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The bispecific SDF1-GPVI fusion protein preserves myocardial function after transient ischemia in mice.
Circulation. 2012 Feb 07; 125(5):685-96.Circ

Abstract

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.

Authors+Show Affiliations

Innere Medizin III, Eberhard Karls Universität, Tübingen, Otfried-Müller-Strasse 10, Tübingen, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22223428

Citation

Ziegler, Melanie, et al. "The Bispecific SDF1-GPVI Fusion Protein Preserves Myocardial Function After Transient Ischemia in Mice." Circulation, vol. 125, no. 5, 2012, pp. 685-96.
Ziegler M, Elvers M, Baumer Y, et al. The bispecific SDF1-GPVI fusion protein preserves myocardial function after transient ischemia in mice. Circulation. 2012;125(5):685-96.
Ziegler, M., Elvers, M., Baumer, Y., Leder, C., Ochmann, C., Schönberger, T., Jürgens, T., Geisler, T., Schlosshauer, B., Lunov, O., Engelhardt, S., Simmet, T., & Gawaz, M. (2012). The bispecific SDF1-GPVI fusion protein preserves myocardial function after transient ischemia in mice. Circulation, 125(5), 685-96. https://doi.org/10.1161/CIRCULATIONAHA.111.070508
Ziegler M, et al. The Bispecific SDF1-GPVI Fusion Protein Preserves Myocardial Function After Transient Ischemia in Mice. Circulation. 2012 Feb 7;125(5):685-96. PubMed PMID: 22223428.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The bispecific SDF1-GPVI fusion protein preserves myocardial function after transient ischemia in mice. AU - Ziegler,Melanie, AU - Elvers,Margitta, AU - Baumer,Yvonne, AU - Leder,Christoph, AU - Ochmann,Carmen, AU - Schönberger,Tanja, AU - Jürgens,Tobias, AU - Geisler,Tobias, AU - Schlosshauer,Burkhard, AU - Lunov,Oleg, AU - Engelhardt,Stefan, AU - Simmet,Thomas, AU - Gawaz,Meinrad, Y1 - 2012/01/05/ PY - 2012/1/7/entrez PY - 2012/1/10/pubmed PY - 2012/4/14/medline SP - 685 EP - 96 JF - Circulation JO - Circulation VL - 125 IS - 5 N2 - 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. SN - 1524-4539 UR - https://www.unboundmedicine.com/medline/citation/22223428/The_bispecific_SDF1_GPVI_fusion_protein_preserves_myocardial_function_after_transient_ischemia_in_mice_ L2 - https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.111.070508?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -