Function and expression of ATIP and its variants in cardiomyoblast cell line H9c2
| Autor: | Simon N S Louis, Michael A Krezel, William J Louis, Laurie T C Chow, Albert G Frauman, Linda Adriana Rezmann, Naghmeh Varghayee |
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| Rok vydání: | 2013 |
| Předmět: |
Medicine (General)
medicine.medical_specialty medicine.medical_treatment Genetic Vectors Muscle Fibers Skeletal Cardiomegaly Biology Receptor Angiotensin Type 2 Cell Line Muscle hypertrophy R5-920 Endocrinology Internal medicine Internal Medicine medicine Animals Myocyte Phosphorylation Receptor Cell Proliferation Cell Size Cell growth Growth factor Intracellular Signaling Peptides and Proteins Angiotensin II Rats Cell biology Cell culture cardiovascular system Myoblasts Cardiac hormones hormone substitutes and hormone antagonists Thymidine circulatory and respiratory physiology |
| Zdroj: | Journal of the Renin-Angiotensin-Aldosterone System, Vol 16 (2015) |
| ISSN: | 1752-8976 1470-3203 |
| DOI: | 10.1177/1470320313483845 |
| Popis: | Hypothesis: Cardiac hypertrophy in myocytes is in part regulated by changes in expression of a novel Ang II type 2 recep- tor (AT2-receptor) interacting protein identified as ATIP. Introduction: The role of the AT2-receptor in cardiac hypertrophy is controversial, with some reports indicating that AT2-receptor activation has detrimental effects on disease progression, whereas others indicate that it has a beneficial role. Materials and methods: In an effort to unravel this paradox, we examined the expression and function of ATIP in cell- based models of cardiac hypertrophy using QPCR, immunohistochemistry, cell proliferation, morphological and transfec- tion techniques in H9c2 cardio-myoblast and myotubules. Results: These studies indicate that in cultured cardio-myoblast and myotubules, Ang II mediates cellular hypertrophy and proliferation solely via the AT1-receptor, the ATIP variants are abundantly expressed and that ATIP3 may play an anti- proliferative/hypertrophic role in these cells in the absence of AT2-receptor expression or activation. Conclusions: Previously ATIP has been shown to inhibit growth factor signalling in cancerous cells via an interaction with the AT2-receptor. This is the first report to identify that ATIP may have a similar role in other disease states charac- terised by excessive growth and indicates that for ATIP3, at least, an interaction with the AT2-receptor may not be necessary. |
| Databáze: | OpenAIRE |
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