| First Author | Banerjee I | Year | 2012 |
| Journal | Circ Res | Volume | 110 |
| Issue | 3 | Pages | 456-64 |
| PubMed ID | 22158707 | Mgi Jnum | J:185264 |
| Mgi Id | MGI:5427986 | Doi | 10.1161/CIRCRESAHA.111.258616 |
| Citation | Banerjee I, et al. (2012) Thymosin beta 4 is dispensable for murine cardiac development and function. Circ Res 110(3):456-64 |
| abstractText | RATIONALE: Thymosin beta 4 (Tbeta4) is a 43-amino acid factor encoded by an X-linked gene. Recent studies have suggested that Tbeta4 is a key factor in cardiac development, growth, disease, epicardial integrity, and blood vessel formation. Cardiac-specific short hairpin (sh)RNA knockdown of tbeta4 has been reported to result in embryonic lethality at E14.5-16.5, with severe cardiac and angiogenic defects. However, this shRNA tbeta4-knockdown model did not completely abrogate Tbeta4 expression. To completely ablate Tbeta4 and to rule out the possibility of off-target effects associated with shRNA gene silencing, further studies of global or cardiac-specific knockouts are critical. OBJECTIVE: We examined the role of Tbeta4 in developing and adult heart through global and cardiac specific tbeta4-knockout mouse models. METHODS AND RESULTS: Global tbeta4-knockout mice were born at mendelian ratios and exhibited normal heart and blood vessel formation. Furthermore, in adult global tbeta4-knockout mice, cardiac function, capillary density, expression of key cardiac fetal and angiogenic genes, epicardial marker expression, and extracellular matrix deposition were indistinguishable from that of controls. Tissue-specific tbeta4-deficient mice, generated by crossing tbeta4-floxed mice to Nkx2.5-Cre and alphaMHC-Cre, were also found to have no phenotype. CONCLUSIONS: We conclude that Tbeta4 is dispensable for embryonic viability, heart development, coronary vessel development, and adult myocardial function. |
