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:3.1.27.5 (RNase)
17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the vasorelaxation by natriuretic peptide (NP) is much less potent in the vein than in the artery, mechanism underlying the phenomenon remains unknown. Since NP receptor consists of three subtypes with different functions, we determined the mRNA level of each NP receptor subtype in the artery and vein by ribonuclease protection assay. In the aorta, NP-A receptor related to the biological action of NP was the predominant form. By contrast, NP-C receptor related mainly to the clearance of NP was the predominant form in the inferior vena cava: NP-C mRNA level was about two fold higher than in the aorta, while both NP-A and NP-B receptor mRNA levels were about half of that in the aorta. These results provide the molecular basis for the different biological response to NP in the artery and vein. Differential gene expression of NP receptor subtype could be an important determinant of the biological actions of NP.
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PMID:Differential gene expression of vascular natriuretic peptide receptor subtype in artery and vein. 748 44

A novel natriuretic peptide receptor, which we have termed natriuretic peptide receptor D (NPR-D), has been cloned and characterized. cDNAs related to the natriuretic peptide receptor (NPR) were amplified by PCR from a template of poly(A)-rich RNA isolated from the eel gill. Sequencing of the PCR products revealed the presence of a new clone that showed about 70% sequence identity to the eel type-C receptor, NPR-C. The PCR fragment was used to determine the tissue distribution of the new NPR-D message by an RNase protection assay, which gave the strongest signal in brain samples, and then used to screen a brain library to obtain a full-length cDNA clone. The cDNA clone predicted a protein of 500 amino acids containing a signal sequence and a hydrophobic transmembrane segment. The predicted sequence also contained the NPR motif which is essential for the binding of natriuretic peptides. The protein NPR-D was expressed in COS cells and shown to have high affinities for eel and rat natriuretic peptides. The newly cloned NPR-D has a short cytoplasmic tail; in this respect, NPR-C and NPR-D are very similar and form a subfamily of the NPR family. Affinity labeling indicated that NPR-D exists as a disulfide-linked tetramer. This is a marked contrast to the homodimeric structure of NPR-C. HS-142-1, a non-peptide natriuretic peptide receptor antagonist of microbial origin previously shown to be selective for the guanylate-cyclase-coupled receptors NPR-A and NPR-B, competitively inhibited the binding of 125I-labeled eel natriuretic peptide to eel NPR-D, whereas it did not affect the binding activity of eel NPR-C, suggesting that HS-142-1 is an antagonist that recognizes the tetrameric structures of NPR since the guanylate-cyclase-coupled receptors have also been demonstrated to exist as tetramers.
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PMID:Cloning and properties of a novel natriuretic peptide receptor, NPR-D. 758 32

Receptors for natriuretic peptide (NP) consist of three subtypes: NP-A, NP-B, and NP-C. Recent studies in cultured aortic cells have suggested a phenotype-related switching of the vascular NP receptor from NP-A to NP-B. To ascertain the biological significance of the phenomenon in vivo, we developed a sensitive and reproducible ribonuclease protection assay and determined each receptor messenger RNA (mRNA) level in the vascular vessels of stroke-prone spontaneously hypertensive rats, deoxycorticosterone acetate-salt hypertensive rats, and genetically hyperglycemic. Wistar fatty rats and in cultured aortic smooth muscle cells. The aortic NP-A receptor mRNA level was significantly up-regulated in both types of hypertensive rats, whereas the NP-B receptor mRNA level did not show any significant change. Both NP-A and NP-B receptor mRNA levels were significantly up-regulated in Wistar fatty rats compared with the control values. There was no significant up-regulation of NP-A receptor mRNA in the inferior vena cava of the stroke-prone spontaneously hypertensive rats. Although the NP-A receptor was always the predominant subtype in rat aortic tissue, NP-B receptor was the predominant subtype in aortic smooth muscle cells in culture. These findings suggest that up-regulation of the NP-A receptor, but not the subtype switching, is the major modulation of receptor gene expression in both hypertensive and diabetic rats.
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PMID:Modulation of vascular natriuretic peptide receptor gene expression in hypertensive and obese hyperglycemic rats. 775 Apr 64

