

Nuclear Factor Κb ◽

Normal Mucosa ◽

Cyclooxygenase 2 ◽

Interleukin 1Β ◽

Nuclear Factor ◽

Gastric Ulcer Healing

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.

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