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Gene Review

COX2  -  cytochrome c oxidase subunit II

Oryctolagus cuniculus

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Disease relevance of COX2

  • Overexpression of PPARdelta using an adenovirus not only drove DRE activity but also prevented RMIC death due to COX2 inhibition [1].
  • The same doses of NS-398 and celecoxib, given 24 h after ischemic PC, completely blocked the cardioprotective effects of late PC against both myocardial stunning and myocardial infarction, indicating that COX-2 activity is necessary for this phenomenon to occur [2].
  • COX-2 protein overexpression by hypoxia and PPAR activation was not associated with a parallel increase in prostaglandin E(2) accumulation [3].
  • CONCLUSIONS: The reduction of stromal edema after topical administration of the inhibitors demonstrates the involvement of the COX-2 enzyme, the matrix metalloproteinase family, plasminogens, and the IL-1 system in the trauma-induced inflammatory response of the rabbit cornea [4].
  • These results demonstrate that activation of delta-opioid receptors induces late PC against both stunning and infarction via a COX-2-dependent mechanism [5].

High impact information on COX2

  • HEK/EP1 [Ca2+]i responses were observed mainly in preparations from rabbits on a low-salt diet and were completely inhibited by either a selective COX-2 inhibitor or an EP1 antagonist, and also by 100 microM luminal furosemide [6].
  • Also, 20-mM graduated reductions in [NaCl]L between 80 and 0 mM caused step-by-step increases in HEK/EP1 [Ca2+]i. Low-salt diet greatly increased the expression of both COX-2 and microsome-associated PGE synthase (mPGES) in the MD [6].
  • Macula densa (MD) cells express COX-2 and COX-2-derived PGs appear to signal the release of renin from the renal juxtaglomerular apparatus, especially during volume depletion [6].
  • Administration of two unrelated COX-2 selective inhibitors (NS-398 and celecoxib) 24 h after ischemic PC abolished the ischemic PC-induced increase in tissue levels of PGE(2) and 6-keto-PGF(1alpha) [2].
  • The analysis of arachidonic acid metabolites strongly points to PGE(2) and/or PGI(2) as the likely effectors of COX-2-dependent protection [2].

Chemical compound and disease context of COX2


Biological context of COX2

  • COX2-selective non-steroidal anti-inflammatory drugs (NSAIDs) cause selective apoptosis of renal medullary interstitial cells (RMIC) in vivo and reduce their ability to tolerate hypertonic stress in vitro [1].
  • These studies indicate C/EBPbeta is required for the transcriptional activation of COX2 by NFkappaB, suggesting a dominant role for the C/EBPbeta pathway in regulating induction of RMIC COX2 by hypertonicity [12].
  • Both trout rTNF1 and rTNF2 induced gene expression of a number of proinflammatory factors including IL1beta, TNF1, TNF2, IL8 and COX2 in freshly isolated head kidney leucocytes and the macrophage cell line RTS11 [13].
  • Antisense downregulation of COX2 was associated with MIC death, whereas a control adenovirus was without effect [7].
  • Taken together, these results demonstrate that, in conscious rabbits, up-regulation of COX-2 plays an essential role in the cardioprotection afforded by the late phase of ischemic PC [2].

Anatomical context of COX2

  • Our results indicate that EGF in articular chondrocytes stimulates COX-2 expression and PGE(2) production via ERK and p38 kinase signaling in association with differentiation status [14].
  • In rabbit corneal epithelial cells, both peroxisome proliferator-activated receptor (PPAR)-inducible cytochrome P450 4B1 and cyclooxygenase-2 (COX-2) mRNAs were increased by hypoxia [3].
  • Disruption of the actin cytoskeleton by cytochalasin D (CD) inhibited NO-induced apoptosis, dedifferentiation, COX-2 expression, and prostaglandin E2 production in chondrocytes cultured on plastic or during cartilage explants culture [15].
  • In duplicate slot blots probed with a cDNA for synovial fluid PLA2, half-maximal induction of PLA2 mRNA was estimated to require 0.15 ng/ml IL-1, approximately 10-fold less IL-1 than required for COX-2 [16].
  • The cultured cells expressed immunoreactive nNOS, and 7-NI inhibited basal COX-2 immunoreactivity expression, which could be partially overcome by cGMP [17].

