Although cardiac hypertrophy is a compensatory mechanism of the stressed heart, it ultimately leads to cardiac dysfunction. GATA-4, a member of the GATA family, plays an essential role in this process, nevertheless, its mechanism of action is still largely unknown. We have isolated a new evolutionarily conserved protein, ENDO1, that belongs to a new subfamily of PHD finger proteins. In adult mouse, ENDO1 was highly expressed in the kidney, lung, spleen, heart and brain. In ventricular cardiomyocytes, endogenous ENDO1 was expressed in the nucleus and cytoplasm. Overexpression analysis of antisense and sense GATA-4 suggests that GATA-4 downregulates endogenous ENDO1 in cardiomyocytes at the mRNA and protein levels. The protein levels of ENDO1 were enhanced in cardiomyocytes stimulated with phenylephrine, a hypertrophy stimulus. Structure-function analysis revealed that ENDO1 inhibits the activity levels of the BNP promoter. Our results indicate that the ENDO1 protein may play a significant role in cardiac development and differentiation.
| Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.80294 |
| Date | January 2004 |
| Creators | Jain, Pooja |
| Contributors | Nemer, Mona (advisor) |
| Publisher | McGill University |
| Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
| Language | English |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Format | application/pdf |
| Coverage | Master of Science (Division of Experimental Medicine.) |
| Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
| Relation | alephsysno: 002141205, proquestno: AAIMQ98663, Theses scanned by UMI/ProQuest. |
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