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

Ribonuclease (RNase) activity measured at pH 7.8 (the alkaline RNase) and pH 6.7 (the acid RNase) was estimated in serum of 54 patients with acute myocardial infarction (AMI). The estimations were performed on the first day of disease, then on the seven consecutive days and on the 14th day. A significant elevation in both alkaline and acid RNase activities on days 1--7 of AMI was found, compared with healthy control subjects. Elevation in both acid and alkaline RNase activity began on the 1st day of AMI and continued to increase up to peak values on the 3rd day for acid RNase and the 5 the day for alkaline RNase. On the 14th day both alkaline and acid RNase activities came back to the range found in normal sera. Increase in serum acid and alkaline RNase activity in AMI showed a time pattern different from that of GOT and GPT aminotransferases. However, the relationship between the elevation of serum RNase activity and severity of the disease was obvious.
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PMID:Serum ribonuclease activity in acute myocardial infarction. 729 72

An increase in myocardial bradykinin (BK) might be a mechanism to protect the heart during acute myocardial infarction (MI). To characterize the regulation of the myocardial B2 receptor during MI, we studied the expression of this BK receptor in the right ventricle (RV), left ventricle (LV) and myocardial septum (S) 24 h after left coronary ligation. Experiments were performed in male Wistar Kyoto rats (n = 10) and compared with sham operated animals (n = 6). After total RNA extraction, the myocardial B2-receptor expression was analyzed by a RNase protection assay (n = 6), using a specific probe from the coding region of the receptor gene. After 24 h, rats with MI were normotensive and showed an impaired left ventricular function. The B2-receptor expression of the LV of these rats was significantly elevated (2.3-fold) compared to sham operated rats. Furthermore, we found a dramatic upregulation of the B2 receptor in the RV (7.8-fold) and a dramatic expression of B2 receptor mRNA in S of infarcted hearts, whereas in the S of sham operated rats no B2 receptor expression could be detected. Our data show clearly that the described increase in BK during myocardial ischemia is accompanied by an elevated B2-receptor expression in the infarcted and non-infarcted parts of cardiac ventricles.
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PMID:Upregulation of the cardiac bradykinin B2 receptors after myocardial infarction. 1060 33

Although cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in non-infarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury.
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PMID:Decreased expression of Na+/H+ exchanger isoform 1 (NHE1) in non-infarcted myocardium after acute myocardial infarction. 1222 2

The proinflammatory cytokines interleukin (IL)-1beta and IL-6 are increased after acute myocardial infarction (MI). Moreover, serum IL-6 level is elevated after MI, but has also been associated with heart failure. In the present study, heart function was monitored in a rat model of chronic MI. Cytokine expression in the infarcted and non-infarcted myocardium as well as in hearts of sham-operated controls was measured by the ribonuclease-protection assay. To identify the cells contributing to the increased cytokine expression, we further analyzed myocytes and non-myocytes isolated in the acute phase as well as during congestive heart failure (CHF) after MI. There was a strong induction in cytokine expression in the myocytes of the infarct area 6 h after MI. In the non-infarcted myocardium, cytokine expression increased only slightly in the non-myocytes after 6 h. This was not different from sham-operated controls and may, therefore, be induced by stress and catecholamines. In CHF, however, cytokine expression level in myocytes was normal. It increased slightly but significantly in the non-myocytes 4 and 8 weeks after MI. In conclusion, we suggest that pro-inflammatory cytokines, produced by the ischemic myocytes may be involved in the initiation of wound healing of the necrotic area, whereas the effect of pro-inflammatory cytokines in CHF, if any, seems not to be crucial.
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PMID:Differential cytokine expression in myocytes and non-myocytes after myocardial infarction in rats. 1261 65

Nucleolytic enzymes are associated with various diseases, and several methods have been developed for their detection. DNase expression is modulated in such diseases as acute myocardial infarction, transient myocardial ischemia, oral cancer, stomach cancer, and malignant lymphoma, and DNase I is used in cystic fibroma therapy. RNase is used to treat mesothelial cancer because of its antiproliferative, cytotoxic, and antineoplastic activities. Angiogenin, an angiogenic factor, is a member of the RNase A family. Angiogenin inhibitors are being developed as anticancer drugs. In this review, we describe fluorometric and electrochemical techniques for detecting DNase and RNase in disease. Oligonucleotides having fluorescence resonance energy transfer (FRET)-causing chromophores are non-fluorescent by themselves, yet become fluorescent upon cleavage by DNase or RNase. These oligonucleotides serve as a powerful tool to detect activities of these enzymes and provide a basis for drug discovery. In electrochemical techniques, ferrocenyl oligonucleotides with or without a ribonucleoside unit are used for the detection of RNase or DNase. This technique has been used to monitor blood or serum samples in several diseases associated with DNase and RNase and is unaffected by interferents in these sample types.
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PMID:Highly sensitive nuclease assays based on chemically modified DNA or RNA. 2501 31