Associations of COX2 with chemical compounds


Analytical, diagnostic and therapeutic context of COX2


  1. Peroxisome proliferator-activated receptor delta activation promotes cell survival following hypertonic stress. Hao, C.M., Redha, R., Morrow, J., Breyer, M.D. J. Biol. Chem. (2002) [Pubmed]
  2. Cyclooxygenase-2 mediates the cardioprotective effects of the late phase of ischemic preconditioning in conscious rabbits. Shinmura, K., Tang, X.L., Wang, Y., Xuan, Y.T., Liu, S.Q., Takano, H., Bhatnagar, A., Bolli, R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  3. Regulation of cyclooxygenase-2 by hypoxia and peroxisome proliferators in the corneal epithelium. Bonazzi, A., Mastyugin, V., Mieyal, P.A., Dunn, M.W., Laniado-Schwartzman, M. J. Biol. Chem. (2000) [Pubmed]
  4. Effect of inhibition of inflammatory mediators on trauma-induced stromal edema. Karon, M.D., Klyce, S.D. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
  5. Delta-opioid receptor-induced late preconditioning is mediated by cyclooxygenase-2 in conscious rabbits. Kodani, E., Xuan, Y.T., Shinmura, K., Takano, H., Tang, X.L., Bolli, R. Am. J. Physiol. Heart Circ. Physiol. (2002) [Pubmed]
  6. Luminal NaCl delivery regulates basolateral PGE2 release from macula densa cells. Peti-Peterdi, J., Komlosi, P., Fuson, A.L., Guan, Y., Schneider, A., Qi, Z., Redha, R., Rosivall, L., Breyer, M.D., Bell, P.D. J. Clin. Invest. (2003) [Pubmed]
  7. Selective targeting of cyclooxygenase-2 reveals its role in renal medullary interstitial cell survival. Hao, C.M., Kömhoff, M., Guan, Y., Redha, R., Breyer, M.D. Am. J. Physiol. (1999) [Pubmed]
  8. Licofelone, a balanced inhibitor of cyclooxygenase and 5-lipoxygenase, reduces inflammation in a rabbit model of atherosclerosis. Vidal, C., G??mez-Hern??ndez, A., S??nchez-Gal??n, E., Gonz??lez, A., Ortega, L., G??mez-Gerique, J.A., Tu????n, J., Egido, J. J. Pharmacol. Exp. Ther. (2007) [Pubmed]
  9. The endocannabinoid arachidonyl ethanolamide (anandamide) increases pulmonary arterial pressure via cyclooxygenase-2 products in isolated rabbit lungs. Wahn, H., Wolf, J., Kram, F., Frantz, S., Wagner, J.A. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
  10. Nicorandil induces late preconditioning against myocardial infarction in conscious rabbits. Tang, X.L., Xuan, Y.T., Zhu, Y., Shirk, G., Bolli, R. Am. J. Physiol. Heart Circ. Physiol. (2004) [Pubmed]
  11. Involvement of cyclooxygenase 2 in the protective effect of 17beta-estradiol on hypercholesterolemic rabbit aorta. Ghanam, K., Lavagna, C., Burgaud, J.L., Javellaud, J., Ea-Kim, L., Oudart, N. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  12. C/EBP{beta} and its binding element are required for NF{kappa}B-induced COX2 expression following hypertonic stress. Chen, J., Zhao, M., Rao, R., Inoue, H., Hao, C.M. J. Biol. Chem. (2005) [Pubmed]
  13. Functional characterisation of the recombinant tumor necrosis factors in rainbow trout, Oncorhynchus mykiss. Zou, J., Peddie, S., Scapigliati, G., Zhang, Y., Bols, N.C., Ellis, A.E., Secombes, C.J. Dev. Comp. Immunol. (2003) [Pubmed]
  14. Differentiation status-dependent regulation of cyclooxygenase-2 expression and prostaglandin E2 production by epidermal growth factor via mitogen-activated protein kinase in articular chondrocytes. Huh, Y.H., Kim, S.H., Kim, S.J., Chun, J.S. J. Biol. Chem. (2003) [Pubmed]
  15. Actin cytoskeletal architecture regulates nitric oxide-induced apoptosis, dedifferentiation, and cyclooxygenase-2 expression in articular chondrocytes via mitogen-activated protein kinase and protein kinase C pathways. Kim, S.J., Hwang, S.G., Kim, I.C., Chun, J.S. J. Biol. Chem. (2003) [Pubmed]
  16. Interleukin-1 differentially modulates chondrocyte expression of cyclooxygenase-2 and phospholipase A2. Lyons-Giordano, B., Pratta, M.A., Galbraith, W., Davis, G.L., Arner, E.C. Exp. Cell Res. (1993) [Pubmed]
  17. Nitric oxide regulates renal cortical cyclooxygenase-2 expression. Cheng, H.F., Wang, J.L., Zhang, M.Z., McKanna, J.A., Harris, R.C. Am. J. Physiol. Renal Physiol. (2000) [Pubmed]
  18. The lipoxygenase-cyclooxygenase inhibitor licofelone prevents thromboxane A2-mediated cardiovascular derangement triggered by the inflammatory peptide fMLP in the rabbit. Rotondo, S., Dell'elba, G., Manarini, S., Cerletti, C., Evangelista, V. Eur. J. Pharmacol. (2006) [Pubmed]
  19. Nimesulide, a cyclooxygenase-2 preferential inhibitor, impairs renal function in the newborn rabbit. Prévot, A., Mosig, D., Martini, S., Guignard, J.P. Pediatr. Res. (2004) [Pubmed]
  20. Induction of rabbit cyclooxygenase 2 in the anterior uvea following glaucoma filtration surgery. Chang, M.S., Tsai, J.C., Yang, R., DuBois, R.N., Breyer, M.D., O'Day, D.M. Curr. Eye Res. (1997) [Pubmed]
  21. Unexpected nanomolar inhibition of carbonic anhydrase by COX-2-selective celecoxib: new pharmacological opportunities due to related binding site recognition. Weber, A., Casini, A., Heine, A., Kuhn, D., Supuran, C.T., Scozzafava, A., Klebe, G. J. Med. Chem. (2004) [Pubmed]
  22. Cyclooxygenase-2 does not mediate late preconditioning induced by activation of adenosine A1 or A3 receptors. Kodani, E., Shinmura, K., Xuan, Y.T., Takano, H., Auchampach, J.A., Tang, X.L., Bolli, R. Am. J. Physiol. Heart Circ. Physiol. (2001) [Pubmed]
  23. Atorvastatin reduces the expression of cyclooxygenase-2 in a rabbit model of atherosclerosis and in cultured vascular smooth muscle cells. Hernández-Presa, M.A., Martín-Ventura, J.L., Ortego, M., Gómez-Hernández, A., Tuñón, J., Hernández-Vargas, P., Blanco-Colio, L.M., Mas, S., Aparicio, C., Ortega, L., Vivanco, F., Gerique, J.G., Díaz, C., Hernández, G., Egido, J. Atherosclerosis (2002) [Pubmed]
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