Disease relevance of mt-Co1

• These data demonstrate that a dramatic decrease in antioxidant defense was initiated during warm renal ischemia, whereas the 8-iso-PGF(2alpha) was related only to arachidonate conversion by COX1 [1].
• However, the concurrent inhibition of endogenous nitric oxide generation and COX1 or COX2 causes overshooting neointimal hyperplasia [2].
• These findings demonstrate that COX-1- and COX-2-derived prostanoids contribute importantly to the development of malignant hypertension in Cyp1a1-Ren2 transgenic rats [3].
• This study was designed to examine the effect of perinatal hypothyroidism on ontogenic change in cytochrome c oxidase subunit I (COX I) gene expression in the rat cerebellum by using quantitative in situ hybridization histochemistry (ISH) [4].

Psychiatry related information on mt-Co1

• These data with exploratory behavior and laparotomy agree with studies with reflexive withdrawal responses after incisional surgery and indicate that COX-1 inhibition reduces pain responses after surgery [5].
• 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 [5].

High impact information on mt-Co1

• Transcriptional activation through ETS domain binding sites in the cytochrome c oxidase subunit IV gene [6].
• A mutational analysis of the rat cytochrome c oxidase subunit IV (RCO4) promoter region revealed the presence of a major control element consisting of a tandemly repeated pair of binding sites for a nuclear factor from HeLa cells [6].
• Complete nucleotide sequence of the gene encoding rat cytochrome c oxidase subunit IV [7].
• We have isolated three members of the rat cytochrome c oxidase subunit IV gene family: one functional gene and two processed pseudogenes [8].
• Basal cells, but not principal cells, and other cells in the epididymis express TRPC3 and COX-1 [9].

Chemical compound and disease context of mt-Co1

• Additional rats received Pio (10 mg.kg-1.day-1) for 3 days and intravenous SC-58125 [a cyclooxygenase-2 (COX-2) inhibitor] or SC-560 (a COX-1 inhibitor) 15 min before ischemia [10].
• Adv-COX-1/PGIS infusion selectively augmented prostacyclin levels, with reduction of other eicosanoids in ischemic cortex and a significant reduction of infarct volume, even when the rAd was administered 5 hours after ischemia [11].

Biological context of mt-Co1

• A murine dopamine neuron-specific cDNA library and microarray: increased COX1 expression during methamphetamine neurotoxicity [12].
• PKC downregulation and COX1/2 inhibition did not alter these inductions [13].
• Prostanoids are arachidonic acid (AA) metabolites derived from the cyclooxygenase (COX1 and COX2 isozymes) pathway and are involved in signal transduction pathways activated by distinct ILs [14].
• The possible role of isoforms of cytochrome c oxidase subunit VIa in mammalian thermogenesis [15].
• Nevertheless, enlarged mitochondria retained immunoreactivity for cytochrome c oxidase subunit 1, implying that mitochondrial genes remain active in defective mitochondria [16].

Anatomical context of mt-Co1

• The mechanism of action involves an over-expression of COX-2, but not COX-1, in dorsal and ventral horn areas of the lumbar spinal cord [17].
• In conclusion, the expression of iNOS in the small intestine following administration of NSAIDs results from COX-1 inhibition and is functionally associated with intestinal hypermotility and bacterial invasion [18].
• COX1 was increased by TGFbeta1, but only in astrocytes [19].
• To determine cellular expression, frozen sections of rat tibial growth plate and primary chondrocyte cultures were stained using immunohistochemistry with polyclonal antibodies directed towards COX-1, COX-2, EP1, EP2, EP3, and EP4 [20].
• Spinal COX-1 inhibition completely restores exploratory activity, including rearing behavior that stretches the abdominal muscles [5].

Associations of mt-Co1 with chemical compounds

• There is a correlation (correlation coefficient = 0.05) between NOS activity and PGE(2) generation through the activation of phosphoinositide by phospholipase C (PLC), phospholipase A(2) (PLA(2)), and cyclooxygenase 1 (COX-1) [21].
• Tissue-specific regulation of cytochrome c oxidase subunit expression by thyroid hormone [22].
• In contrast, 2-[2-(3-fluorophenyl)ethynyl]benzenesulfonamide (11c) possessing a SO2NH2 COX-2 pharmacophore at the ortho-position of the C-1 phenyl ring exhibited COX-1 inhibition and selectivity (COX-1 IC50=3.6 microM) [23].
• Therefore the two metabolites of arachidonic acid seemed to be produced via an enzymatic COX1-dependent pathway [1].
• COX function was assessed using COX activity inhibitors: indomethacin (INDO; COX1 and COX2 inhibitor) and NS-398 (COX2 selective inhibitor) [14].

Other interactions of mt-Co1

• Moreover, E2 and flutamide normalized expression of cardiac PGC-1, NRF-2, Tfam, cytochrome-c oxidase subunit IV, and the mitochondrial DNA-encoded gene cytochrome-c oxidase subunit I and beta-ATP synthase, mitochondrial ATP, and cytochrome-c oxidase activity [24].
• Northern blot analysis demonstrated that CO-III and ATPase-6 were downregulated 1.8- and 2.3-fold by 400-lux cyclic light compared with 5-lux cyclic light, respectively; however, there was no change in cytochrome c oxidase subunit I and II (CO-I and -II) or in 12S ribosomal RNA (12S rRNA), a mitochondrial housekeeping gene [25].
• The content of DNA and of 16S rRNA and of two mRNAs, i.e., the mRNA for the cytochrome c oxidase subunit I and the mRNA for one subunit of the NADH dehydrogenase (ND4), in free (nonsynaptic) mitochondria of developing and adult rat cerebellum has been determined [26].
• Clofibrate, perfluorooctanoic acid, and acetylsalicylic acid all increased the mRNA levels for the mitochondrial-encoded respiratory-chain components cytochrome c oxidase subunit I and NADH dehydrogenase subunit I. Mitochondrial 16S rRNA was also induced by clofibrate [27].
• Catalase, epithelial glycoprotein (EGP-314), cytochrome C oxidase-subunit 1, ribosomal L31 protein, and ceruloplasmin were found to be differentially expressed [28].

Analytical, diagnostic and therapeutic context of mt-Co1

• These data suggest that targeting COX-1 in the spinal cord may produce postoperative analgesia [5].
• Expressions of cytochrome c oxidase subunit mRNAs were measured by real-time quantitative polymerase chain reaction [29].
• Sequence analysis of these clones revealed that all isolated clones encode cytochrome c oxidase subunit I (COX I), which is located in the mitochondrial DNA [30].
• The labeled translation products were incubated with an antiserum against cytochrome c oxidase subunit V. After immunoprecipitation and affinity chromatography with protein-A-Sepharose, the isolated antigen-immunoglobulin complexes were analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and fluorography [31].
• Specific cyclooxygenase-1 (COX-1) immunoprecipitation was associated to co-precipitation of four proteins [32].

References