Key result
Administration of the bifunctional SDF1-GPVI fusion protein in a mouse model of myocardial infarction enhanced recruitment of bone marrow cells, reduced infarct size, and preserved cardiac function.
Why the study?
Does the bispecific SDF1-GPVI fusion protein improve myocardial repair and preserve cardiac function in a mouse model of myocardial infarction?
Does the bispecific SDF1-GPVI fusion protein improve myocardial repair and preserve cardiac function in a mouse model of myocardial infarction?
The novel bispecific SDF1-GPVI fusion protein demonstrates potential for promoting myocardial repair and preserving cardiac function following myocardial infarction in preclinical models.
Answers are grounded in this paper and cite their sources.
Premature for clinical use; leaves open whether SDF1-GPVI fusion protein aids human post-MI repair.
BACKGROUND: CXCR4-positive bone marrow cells (BMCs) are critically involved in cardiac repair mechanisms contributing to preserved cardiac function. Stromal cell-derived factor-1 (SDF-1) is the most prominent BMC homing factor known to augment BMC engraftment, which is a limiting step of stem cell-based therapy. After myocardial infarction, SDF-1 expression is rapidly upregulated and promotes myocardial repair. METHODS AND RESULTS: We have established a bifunctional protein consisting of an SDF-1 domain and a glycoprotein VI (GPVI) domain with high binding affinity to the SDF-1 receptor CXCR4 and extracellular matrix proteins that become exposed after tissue injury. SDF1-GPVI triggers chemotaxis of CXCR4-positive cells, preserves cell survival, enhances endothelial differentiation of BMCs in vitro, and reveals proangiogenic effects in ovo. In a mouse model of myocardial infarction, administration of the bifunctional protein leads to enhanced recruitment of BMCs, increases capillary density, reduces infarct size, and preserves cardiac function. CONCLUSIONS: These results indicate that administration of SDF1-GPVI may be a promising strategy to treat myocardial infarction to promote myocardial repair and to preserve cardiac function.
No takes yet. Share an insight, caveat, or question.
Ziégler et al. (2012) studied Myocardial infarction. SDF1-GPVI fusion protein was evaluated on Recruitment of BMCs, capillary density, infarct size, and cardiac function. Administration of the bifunctional SDF1-GPVI fusion protein in a mouse model of myocardial infarction enhanced recruitment of bone marrow cells, reduced infarct size, and preserved cardiac function.
Synapse has enriched 10 related papers. Consider them for comparative context: