Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Senescence may contribute to the pathogenesis of atherosclerosis. Although the bioavailability of nitric oxide (NO) is limited in senescence, the effect of NO on senescence and its relationship to cardiovascular risk factors have not been investigated fully. We studied these factors by investigating senescence-associated beta-galactosidase (SA-beta-gal) and human telomerase activity in human umbilical venous endothelial cells (HUVECs). Treatment with NO donor (Z)-1-[2-(2-aminoethyl)-N-(2-aminoethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) and transfection with endothelial NO synthase (eNOS) into HUVECs each decreased the number of SA-beta-gal positive cells and increased telomerase activity. The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) abolished the effect of eNOS transfection. The physiological concentration of 17beta-estradiol activated hTERT, decreased SA-beta-gal-positive cells, and caused cell proliferation. However, ICI 182780, an estrogen receptor-specific antagonist, and L-NAME each inhibited these effects. Finally, we investigated the effect of NO bioavailability on high glucose-promoted cellular senescence of HUVECs. Inhibition by eNOS transfection of this cellular senescence under high glucose conditions was less pronounced. Treatment with L-arginine or L-citrulline of eNOS-transfected cells partially inhibited, and combination of L-arginine and L-citrulline with antioxidants strongly prevented, high glucose-induced cellular senescence. These data demonstrate that NO can prevent endothelial senescence, thereby contributing to the anti-senile action of estrogen. The ingestion of NO-boosting substances, including L-arginine, L-citrulline, and antioxidants, can delay endothelial senescence under high glucose. We suggest that the delay in endothelial senescence through NO and/or eNOS activation may have clinical utility in the treatment of atherosclerosis in the elderly.
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PMID:Endothelial cellular senescence is inhibited by nitric oxide: implications in atherosclerosis associated with menopause and diabetes. 1707 48

In this study we sought to determine whether contractile activity has a role as a signalling mechanism in the activation of intracellular nitric oxide (NO(i)) production induced by electrical stimulation of cat ventricular myocytes. Field stimulation (FS) of single ventricular myocytes elicited frequency-dependent increases in NO(i) that were blocked by the calmodulin (CaM) inhibitor 10 microM W-7 and partially inhibited by the phosphatidylinositol 3'-kinase (PI-(3)K) inhibitor 10 microMm LY294002. Increasing extracellular [Ca(2+)] caused a concentration-dependent increase in FS-induced NO(i) that was partially inhibited by LY294002. The negative inotropic agents BDM (5 mm) or blebbistatin (10 microM) decreased cell shortening and NO(i) production without concomitant changes in L-type Ca(2+) current (I(Ca,L)) or [Ca(2+)](i) transients. The positive inotropic agents EMD 57033 or CGP 48506 (1 microM) increased cell shortening and NO(i) production without concomitant changes in I(Ca,L) or [Ca(2+)](i) transients. FS-induced NO(i) production was decreased in myocytes infected (100 multiplicity of viral infection (MOI); 24 h) with a replication-deficient adenovirus expressing a dominant-negative mutant of protein kinase B (Akt) compared with cells infected with a control adenovirus expressing beta-galactosidase. FS-induced NO(i) was partially inhibited by either endothelial (eNOS) or neuronal nitric oxide synthase (nNOS) inhibitors and completely blocked by simultaneous exposure to both. FS-induced [Ca(2+)](i) transients were increased by the nNOS inhibitor nNOS-I (0.24 microM), decreased by the eNOS inhibitor L-NIO (1 microM) and unchanged by exposure to both inhibitors. We conclude that in cat ventricular myocytes, FS-induced NO(i) production requires both Ca(2+)-dependent CaM signalling and Ca(2+)-independent PI-(3)K-Akt signalling activated by contractile activity. FS activates NO(i) production from both eNOS and nNOS, and each source of NO(i) exerts opposing effects on [Ca(2+)](i) transient amplitude. These findings are important for understanding the regulation of NO(i) signalling in the normal and mechanically failing heart.
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PMID:Signalling mechanisms in contraction-mediated stimulation of intracellular NO production in cat ventricular myocytes. 1723 90

Fluorescence imaging is the most powerful technique currently available for continuous observation of dynamic intracellular processes in living cells. However, only a very limited range of biomolecules can be visualized because of the lack of flexible design strategies for fluorescence probes. In our laboratory, it was elucidated that fluorescein which has been widely employed as a core of fluorescence probes could be understood as a directly linked electron donor/fluorophore acceptor system. Fluorescence properties of fluorescein derivatives could be easily anticipated and modulated by controlling the rate of photoinduced electron transfer (PeT) from the donor moiety to the xanthene fluorophore. Further, we found that the opposite direction of PeT from the singlet excited fluorophore to the electron acceptor moiety could be occurred. More than twenty probes for imaging of nitric oxide, beta-galactosidase, highly reactive oxygen species, zinc ion et al. have been developed according to precise and rational design strategies based on PeT mechanism.
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PMID:[How to develop custom-designed fluorescence probes for molecular imaging]. 1730 68

