ArticleExperimental and therapeutic medicine2018
Effect of transplantation of cardiac stem cells overexpressing integrin-linked kinase on cardiac function of rats with acute myocardial infarction.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Endothelial Integrin-Linked Kinase (ILK) Deficiency Promotes Endothelial Activation and Cardiovascular Dysfunction via Receptor Interacting Protein Kinase-1 (RIPK1) Enriched-Extracellular Vesicle Signalling.Journal of extracellular vesicles · 2026Article
- Endothelial ILK induces cardioprotection by preventing coronary microvascular dysfunction and endothelial-to-mesenchymal transition.Basic research in cardiology · 2023Article
- Roles of TRPV4 in Regulating Circulating Angiogenic Cells to Promote Coronary Microvascular Regeneration.Journal of cardiovascular translational research · 2023Article
- A Potential Role for Integrin-Linked Kinase in Colorectal Cancer Growth and Progression via Regulating Senescence and Immunity.Frontiers in genetics · 2021Review
- Therapeutic effect of integrin-linked kinase gene-modified bone marrow-derived mesenchymal stem cells for streptozotocin-induced diabetic cystopathy in a rat model.Stem cell research & therapy · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we aimed to investigate the effect of transplantation of cardiac stem cells (CSCs) overexpressing integrin-linked kinase (ILK) on cardiac function of rats with acute myocardial infarction (MI). A total of 60 rats were randomly divided into normal saline (NS) group (n=20), green fluorescent protein (GFP)-CSC group (n=20) and ILK-CSC group (n=20). In the ILK-CSC group, CSCs in rats were transfected with GFP adenovirus vector overexpressing ILK. The rat model of MI was established. The cardiac function 4 weeks after transplantation was detected via echocardiography, and the exhaustive swimming experiment was performed to observe the exercise load capacity. Moreover, Ki-67 and P-H3 proteins in myocardial tissues of rats were detected via immunohistochemistry, and the expression of GFP was observed under a fluorescence microscope. Cells in the GFP-CSC group were transfected with the empty GFP adenovirus, while those in NS group were not transfected, and other treatments in these two groups were the same as those in the ILK-CSC group. Four weeks after transplantation, left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD) of rats in the ILK-CSC group were smaller than those in the GFP-CSC group, but left ventricular ejection fraction (LVEF) (69.88±5.61 mm) was higher than that in the GFP-CSC group (P<0.05). The exercise time in the ILK-CSC group (12.69±0.58 min) was longer than that in the GFP-CSC and NS groups (P<0.05). The expression levels of Ki-67 and P-H3 proteins in myocardial cells of rats in the ILK-CSC group were higher than those in the GFP-CSC and NS groups (P<0.05). The number of transplanted cells retained around the infarct region in the ILK-CSC group 3 days after transplantation was obviously larger than that in the GFP-CSC group (P<0.001). Intramyocardial injection of CSCs overexpressing ILK immediately after the establishment of rat model of MI can promote myocardial cell proliferation, improve cardiac function and increase exercise capacity of rats.
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