Please use this identifier to cite or link to this item:
|Title:||Reversal of myocardial injury using genetically modulated human skeletal myoblasts in a rodent cryoinjured heart model|
|Authors:||Ye, L. |
|Citation:||Ye, L., Sim, E.K.W., Haider, H.Kh., Jiang, S., Ling, L.H., Ge, R., Law, P.K. (2005). Reversal of myocardial injury using genetically modulated human skeletal myoblasts in a rodent cryoinjured heart model. European Journal of Heart Failure 7 (6) : 945-952. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ejheart.2005.03.012|
|Abstract:||Background: We hypothesized that combination therapy using human myoblasts and VEGF165 will lead to better prognosis in a failing heart. Methods: Forty-eight female Wistar rats with cryoinjured hearts were randomized into non-treated normal (group-1, n = 12), DMEM injected (group-2, n = 10), myoblast-transplanted (group-3, n = 12) and myoblast-hVEGF165 (group-4, n = 14). Ten days after cryoinjury, 200 μl DMEM containing 3 × 106 cells or without cells was injected into the injured myocardium. Animals were maintained on cyclosporine for 6 weeks post cell transplantation. Heart function was assessed by echocardiography. Animals were sacrificed and hearts were processed for histochemical and immunohistochemical studies. Results: Histological examination showed survival of the donor myoblasts expressing lac-z and hVEGF165 in rat cardiac tissue. Fluorescent immunostaining for vWillebrand Factor-VIII and smooth muscle actin expression at low power microscope (× 100) showed significantly higher blood vessel density in group-4 (31.25 ± 1.82; 24.63 ± 0.92) as compared to group-2 (13.29 ± 1.0; p < 0.001; 9.71 ± 0.81, p < 0.001) and group-3 (16.50 ± 1.43, p < 0.001; 14.5 ± 1.34, p < 0.001). Echocardiography showed that ejection fraction and fractional shortening of group-3 (93.36 ± 1.52%, p = 0.005; 75 ± 3.75%, p = 0.024) and group-4 (94.8 ± 1.62%, p = 0.003; 76.13 ± 2.15%, p = 0.011) significantly improved as compared to group-2 (81.8 ± 3.3%, 55.1 ± 7.18%). Conclusion: Myoblasts carrying of hVEGF165 are potential therapeutic transgene carriers for cardiac repair. © 2005 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.|
|Source Title:||European Journal of Heart Failure|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Oct 20, 2018
WEB OF SCIENCETM
checked on Oct 3, 2018
checked on Oct 13, 2018
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.