The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Regulation of gene transcription of angiotensin II receptor subtypes in myocardial infarction.
Open accessAbstract
Increasing evidence suggests that angiotensin II (AngII) acts as a modulator for ventricular remodeling after myocardial infarction. Using competitive reverse-transcriptase polymerase chain reaction, nuclear runoff, and binding assays, we examined the regulation of AngII type 1a and 1b (AT1a-R and AT1b-R) and type 2 receptor (AT2-R) expression in the infarcted rat heart as well as the effects of AngII receptor antagonists. AT1a-R mRNA levels were increased in the infarcted (4.2-fold) and noninfarcted portions (2.2-fold) of the myocardium 7 d after myocardial infarction as compared with those in sham-operated controls, whereas AT1b-R mRNA levels were unchanged. The amount of detectable AT2-R mRNA increased in infarcted (3.1-fold) and noninfarcted (1.9-fold) portions relative to that in the control. The transcription rates for AT1a-R and AT2-R genes, determined by means of a nuclear runoff assay, were significantly increased in the infarcted heart. The AngII receptor numbers were elevated (from 12 to 35 fmol/mg protein) in the infarcted myocardium in which the increases in AT1-R and AT2-R were 3.2- and 2.3-fold, respectively, while the receptor affinity was unchanged. Therapy with AT1-R antagonist for 7 d reduced the increase in AT1-R and AT2-R expressions in the infarcted heart together with a decrease in blood pressure, whereas therapy with an AT2-R antagonist did not affect mRNA levels and blood pressure. Neither AT1-R nor AT2-R antagonists affected the infarct sizes. These results demonstrated that myocardial infarction causes an increase in the gene transcription and protein expression of cardiac AT1a-R and AT2-R, whereas the AT1b-R gene is unaffected, and that therapy with an AT1-R antagonist, but not with an AT2-R antagonist, is effective in reducing the increased expression of AngII receptor subtypes induced by myocardial infarction.
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Identification of angiotensin II receptor subtypes
Chiu, A. T., Herblin, W. F., McCall, D. E., Ardecky, R. J., Carini, D. J., Duncia, J. V., Pease, L. J., Wong, P. C., Wexler, R. R., Johnson, A. L., et al. (1989) · Biochemical and Biophysical Research Communications · doi:10.1016/0006-291x(89)91054-1 · Cited by 819
Cited by
Goette, A., Staack, T., Röcken, C., Arndt, M., Geller, J. C., Huth, C., Ansorge, S., Klein, H. U., & Lendeckel, U. (2000) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(00)00611-2 · Cited by 583
Horiuchi, M., Hayashida, W., Kambe, T., Yamada, T., & Dzau, V. J. (1997) · Journal of Biological Chemistry · doi:10.1074/jbc.272.30.19022 · Cited by 295
Tsutsumi, Y., Matsubara, H., Ohkubo, N., Mori, Y., Nozawa, Y., Murasawa, S., Kijima, K., Maruyama, K., Masaki, H., Moriguchi, Y., et al. (1998) · Circulation Research · doi:10.1161/01.res.83.10.1035 · Cited by 241
Self-citationThe Angiotensin AT2 Receptor: From a Binding Site to a Novel Therapeutic Target
Steckelings, U. M., Widdop, R. E., Sturrock, E. D., Lubbe, L., Hussain, T., Kaschina, E., Unger, T., Hallberg, A., Carey, R. M., & Sumners, C. (2022) · Pharmacological Reviews · doi:10.1124/pharmrev.120.000281 · Cited by 97
Wilms, H., Rosenstiel, P., Unger, T., Deuschl, G., & Lucius, R. (2005) · American Journal of Cardiovascular Drugs · doi:10.2165/00129784-200505040-00004 · Cited by 52
Metadata
- Authors
- Nio, Y., Matsubara, H., Murasawa, S., Kanasaki, M., & Inada, M.
- Venue
- Journal of Clinical Investigation
- Published
- 1995-01-01
- Volume
- 95
- Issue
- 1
- Pages
- 46-54
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2149060182
- Cited by
- 435
- References
- 42
- FWCI
- 27.46
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Nio, Y., Matsubara, H., Murasawa, S., Kanasaki, M., & Inada, M. (1995). Regulation of gene transcription of angiotensin II receptor subtypes in myocardial infarction. Journal of Clinical Investigation. https://doi.org/10.1172/jci117675
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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