Thymosin beta 4 is dispensable for murine cardiac development and function.
Open accessAbstract
Rationale: Thymosin beta 4 (Tβ4) is a 43–amino acid factor encoded by an X-linked gene. Recent studies have suggested that Tβ4 is a key factor in cardiac development, growth, disease, epicardial integrity, and blood vessel formation. Cardiac-specific short hairpin (sh)RNA knockdown of tβ4 has been reported to result in embryonic lethality at E14.5–16.5, with severe cardiac and angiogenic defects. However, this shRNA tβ4 -knockdown model did not completely abrogate Tβ4 expression. To completely ablate Tβ4 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 Tβ4 in developing and adult heart through global and cardiac specific t β4-knockout mouse models. Methods and Results: Global t β 4 -knockout mice were born at mendelian ratios and exhibited normal heart and blood vessel formation. Furthermore, in adult global t β 4 -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 t β 4 -deficient mice, generated by crossing t β 4 -floxed mice to Nkx2.5-Cre and α MHC-Cre , were also found to have no phenotype. Conclusions: We conclude that Tβ4 is dispensable for embryonic viability, heart development, coronary vessel development, and adult myocardial function.
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- Authors
- Banerjee, I., Zhang, J., Moore-Morris, T., Lange, S., Shen, T., Dalton, N. D., Gu, Y., Peterson, K. L., Evans, S. M., & Chen, J.
- Affiliations
- University of California San Diego (US)
- From the Department of Medicine (I.B., J.Z., S.L., T.S., N.D.D., Y.G., K.L.P., S.M.E., J.C.) and Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California–San Diego, La Jolla, CA (T.M.M., T.S., S.M.E.).
- Corresponding author
- Chen, Ju
- Venue
- Circulation Research
- Published
- 2012-02-03
- Volume
- 110
- Issue
- 3
- Pages
- 456-464
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC3739283
- OpenAlex
- W2020964402
- Cited by
- 59
- References
- 31
- Citations by year
- 2023: 2 · 2022: 3 · 2021: 4 · 2020: 1 · 2019: 4 · 2018: 8 · 2016: 5 · 2015: 5 · 2014: 7 · 2013: 10 · 2012: 10
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1r01hl106968-01)
- National Heart, Lung, and Blood Institute (R01-HL106968, R01HL066100, DP1HL117649, T32HL007444)
- National Institute of Neurological Disorders and Stroke (P30NS047101)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- thymosin beta 4, heart development, cardiac function, cardiac-specific knockout, coronary vessel development, angiogenesis, epicardium, capillary density, extracellular matrix, embryonic lethality
- MeSH terms
- Thymosin beta(4), Animals, Coronary Vessels, Female, Heart, Male, Thymosin, Mice, Knockout, Gene Expression Regulation, Developmental, Neovascularization, Physiologic, Models, Animal, RNA, Small Interfering, Embryonic Development, Mice
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