A Tissue Engineered Blood Vessel Model of Hutchinson-Gilford Progeria Syndrome Using Human iPSC-derived Smooth Muscle Cells
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-017-08632-4.pdf
Reference49 articles.
1. Gonzalo, S., Kreienkamp, R. & Askjaer, P. Hutchinson-Gilford Progeria Syndrome: a premature aging disease caused by LMNA gene mutations. Ageing Res. Rev. 33, 18–29, doi: 10.1016/j.arr.2016.06.007 (2017).
2. Booth-Gauthier, Ea et al. Hutchinson-Gilford progeria syndrome alters nuclear shape and reduces cell motility in three dimensional model substrates. Integr. Biol. 5, 569–77, doi: 10.1039/c3ib20231c (2013).
3. Gonzalo, S. & Kreienkamp, R. DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome. Curr. Opin. Cell Biol. 34, 75–83, doi: 10.1016/j.ceb.2015.05.007 (2015).
4. McClintock, D., Gordon, L. B. & Djabali, K. Hutchinson–Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody. Proc. Natl. Acad. Sci. USA 103, 2154–2159, doi: 10.1073/pnas.0511133103 (2006).
5. Choi, K.-M. et al. Effect of ascorbic acid on bone marrow-derived mesenchymal stem cell proliferation and differentiation. J. Biosci. Bioeng. 105, 586–594, doi: 10.1263/jbb.105.586 (2008).
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