Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.27.1 (RNase)
 16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of ANP prohormone immunoreactivity in rat GI tract suggests that it may be an extracardiac site of ANP synthesis. The aim of this study was to investigate the expression of ANP mRNA in the adult rat GI tract. ANP mRNA was detected by ribonuclease protection analysis in stomach, small and large intestines, and rectum/anus. The highest concentrations of ANP transcripts were found in the proximal stomach, antrum, proximal colon, and rectum/anus at levels that ranged from 1 to 10% of that found in cardiac ventricle. Northern blot analysis of total RNA from these tissues identified a single 0.9 kb ANP transcript similar to that detected in heart. Gel filtration chromatography of tissue extracts provided evidence for the presence of the complete ANP prohormone in proximal stomach, antrum, proximal colon and rectum/anus. These results demonstrate that the gene for ANP is expressed in specific regions of the rat GI tract, suggesting that tissue-specific differential regulation of ANP synthesis occurs within the GI tract.
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PMID:Atrial natriuretic peptide gene expression in the rat gastrointestinal tract. 803 63

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

C-type natriuretic peptide (CNP), a recent addition to the family of natriuretic peptides including atrial and brain natriuretic peptide (ANP, BNP), is believed to be an endothelium-derived vasodilator and to have an antimitotic effect. ANP and BNP concentrations are increased in conditions such as congestive heart failure, but cardiac CNP concentrations have not been investigated in this connection. Diabetes mellitus also involves myocardial dysfunctions without coronary artery disease or systemic hypertension. We therefore investigated the cardiac expression of CNP mRNA compared with that of BNP mRNA in streptozotocin (STZ)-diabetic rats. STZ- diabetic male Wistar rats (n=6) were studied in comparison with controls (n=6). The animals were characterised by their mean arterial blood pressure and plasma glucose concentrations. After extraction of total cardiac RNA, a specific cDNA probe of BNP was used for northern blot analysis, whereas myocardial CNP expression was analysed by an RNase-protection assay. Twelve weeks after diabetes was induced, the rats were normotensive (96.4+/-2.0 compared with 95.1+/-1.9 mmHg) and hyperglycaemic (615+/-61 compared with 165+/-21 mg/dl; P<0.001). Left ventricular pressure was significantly impaired (76.8+/-6.4 compared with 51.2+/-3.6 mmHg). STZ-diabetic rats had a 3.2-fold increase in cardiac BNP expression compared with controls. In contrast, cardiac CNP mRNA concentrations were decreased 2.6-fold. CNP seems to be downregulated like other peptides with antimitotic and vasodilator activities (nitric oxide, prostacyclin, kinins). This may contribute to cardiac dysfunction in diabetes mellitus and suggests that stimulation of CNP expression could provide cardiac protection in such cases.
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PMID:Opposite regulation of brain and C-type natriuretic peptides in the streptozotocin-diabetic cardiopathy. 1082 32

The aim of our study was to clarify whether atrial (ANP) and brain (BNP) natriuretic peptides and the hypotensive peptide adrenomedullin (ADM) are regulated differently in the rat heart in the two-kidney, one-clip model of renovascular hypertension. We assessed messenger ribonucleic acid (mRNA) abundance and distribution of ANP, BNP and ADM in the ventricles and atria of rats after unilateral renal artery stenosis (clipping). Rats were clipped for 6 h or 1, 2 or 4 days and mRNA levels were assessed semiquantitatively in left and right atria and ventricles by RNase protection assay. Left ventricular BNP mRNA up-regulation (4.3-fold after 6 hours) preceded ANP up-regulation (4.5-fold after 1 day) and seemed to be transient, whereas ANP mRNA levels were still elevated at day 4 (2.4-fold vs. sham). The right ventricle and the atria did not participate in these responses. Despite the massive changes of natriuretic peptide mRNAs, ADM mRNA did not change in either the ventricles or the atria. In contrast to ANP and BNP mRNA, which predominate in atrial tissue, mRNA for adrenomedullin is equally distributed in ventricles and atria. Plasma levels of immunoreactive (ir)-ANP and ir-BNP changed in parallel with left ventricular mRNA levels. Our findings suggest that renovascular hypertension induced by clipping the renal artery leads to immediate, but independent, up-regulation of ANP and BNP mRNA in the left ventricle whereas adrenomedullin mRNA is not changed.
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PMID:Different regulation of left ventricular ANP, BNP and adrenomedullin mRNA in the two-kidney, one-clip model of renovascular hypertension. 1141 16

