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Updated: Jun 25, 2026

In Vitro Generation of Heart Field-specific Cardiac Progenitor Cells
Published on: July 3, 2019
In vitro cardiogenesis can be initiated in human CD34+ cells
1Department of Biotechnology, Sri Venkateswara Institute of Medical Sciences, Tirupati 517507, India.
Insights
Stem cells can be differentiated into cardiomyocytes in vitro. Transplanting these lab-grown cardiomyocytes may prevent heart failure after myocardial infarction, offering a future therapeutic strategy.
Area of Science:
- Regenerative Medicine
- Cardiovascular Biology
- Stem Cell Biology
Background:
- Myocardial infarction causes extensive cardiac tissue damage, a major concern in post-infarct management.
- Adult stem cells, mobilized by granulocyte-colony stimulating factor (G-CSF), home to damaged myocardium due to their proliferative and differentiation capacities.
Purpose of the Study:
- To investigate the potential of in vitro cardiogenesis from CD34+ stem cells.
- To evaluate the therapeutic potential of cardiomyocytes derived from autologous stem cells for myocardial repair.
Main Methods:
- Stem cells were harvested from peripheral blood of a healthy donor after G-CSF administration.
- Peripheral blood stem cells (PBSC) were identified using CD34+ monoclonal antibodies.
- In vitro cardiogenesis was induced using 5'Azacytidine, followed by culture for 17 weeks.
Main Results:
- In vitro cardiogenesis was successfully initiated in CD34+ cells with 5'Azacytidine.
- Cells exhibited spontaneous beating within 24 hours and formed myotubes after 5 weeks.
- Expression of cardiomyocyte markers (MLC2v, GATA-4) confirmed successful differentiation.
Conclusions:
- Transplantation of autologous stem cells or derived cardiomyocytes into infarct scar tissue can limit scar expansion and prevent heart failure.
- While stem cell homing is time-consuming, transplanting pre-developed cardiomyocytes offers a promising future approach for infracted myocardium repair.
Background:
The extensive damage that occurs in the cardiac tissue after myocardial infarct is the major concern in post infarct management. It is very well known that adult stem cells mobilized by administration of G-CSF result in homing of stem cells into the damaged myocardium. This is because of the fact that stem cells have the ability to proliferate and capacity to generate into multiple cell lineages.
Method:
A healthy donor was selected as per the guidelines given by the institutional ethical committee and Helsinki declaration. The donor was given G-CSF 5 microg/kg/day and stem cells were harvested from the peripheral blood using Fresenius ASTec204 cell separator. The PBSC were then evaluated by immunohistochemical staining using anti-human CD34 monoclonal antibodies. The cells were then cultured in DMEM with 10% FCS for 17 weeks and in vitro cardiogenesis was initiated by adding 4 microM/l 5'Azacytidine.
Results:
In vitro cardiogenesis was initiated in pure CD34+ cells with 5' Azacytidine. The cells showed spontaneous beating after 24 hours of treatment and after 5 weeks, the cells connected with the adjoining cells by a myotube. In these cells, expression of myosin light chain (MLC2v) gene and GATA-4 transcription factor validated the development of cardiomyocytes.
Conclusion:
It is observed that the transplantation of autologous stem cells/fetal cardiomyocytes in the heart scar tissue developed due to infarct, limited the scar expansion, and prevented post infarct heart failures. Homing process due to the transplantation of autologous stem cells is time consuming; therefore, transplantation of cardiomyocytes developed from autologous stem cells could be the future method of correcting the infracted myocardium.

