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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #242706

Title: Serum amyloid P inhibits dermal wound healing

item Naik-mathuria, Bindi - Baylor College Of Medicine
item Pilling, Darrell - Rice University
item Crawford, Jeff - Rice University
item Gay, Andre - Baylor College Of Medicine
item Smith, C. Wayne - Children'S Nutrition Research Center (CNRC)
item Gomer, Richard - Rice University
item Olutoye, Oluyinka - Children'S Nutrition Research Center (CNRC)

Submitted to: Journal of Wound Repair and Regeneration
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/12/2007
Publication Date: 3/2/2008
Citation: Naik-Mathuria, B., Pilling, D., Crawford, J.R., Gay, A.N., Smith, C.W., Gomer, R.H., Olutoye, O.0. 2008. Serum amyloid P inhibits dermal wound healing. Journal of Wound Repair and Regeneration. 16(2):266-273.

Interpretive Summary: This research deals with the mechanisms of wound healing, a process that is delayed in patients with obesity and/or diabetes. We studied the ability of a protein found in blood to influence wound healing in a mouse model of skin wounds, and we found for the first time that this protein delays healing. Future studies will investigate this protein and its functions in obesity and diabetes in a mouse model.

Technical Abstract: The repair of open wounds depends on granulation tissue formation and contraction, which is primarily mediated by myofibroblasts. A subset of myofibroblasts originates from bone-marrow-derived monocytes which differentiate into fibroblast-like cells called fibrocytes. Serum amyloid P (SAP) inhibits differentiation of monocytes into fibrocytes. Thus, we hypothesized that the addition of exogenous SAP would hinder the normal wound healing process. Excisional murine dorsal wounds were injected with SAP (intradermal group) or the mice were treated with systemic SAP (intraperitoneal group) and compared with animals treated with vehicle. Grossly, SAP-treated wounds closed slower than respective controls in both groups. Histologically, the contraction rate was slower in SAP-treated wounds in both groups and the reepithelialization rate was slower in the intraperitoneal group. Furthermore, significantly less myofibroblasts expressing alpha-smooth muscle actin were noted in the intraperitoneal group wounds compared with controls. These data suggest that SAP delays normal murine dermal wound healing, probably due to increased inhibition of fibrocyte differentiation, and ultimately a decreased wound myofibroblast population. SAP may provide a potential therapeutic target to prevent or limit excessive fibrosis associated with keloid or hypertrophic scar formation. Furthermore, SAP removal from wound fluid could potentially accelerate the healing of chronic, nonhealing wounds.