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Poly-N-acetyl glucosamine fibers induce angiogenesis in ADP inhibitor-treated diabetic mice.
J Trauma 2011; 71(2 Suppl 1):S183-6JT

Abstract

BACKGROUND

It has been previously demonstrated that short-fiber poly-N-acetyl-glucosamine (sNAG) nanofibers specifically interact with platelets, are hemostatic, and stimulate diabetic wound healing by activating angiogenesis, cell proliferation, and reepithelialization. Platelets play a significant physiologic role in wound healing. The influence of altered platelet function by treatment with the ADP inhibitor Clopidogrel (CL) on wound healing and the ability of sNAG to repair wounds in diabetic mice treated with CL were studied.

METHODS

Dorsal 1 cm2 skin wounds were excised on genetically diabetic 8-week to 12-week-old, Lep/r-db/db male mice, and wound healing kinetics were determined. Microscopic analysis was performed for angiogenesis (PECAM-1) and cell proliferation (Ki67). Mice were either treated with CL (P2Y12 ADP receptor antagonist, CL) or saline solution (NT). CL wounds were also treated with either a single application of topical sNAG (CL-sNAG) or were left untreated (CL-NT).

RESULTS

CL treatment did not alter wound healing kinetics, while sNAG induced faster wound closure in CL-treated mice compared with controls. CL treatment of diabetic mice caused an augmentation of cell proliferation and reduced angiogenesis compared with nontreated wounds. However, sNAG reversed the effects of CL on angiogenesis and partially reversed the effect on cell proliferation in the wound beds. The sNAG-treated wounds in CL-treated mice showed higher levels of cell proliferation and not did inhibit angiogenesis.

CONCLUSIONS

CL treatment of diabetic mice decreased angiogenesis and increased cell proliferation in wounds but did not influence macroscopic wound healing kinetics. sNAG treatment did not inhibit angiogenesis in CL-treated mice and induced faster wound closure; sNAG technology is a promising strategy to facilitate the healing of complex bleeding wounds in CL-treated diabetic patients.

Authors+Show Affiliations

Department of Plastic Surgery, University Hospital of Lausanne (CHUV), Lausanne, Switzerland.No 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

21814116

Citation

Scherer, Saja S., et al. "Poly-N-acetyl Glucosamine Fibers Induce Angiogenesis in ADP Inhibitor-treated Diabetic Mice." The Journal of Trauma, vol. 71, no. 2 Suppl 1, 2011, pp. S183-6.
Scherer SS, Pietramaggiori G, Matthews JC, et al. Poly-N-acetyl glucosamine fibers induce angiogenesis in ADP inhibitor-treated diabetic mice. J Trauma. 2011;71(2 Suppl 1):S183-6.
Scherer, S. S., Pietramaggiori, G., Matthews, J. C., Gennaoui, A., Demcheva, M., Fischer, T. H., ... Orgill, D. P. (2011). Poly-N-acetyl glucosamine fibers induce angiogenesis in ADP inhibitor-treated diabetic mice. The Journal of Trauma, 71(2 Suppl 1), pp. S183-6. doi:10.1097/TA.0b013e318225585b.
Scherer SS, et al. Poly-N-acetyl Glucosamine Fibers Induce Angiogenesis in ADP Inhibitor-treated Diabetic Mice. J Trauma. 2011;71(2 Suppl 1):S183-6. PubMed PMID: 21814116.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Poly-N-acetyl glucosamine fibers induce angiogenesis in ADP inhibitor-treated diabetic mice. AU - Scherer,Saja S, AU - Pietramaggiori,Giorgio, AU - Matthews,Jasmine C, AU - Gennaoui,Anthony, AU - Demcheva,Marina, AU - Fischer,Thomas H, AU - Valeri,C Robert, AU - Orgill,Dennis P, PY - 2011/8/5/entrez PY - 2011/9/20/pubmed PY - 2011/10/25/medline SP - S183 EP - 6 JF - The Journal of trauma JO - J Trauma VL - 71 IS - 2 Suppl 1 N2 - BACKGROUND: It has been previously demonstrated that short-fiber poly-N-acetyl-glucosamine (sNAG) nanofibers specifically interact with platelets, are hemostatic, and stimulate diabetic wound healing by activating angiogenesis, cell proliferation, and reepithelialization. Platelets play a significant physiologic role in wound healing. The influence of altered platelet function by treatment with the ADP inhibitor Clopidogrel (CL) on wound healing and the ability of sNAG to repair wounds in diabetic mice treated with CL were studied. METHODS: Dorsal 1 cm2 skin wounds were excised on genetically diabetic 8-week to 12-week-old, Lep/r-db/db male mice, and wound healing kinetics were determined. Microscopic analysis was performed for angiogenesis (PECAM-1) and cell proliferation (Ki67). Mice were either treated with CL (P2Y12 ADP receptor antagonist, CL) or saline solution (NT). CL wounds were also treated with either a single application of topical sNAG (CL-sNAG) or were left untreated (CL-NT). RESULTS: CL treatment did not alter wound healing kinetics, while sNAG induced faster wound closure in CL-treated mice compared with controls. CL treatment of diabetic mice caused an augmentation of cell proliferation and reduced angiogenesis compared with nontreated wounds. However, sNAG reversed the effects of CL on angiogenesis and partially reversed the effect on cell proliferation in the wound beds. The sNAG-treated wounds in CL-treated mice showed higher levels of cell proliferation and not did inhibit angiogenesis. CONCLUSIONS: CL treatment of diabetic mice decreased angiogenesis and increased cell proliferation in wounds but did not influence macroscopic wound healing kinetics. sNAG treatment did not inhibit angiogenesis in CL-treated mice and induced faster wound closure; sNAG technology is a promising strategy to facilitate the healing of complex bleeding wounds in CL-treated diabetic patients. SN - 1529-8809 UR - https://www.unboundmedicine.com/medline/citation/21814116/Poly_N_acetyl_glucosamine_fibers_induce_angiogenesis_in_ADP_inhibitor_treated_diabetic_mice_ L2 - http://Insights.ovid.com/pubmed?pmid=21814116 DB - PRIME DP - Unbound Medicine ER -