Disease relevance of mt-Co2

• In conclusion, L-arginine can educe the role of pulmonary tissue protection through up-regulating the expression of intra-pulmonary NOS and down -regulating COX2 in pulmonary thromboembolism [1].
• Purpose: To prospectively evaluate the ability of macromolecular contrast medium (MMCM)-enhanced dynamic magnetic resonance (MR) imaging to depict vascular changes in response to cyclooxygenase-2 (COX-2) inhibition of angiogenesis in a human breast cancer model [2].
• Expression of both COX2 mRNA and protein was increased after ischemia in CA1 hippocampal neurons before their death [3].
• This study demonstrates a distinctive pattern of COX2 increases in the brain over time following traumatic brain injury (TBI) [4].
• A selective COX-2 inhibitor suppresses chronic pancreatitis in an animal model (WBN/Kob rats): significant reduction of macrophage infiltration and fibrosis [5].

Psychiatry related information on mt-Co2

• Exploratory locomotor activity was measured on the first postoperative day after intrathecal injection of dimethyl sulfoxide (vehicle) or COX-1 (SC-560) or COX-2 (NS-398) inhibitors [6].

High impact information on mt-Co2

• Here we report that increases in prostaglandin-E(2) (PGE(2)), resulting from changes in cyclooxygenase-2 (COX-2) regulation induced by perinatal exposure to estradiol, are necessary and sufficient to organize the crucial neural substrate that mediates male sexual behavior [7].
• CONCLUSIONS: Inducible Ha-Ras(V12) increases the production of PGI(2) through the coordinate up-regulation of cPLA(2), COX-2, and prostacyclin synthase (PGIS) [8].
• CONCLUSIONS: Aspirin administration results in elevated production of 15(R)-epi-LXA4 via COX-2 [9].
• The inducible isoform of the enzyme cyclooxygenase-2 (COX2) is an immediate early gene induced by synaptic activity in the brain [3].
• There was increased survival of CA1 neurons in rats treated with the COX2-selective inhibitor SC58125 [1-[(4-methylsulfonyl) phenyl]-3-trifluoro-methyl-5-[(4-fluoro)phenyl] pyrazole] before or after global ischemia compared with vehicle controls [3].

Chemical compound and disease context of mt-Co2

• Influence of L-arginine on the expression of eNOS and COX2 in experimental pulmonary thromboembolism [1].
• The effect of selective inhibition of COX2 was evaluated by intraperitoneal administration of NS-398, a selective COX2 inhibitor, before and after 2 h of temporary focal ischemia in rats [10].
• This study examines the antifibrotic effect of losartan, an angiotensin II type 1 receptor antagonist, in bleomycin induced lung fibrosis and its possible implication in the regulation of prostaglandin E(2) (PGE(2)) synthesis and cyclooxygenase-2 (COX-2) expression [11].
• CONCLUSION: Curcumin has therapeutic effects on TNBS acid-induced colitis, the mechanisms seem to be related to COX-2 inhibition and PGE(2) improvement [12].
• Activation of HSP70 by the combined actions of DHA and celecoxib in the presence of wild-type p53 reveals a unique COX-2 independent mode of action against prostate cancer [13].

Biological context of mt-Co2

• Conversion of a mitochondrial gene for mammalian cytochrome c oxidase subunit II into its universal codon equivalent and expression in vivo and in vitro [14].
• Partial injury induced greater COX2 up-regulation than complete injury [15].
• To determine whether COX2 might be an effector of excitotoxic cell death, cerebellar granule cells were pretreated (24 h) with the COX2-specific enzyme inhibitor, DFU (5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl) phenyl-2((5)H)-furanone) prior to glutamate challenge [16].
• These findings demonstrate that inhibitors of COX-2 and sPLA2-IIa can effectively suppress OVX-induced bone loss in the adult rat by conserving trabecular bone mass and architecture through reduced bone remodeling and decreased resorptive activity [17].
• Experimental study of the action of COX-2 selective nonsteroidal anti-inflammatory drugs and traditional anti-inflammatory drugs in bone regeneration [18].

Anatomical context of mt-Co2

• Binge ethanol treatment also caused microglia activation, increased NF-kappaB-DNA binding and COX2 expression [19].
• The COX2 protein was detected in the corneal epithelium throughout the epithelial layers from 3 to 72 hours, but not at 7 days [20].
• RESULTS: In the uninjured corneas, faint immunoreactivity for COX2 was detected in the basal cells of the corneal epithelium, but not in other cell layers [20].
• COX-2 was also expressed in the hypothalamus under normal and stressed conditions [21].
• Immunoblot analyses confirm increased levels of COX2 protein in the cortex and hippocampus [4].

Associations of mt-Co2 with chemical compounds

• CONCLUSION: Ethanol exposure activated NF-kappaB and upregulated COX2 expression, which may cause inflammation in corneal tissue [20].
• Butylated hydroxytoluene reduced binge-induced NF-kappaB-DNA binding and COX2 expression [19].
• For comparative purposes we also determined the effects of the mu-opioid receptor agonist morphine and the COX2 inhibitor rofecoxib in this model [22].
• Therefore, glutamate-mediated COX2 induction contributes to excitotoxic neuronal death [16].
• Treatment with excitotoxic concentrations of glutamate or kainate transiently induced COX2 mRNA (two- and threefold at 6 h, respectively, p < 0.05, Dunnett) and prostaglandin production (five- and sixfold at 30 min, respectively, p < 0.05, Dunnett) [16].

Other interactions of mt-Co2

• Other glutamate receptor antagonists, such as MK-801 (1 microM, NMDA receptor) or MCPG (500 microM, class 1 metabotropic receptors), partially attenuated glutamate-induced COX2 mRNA [16].
• Sequence analysis confirmed that four of these clones contained DNA sequences from cytochrome-c oxidase subunit II (COX II), and one contained a DNA sequence from cytochrome-c oxidase subunit I (COX I) [23].

Analytical, diagnostic and therapeutic context of mt-Co2

• Some animals were used for determination of nuclear factor kappa B (NF-kappaB)-DNA binding by electrophoretic mobility shift assay (EMSA) or for reverse transcription-polymerase chain reaction (RT-PCR) of cyclooxygenase 2 (COX2) [19].
• The expression of eNOS and COX2 protein and mRNA in pulmonary tissues was detected by immunohistochemistry and RT-PCR respectively [1].
• The cellular pattern of COX2 induction following TBI has been characterized using immunohistochemistry [4].
• We previously reported that cyclooxygenase 2 (COX2) is up-regulated in macrophages in injured nerve of rats with partial sciatic nerve ligation (PSNL) and that local injection of the COX inhibitor ketorolac reversed tactile allodynia (Eur. J. Neurosci. 15: 1037-1047, 2002) [24].
• In the current study, we observed that abundant COX2 immunoreactive (IR) cell profiles appeared in injured nerves of rats following spinal nerve ligation (SNL), chronic constriction injury (CCI) and complete sciatic nerve transection [15].

References