A novel membrane guanylyl cyclase (membrane GC), OlGC8, was identified in the medaka fish Oryzias latipes by the isolation of full-length cDNA (4958 bp) and genomic DNA (14.3 kbp) clones. Phylogenetic analysis indicated that OlGC8 does not belong in any known vertebrate membrane GC subfamily. OlGC8 consists of an extracellular domain (214 residues), a transmembrane segment (19 residues), and an intracellular protein kinase-like domain (284 residues) and a cyclase catalytic domain (228 residues), although the extracellular domain is about half the length (around 450 residues) of other known vertebrate membrane GCs. OlGC8 transiently expressed in COS-7 cells exhibited only basal guanylyl cyclase activity. None of the known ligands (rat ANP, BNP, CNP, and C-ANF) and various medaka fish tissue extracts, which activated OlGC1, OlGC2, and OlGC7 differentially, stimulated basal activity, suggesting that OlGC8 is an orphan receptor. The OlGC8 gene consists of 24 exons and exists as a single copy on the medaka fish genome. Northern blot hybridization showed that a 5 kb-OlGC8 mRNA was expressed in the kidney and the testis at a high level and a 3.3 kb-OlGC8 mRNA was expressed only in the brain. The RNase protection, RNA Ligase-Mediated Rapid Amplification of cDNA Ends (RLM-RACE), and reverse transcription-polymerase chain reaction (RT-PCR) analyses demonstrated that the 3.3 kb-OlGC8 mRNA detected in the brain is transcribed from the second transcription initiation site, and contains an intron at the position prior to the catalytic domain, the translation product of which appears to be a protein lacking the cyclase catalytic domain.
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PMID:Expression and genomic organization of a medaka fish novel membrane form of guanylyl cyclase/orphan receptor. 1277 30

Stored cardiac pro-atrial natriuretic peptide (pro-ANP) is converted to ANP and released upon stretch from the atria into the circulation. Corin is a serin protease with pro-ANP-converting properties and may be the rate-limiting enzyme in ANP release. This study was aimed to clone and sequence corin in the rat and to analyze corin mRNA expression in heart failure when ANP release upon stretch is blunted. Full-length cDNA of rat corin was obtained from atrial RNA by RT-PCR and sequenced. Tissue distribution as well as regulation of corin mRNA expression in the atria were determined by RT-PCR and RNase protection assay. Heart failure was induced by an infrarenal aortocaval shunt. Stretch was applied to the left atrium in a working heart modus, and ANP was measured in the perfusates. The sequence of rat corin cDNA was found to be 93.6% homologous to mouse corin cDNA. Corin mRNA was expressed almost exclusively in the heart with highest concentrations in both atria. The aortocaval shunt led to cardiac hypertrophy and heart failure. Stretch-induced ANP release was blunted in shunt animals (control 1,195 +/- 197 fmol.min(-1).g(-1); shunt: 639 +/- 99 fmol.min(-1).g(-1), P < 0.05). Corin mRNA expression was decreased in both atria in shunt animals [right atrium: control 0.638 +/- 0.004 arbitrary units (AU), shunt 0.566 +/- 0.014 AU, P < 0.001; left atrium: control 0.564 +/- 0.009 AU, shunt 0.464 +/- 0.009 AU, P < 0.001]. Downregulation of atrial corin mRNA expression may be a novel mechanism for the blunted ANP release in heart failure.
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PMID:Rat corin gene: molecular cloning and reduced expression in experimental heart failure. 1515 64