We have recently found that vascular natriuretic peptide (NP)-A receptor mRNA is upregulated in genetically hypertensive (SHR-SP/Izm) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In the present study, we examined the effects of antihypertensive treatments on aortic NP-A receptor mRNA expression in these hypertensive rats using ribonuclease protection assay. Oral administration of an angiotensin converting enzyme inhibitor, derapril, but not a calcium channel blocker, manidipine, produced a significant decrease of the NP-A receptor mRNA level after 4 weeks, while both antihypertensive agents showed similar hypotensive effects. Plasma renin was high in SHR-SP/Izm and low in DOCA-salt rats. These results suggest that the vascular renin-angiotensin system rather than the blood pressure has an important role in the regulation of the vascular NP-A receptor.
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PMID:Angiotensin converting enzyme inhibitor but not calcium blocker down-regulates gene expression of vascular natriuretic peptide receptor in hypertensive rats. 781 Dec 41

The structure of the mouse natriuretic peptide type-B (BNP) gene was determined by isolating and sequencing genomic clones. The mouse BNP gene was structurally similar to other natriuretic peptide genes and comprised three exons and two introns. Expression of the mouse BNP gene was found only in cardiac tissue as determined by ribonuclease protection analyses. Initiation of transcription was 31 bp downstream from a consensus TATA box as determined by primer extension analysis of cardiac RNA. Comparative DNA sequence analysis identified several DNA elements with potential transcriptional regulatory function. Comparative amino acid sequence analysis showed that the N-terminal portion of the mouse and rat BNP precursors was more conserved than the C-terminal 45-amino-acid sequence that constitute the bioactive BNP-45 peptide. The proteolytic processing site (RXXR-S) generating bioactive BNPs was highly conserved among all BNP precursors and was identical to the consensus site of furin, a calcium-dependent serine endoprotease. Finally, the BNP gene was mapped using recombinant inbred DNA and a polymerase chain reaction-based restriction fragment-length polymorphism assay to mouse chromosome 4 near the atrial natriuretic factor (Anf) locus. No recombination event between Bnp and Anf was evident in the 39 recombinant inbred and inbred strains examined. This physical linkage between the two natriuretic peptide genes expressed in cardiac tissue may be important for their transcriptional regulation.
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PMID:Structure, expression, and genomic mapping of the mouse natriuretic peptide type-B gene. 809 40

The localization of mRNA encoding preproatrial natriuretic peptide (ANP) was investigated in cultured human umbilical vein endothelial cells (HUVEC) and tissue preparations of umbilical vein and artery. The techniques used were in situ hybridization and in situ hybridization combined with immunocytochemistry, using 32P-radiolabelled and non-radioactive digoxigenin labelled complementary RNA probes. Human ANP mRNAs are mainly localized in the endothelial cells of the umbilical vein and, to a lesser extent, in the endothelial cells of the umbilical artery. The autoradiographic labelling and the intensity of digoxigenin staining were significantly reduced by treatment with RNase before in situ hybridization. This study provides unequivocal evidence for the expression of the ANP gene in the endothelial cells of human umbilical vessels, confirming that these endothelial cells have the ability to synthesize this peptide. The functional significance of the presence of the ANP mRNA in the endothelial cells of human umbilical vessels is discussed.
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PMID:In situ hybridization of atrial natriuretic peptide mRNA in the endothelial cells of human umbilical vessels. 827 42

We previously demonstrated that angiotensin converting enzyme (ACE) inhibitor normalizes the up-regulated gene expression of vascular natriuretic peptide type A (NP-A) receptor in hypertensive rats. To elucidate the mechanism, we examined the effect of angiotensin II receptor (AT1) antagonist (TCV-116) and bradykinin receptor (B2) antagonist (Hoe 140) on the NP-A receptor mRNA level in the aorta of genetically hypertensive rats (SHR-SP/Izm) using ribonuclease protection assay. The effect of ACE inhibitor on the NP-A receptor mRNA level was completely abolished by a concomitant administration of Hoe 140, while TCV-116 did not show any significant effect on the NP-A receptor mRNA level. These results suggest that bradykinin plays an important role in the regulation of the vascular NP-A receptor gene expression.
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PMID:Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats. 857 74