Akt is expected to be an effective target for the treatment of ischemia-reperfusion injury (I/R) due to its anti-apoptotic properties and its ability to activate the endothelial nitric oxide synthase (eNOS) enzyme. Therefore, this study was aimed to determine the efficacy of an active mutant of Akt (myr-Akt) to decrease I/R injury in a model of orthotopic liver transplantation in pigs. In addition, we analyzed the contribution of nitric oxide in the Akt-mediated effects by using an eNOS mutant (S1179DeNOS) that mimics the phosphorylation promoted by Akt in the eNOS sequence. Donors were treated with adenoviruses codifying for myr-Akt, S1179DeNOS or beta-galactosidase 24 h before liver harvesting. Then, liver grafts were orthotopically transplanted into their corresponding recipients. Levels of transaminases and lactate dehydrogenase (LDH) increased in all recipients after 24 h of transplant. However, transaminases and LDH levels were significantly lower in the myr-Akt group compared with vehicle. The percentage of apoptotic cells and the amount of activated-caspase 3 protein were also markedly reduced in myr-Akt-treated grafts after 4 days of liver transplant compared with vehicle and S1179DeNOS groups. In conclusion, myr-Akt gene therapy effectively exerts cytoprotection against hepatic I/R injury regardless of the Akt-dependent eNOS activation.
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PMID:Gene transduction of an active mutant of akt exerts cytoprotection and reduces graft injury after liver transplantation. 1739 Nov 22

To elicit the physiological roles of Pbh1, a baculoviral IAP repeat (BIR) domain-containing protein, in Schizosaccharomyces pombe, we investigated if Pbh1 expression is regulated by stress. The upstream region (1221 bp) of the pbh1 gene was fused into the promoterless beta-galactosidase gene of the shuttle vector YEp367R, and the resultant fusion plasmid was named pPbh04. The synthesis of beta-galactosidase from the pbh1-lacZ fusion gene was markedly enhanced by sodium nitroprusside (SNP) generating nitric oxide. The basal expression of the pbh1 gene required the presence of Pap1. Pap1 also mediated the induction of the pbh1 gene by SNP and nitrogen starvation. Pap1-dependent induction of the pbh1 gene by SNP was confirmed by the enhanced level of the pbh1 mRNA in Pap1-positive cells but not in Pap1-negative cells. Taken together, it was demonstrated that the pbh1 genes are positively regulated by nitrosative and nitrogen starvation stresses in Pap1-dependent manner.
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PMID:Stress-dependent regulation of Pbh1, a BIR domain-containing protein, in the fission yeast. 1747 96

To assess novel cellular roles and regulation of Rad9 in the fission yeast Schizosaccharomyces pombe, the full-length rad9 gene was cloned into the shuttle vector pRS316, generating pYFRad9. The rad9 mRNA level was significantly increased in the S. pombe cells harboring the plasmid pYFRad9, suggesting that the cloned rad9 gene is functioning. The S. pombe cells harboring pYFRad9 showed higher survival in the minimal media containing nitric oxide (NO)-generating sodium nitroprusside (SNP, 20 muM) and no nitrogen than the vector control cells. SNP and nitrogen starvation notably enhanced the synthesis of beta-galactosidase from the rad9-lacZ fusion gene in the Pap1-positive cells but not in the Pap1-negative cells. The rad9 mRNA level, detected by semi-quantitative reverse transcriptase (RT)-PCR, was elevated in the Pap1-positive cells but not in the Pap1-negative cells by SNP and nitrogen starvation. It was also increased only in the Pap1-positive cells by diethylmaleate, which activates Pap1. Collectively, the results imply that Rad9 plays a protective role against nitrosative and nutritional stress and is positively regulated by NO and nitrogen starvation in a Pap1-dependent manner.
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PMID:Protective role and regulation of Rad9 from the fission yeast Schizosaccharomyces pombe. 1772 19

In the current work, regulation of the pap1(+) gene was investigated by the use of the pap1(+)-lacZ fusion gene and semi-quantitative reverse transcriptase-PCR. The synthesis of beta-galactosidase from the pap1(+)-lacZ fusion gene was significantly enhanced by nitric oxide (NO)-generating sodium nitroprusside (SNP) and nitrogen starvation. However, the induction by SNP and nitrogen starvation was observed to be much less in the Pap1p-negative cells harboring the fusion gene. Exogenous NO was more effectively scavenged in the Pap1p-positive cells than in the Pap1p-negative cells. Oxidative stress such as superoxide anion, hydrogen peroxide and cadmium could not give rise to an effect on the synthesis of beta-galactosidase from the fusion gene. The pap1(+) mRNA level was elevated in the wild-type cells by SNP and nitrogen starvation. Catalase activity, a major enzyme positively regulated by Pap1p, was significantly increased only in the Pap1p-positive cells by SNP. In brief, it is demonstrated that transcription of the Schizosaccharomyces pombe pap1(+) gene is positively regulated by nitrosative and nutritional stress in a Pap1p-dependent manner.
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PMID:The pap1(+) gene of fission yeast is transcriptionally regulated by nitrosative and nutritional stress. 1824 28

