Increased Angiotensin II AT1 receptor mRNA and binding in spleen and lung of AT2 receptor gene disrupted mice
| Autor: | José A. Terrón, Julius Benicky, Jaroslav Pavel, Amita Rachakonda, Alicia Falcón-Neri, Tadashi Inagami, Juan M. Saavedra |
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| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
medicine.medical_specialty
Angiotensin receptor endocrine system Physiology Clinical Biochemistry Biology Biochemistry Polymerase Chain Reaction Article Receptor Angiotensin Type 1 Cellular and Molecular Neuroscience Estrogen-related receptor alpha Mice Endocrinology Internal medicine medicine Animals RNA Messenger Receptor Lung In Situ Hybridization Common gamma chain Insulin-like growth factor 1 receptor DNA Primers Angiotensin II receptor type 1 Receptors Angiotensin Base Sequence Liver X receptor alpha respiratory system Angiotensin II Molecular biology Mice Inbred C57BL cardiovascular system Autoradiography hormones hormone substitutes and hormone antagonists Spleen circulatory and respiratory physiology Protein Binding |
| Popis: | To clarify the relationship between Angiotensin II AT(1) and AT(2) receptors, we studied AT(1) receptor mRNA and binding expression in tissues from AT(2) receptor gene disrupted (AT(2)(-/-)) female mice, where AT(2) receptors are not expressed in vivo, using in situ hybridization and quantitative autoradiography. Wild type mice expressed AT(1A) receptor mRNA and AT(1) receptor binding in lung parenchyma, the spleen, predominantly in the red pulp, and in liver parenchyma. In wild type mice, lung AT(2) receptors were expressed in lung bronchial epithelium and smooth muscle, and were not present in the lung parenchyma, the spleen or the liver. This indicates that AT(1) and AT(2) receptors were not expressed in the same cells. In AT(2)(-/-) mice, we found higher AT(1A) receptor mRNA and AT(1) receptor binding in lung parenchyma and in the red pulp of the spleen, but not in the liver, when compared to littermate wild type controls. Our results suggest that impaired AT(2) receptor function upregulates AT(1) receptor transcription and expression in a tissue-specific manner and in cells not expressing AT(2) receptors. AT(1) upregulation explains the increased sensitivity to Angiotensin II characteristic of the AT(2)(-/-) phenotype, consistent with enhanced AT(1) receptor activation in a number of tissues. |
| Databáze: | OpenAIRE |
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