Biological actions of natriuretic peptide (NP) are determined by the condition of the receptor as well as that of the hormone. Although we previously demonstrated in hypertensive rats the up-regulation of NP-A receptor that mediates various biological actions of NPs, the pathophysiologic significance of NP-C receptor, another subtype thought to be related to clearance of NPs and possibly to biological actions, remains unknown. In the present study, we determined NP-C receptor messenger RNA (mRNA) level in the aortic tissue of stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and in cultured aortic smooth muscle cells by ribonuclease protection assay. The aortic NP-C receptor mRNA level in SHR-SP/Izm was significantly lower than that in the control WKY/Izm. Oral administration of an angiotensin (Ang) II receptor (AT1) antagonist, TCV-116, but not a calcium channel blocker, manidipine, reversed the down-regulated NP-C receptor mRNA in SHR-SP/Izm to the level in WKY/Izm, whereas the latter was more potent in decreasing the blood pressure. In cultured aortic smooth muscle cells, the NP-C receptor was the predominant subtype. Ang II decreased the NP-C receptor mRNA level in a dose-dependent manner, but this effect was reversed by an AT1 antagonist, CV-11974. Neither the NP-A nor NP-B receptor mRNA level was altered by Ang II. These findings indicate that vascular NP-C receptor is down- regulated via Ang-II-mediated mechanism in SHR-SP/Izm. The phenomenon, together with the up-regulation of the NP-A receptor, may play an important role in counteracting hypertension by enhancing the action of NPs.
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PMID:Angiotensin II-dependent down-regulation of vascular natriuretic peptide type C receptor gene expression in hypertensive rats. 860 80

Chondrocytes derived from rat xiphoid cartilage dedifferentiated into fibroblast-like cells as the number of passages of the cells in culture increased. During in vitro dedifferentiation the growth of the cells was markedly suppressed. We had proposed previously that C-type natriuretic peptide (CNP) might be a potent antimitogenic factor for chondrocytes, and TGF-beta 1 induced a marked increase in CNP secretion of chondrocytes. Therefore, we investigated the expression of CNP, B-type natriuretic peptide receptor (NPR-B or GC-B), and TGF-beta 1 in this process. Radioimmunoassay and RNase protection analyses revealed passage-associated increase in CNP-like immunoreactivity and in levels of NPR-B mRNA, respectively. Northern blot analyses showed that the level of TGF-beta 1 mRNA decreased with increasing passage number. These results suggest that the expression of CNP and NPR-B might be involved in in vitro dedifferentiation of chondrocytes and TGF-beta 1 does not affect the increasing level of CNP during in vitro dedifferentiation.
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PMID:Change in the expression of C-type natriuretic peptide and its receptor, B-type natriuretic peptide receptor, during dedifferentiation of chondrocytes into fibroblast-like cells. 888 16

Genomic sequences encoding mouse C-type natriuretic peptide (CNP) were isolated from bacteriophage libraries and characterized by restriction enzyme and sequence analysis. The mouse CNP gene (Nppc) comprised at least two exons and one intron and included several cis-regulatory elements in the 5'-flanking sequence. The deduced amino acid sequence of mouse CNP-22 was identical to other mammalian CNPs. Analysis of allele distributions in interspecific back-cross and recombinant inbred strains assigned Nppc to chromosome 1. CNP transcripts were detected by ribonuclease protection analysis in brain, ovary, and uterus, with lower levels in testes and epididymus. Uterine CNP transcripts and protein were low in sexually immature mice and adults at estrus and increased at proestrus, but similar variations in ovarian CNP expression were not statistically significant. Atrial natriuretic peptide and B-type natriuretic peptide transcripts were not detected in mouse ovary or uterus. Thus CNP gene expression is regulated by tissue-specific and inducible mechanisms in female reproductive organs. Correlations between CNP expression and uterine fluid content suggest that CNP may regulate uterine fluid balance in mice and other mammals.
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PMID:Isolation, mapping, and regulated expression of the gene encoding mouse C-type natriuretic peptide. 889 53


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