This work was designed to assess regulation of the atf1+ gene in the fission yeast Schizosaccharomyces pombe under nitrosative and nutritional stresses, using the atf1+-lacZ fusion gene and RT-PCR. Nitric oxide (NO)-generating sodium nitroprusside (SNP; 10 micromol/L) and nitrogen depletion significantly enhanced synthesis of beta-galactosidase from the atf1+-lacZ fusion gene in S. pombe Pap1-positive KP1 cells, but not in S. pombe Pap1-negative TP108-3C cells. SNP (10 micromol/L) and nitrogen depletion also caused a significant increase in atf1+ mRNA levels in Pap1-positive cells, but not in Pap1-negative cells. Depletion of glucose marginally increased synthesis of beta-galactosidase from the fusion gene in S. pombe Pap1-positive cells. Taken together, the S. pombe atf1+ gene is upregulated by nitrosative and nutritional stresses on a transcriptional level, possibly via the mediation of Pap1.
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PMID:Expression of the atf1+ gene is upregulated in fission yeast under nitrosative and nutritional stresses. 1994 Sep 42

Nitric oxide (NO) has gained interest as a major signaling molecule during plant development and in response to environmental cues. Formation of NO during symbiotic interactions has been reported, but the role and sources of NO in nodules remain unclear. In this work, the involvement of denitrification, performed by the symbiont Bradyrhizobium japonicum, in NO formation in soybean nodules in response to flooding conditions has been investigated by inoculating plants with napA-, nirK-, or norC-deficient mutants. Levels of nitrosylleghemoglobin (LbNO) in flooded nirK and norC nodules were significantly higher than those observed in wild-type nodules. In addition, nirK and norC nodules accumulated more nitrite and NO, respectively, than wild-type nodules. By contrast, levels of LbNO, nitrite, and NO in flooded napA nodules were lower than in wild-type nodules. These results suggest that LbNO formation in soybean nodules in response to flooding conditions is caused by nitrite and NO generated from periplasmic nitrate reductase (Nap) and also containing nitrite reductase (NirK) denitrification enzymes. Flooding caused a decrease of nifH expression and nitrogenase activity in wild-type and norC nodules but not in napA or nirK nodules. Incubation of wild-type and norC nodules with a NO scavenger counteracted the effect of flooding. Under free-living conditions, beta-galactosidase activity from a nifD'-'lacZ fusion decreased in a norC mutant, which also accumulated NO in the medium. These results suggest that NO formed by Cu-containing nitrite reductase in soybean nodules in response to flooding has a negative effect on expression of nitrogenase. We propose that Lb has a major role in detoxifying NO and nitrite produced by bacteroidal denitrification in response to flooding conditions.
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PMID:Production of nitric oxide and nitrosylleghemoglobin complexes in soybean nodules in response to flooding. 2036 76

The renin-angiotensin system is activated in the early phase of two-kidney, one-clip (2K-1C) hypertension. The paraventricular nucleus (PVN) integrates inputs regulating sympathetic outflow. The PVN receives inputs from plasma angiotensin II via projections from circumventricular organs and from renal afferent nerves transmitted via the nucleus tractus solitarii. Nitric oxide within the PVN may exert a sympathoinhibitory effect. These studies tested whether decreasing endogenous nitric oxide by introducing dominant negative (DN) constructs for neuronal nitric oxide synthase (nNOS) into PVN chronically augments hypertension and/or modulates baroreflex function. Male 6-week-old Sprague-Dawley rats underwent sham surgery or right renal artery clipping and placement of radiotelemetry transmitters. One week later, the PVN was injected bilaterally with 250 nl artificial cerebrospinal fluid containing 250 ng microl(-1) of RSV beta-galactosidase (beta-Gal), cytomegalovirus (CMV) wild-type (WT nNOS), or respiratory syncytial virus (RSV) haeme domain or RSV haemeRedF (DN nNOS). Haemodynamics were monitored for 5 weeks. Then left renal nerve electrodes were placed, and 2 days later the rats underwent baroreflex testing in the conscious state. The rise in mean arterial pressure (MAP) was significantly potentiated in the DN nNOS 2K-1C group beyond 15 days after PVN injection. By day 35, MAP in the 2K-1C groups was 152 +/- 6.3 (beta-Gal), 155.1 +/- 6.6 (WT nNOS) and 179 +/- 5.4 mmHg (DN nNOS; P < 0.01 versus all other groups). Sham-clipped rats remained normotensive. All groups displayed progressive bradycardia over time that was attenuated in the DN nNOS 2K-1C group. Baroreflex curves shifted to higher pressures, and baroreflex sensitivity of heart rate was diminished to a similar extent in all groups of 2K-1C rats. The baroreflex response of renal sympathetic nerve activity was preserved. The PVN tissue from DN nNOS rats had decreased dimerization of nNOS and generation of total nitric oxide. These findings indicate that chronic interference of nNOS dimerization required for generation of nitric oxide within the PVN potentiates the increase of blood pressure by modulating the sympathoexcitation that accompanies renovascular hypertension.
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PMID:Neuronal nitric oxide synthase within paraventricular nucleus: blood pressure and baroreflex in two-kidney, one-clip hypertensive rats. 2049 20


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