Key result
Patients undergoing percutaneous coronary intervention had significantly higher blood levels of PMNs (7.68 vs 4.82 x 10^9/L) and SDF-1α compared to healthy controls.
Why the study?
Only part of BMSC is recruited to the site of myocardial injury in the treatment of ischemic heart disease, warranting study into whether BMSC overexpressing SDF-1α improves protection against myocardial I/R.
Does BMSC overexpressing SDF-1α reduce myocardial ischemia/reperfusion injury caused by PMNs in preclinical models?
Cross-Sectional (n=175)
No
Does BMSC overexpressing SDF-1α reduce myocardial ischemia/reperfusion injury caused by PMNs in preclinical models?
Absolute Event Rate: 7.68% vs 4.82%
p-value: p=<0.001
BMSCs overexpressing SDF-1α demonstrate enhanced repair capabilities and reduce myocardial ischemia/reperfusion injury by modulating PMN migration, suggesting a potential novel stem cell therapy approach.
Should not yet change I/R practice; hypothesis-generating for SDF-1α-overexpressing BMSC.
Background: To study the protective effect of BMSC overexpressing SDF-1α on myocardial ischemia/reperfusion (I/R), to improve the limitation that only part of BMSC is recruited to the site of myocardial injury in the treatment of ischemic heart disease. It provides a new scheme for stem cell therapy for clinical treatment of reperfusion injury.Methods: Collect blood samples from PCI patients and healthy individuals to detect PMN and SDF-1α expression; Construction of BMSC overexpressing SDF-1α (oe-SDF-1α); In the case of no intervention or intervention by BMSC respectively, cell level: the migration ability of PMN to hypoxia/reoxygenation (H/R) cardiomyocytes and the expression of SDF-1α, CXCR4, apoptosis, oxidative stress and other indicators of cardiomyocytes were detected; In vivo level: PMN, SDF-1α, CXCR4, oxidative stress and inflammatory factor levels were detected in I/R mice. And carry out statistical analysis.Results: ① In the clinic, compared with the control group, the expression levels of SDF-1α and PMN in the blood of PCI patients increased. ② Under H/R conditions, cardiomyocytes express and secrete SDF-1α, activate PMN migration and infiltration mediated by SDF-1/CXCR4 signal pathway, promote cardiomyocyte apoptosis and increase the level of oxidative stress; oe-SDF-1α has a stronger ability to migrate to H/R cardiomyocytes and has more repair ability than BMSC.It is more suitable as a tool cell for stem cell therapy. ③ The expression levels of SDF-1α and PMN are increased in I/R mice. oe-SDF-1α can reduce the ability of PMN to reside to the damaged part of myocardial tissue significantly, thereby reducing myocardial tissue damage, oxidative stress, inflammatory factor levels in I/R mice. Conclusions: The SDF-1/CXCR4 biological axis not only plays an important role in BMSC migration, but also helps to enhance the therapeutic effect of BMSC-based therapy. Oe-SDF-1α has a more repairing effect on reducing cell damage caused by PMN, and can be used as a new type of cell for the treatment of IRI.
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Wang et al. (2021) conducted a cross-sectional in Ischemic heart disease (patients undergoing PCI) (n=175). Percutaneous coronary intervention (PCI) / Ischemic heart disease vs. Healthy controls was evaluated on Blood PMN levels (10^9/L) (p=<0.001). Patients undergoing percutaneous coronary intervention had significantly higher blood levels of PMNs (7.68 vs 4.82 x 10^9/L) and SDF-1α compared to healthy controls.
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