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Updated: Aug 17, 2026
Murine Model of Wound Healing
Published on: May 28, 2013
Impaired wound healing in mice deficient in a matricellular protein SPARC (osteonectin, BM-40)
A Basu1, L H Kligman, S J Samulewicz
1The Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA. amitbasu72@hotmail.com
Background:
SPARC is a matricellular protein involved in cell-matrix interactions. From expression patterns at the wound site and in vitro studies, SPARC has been implicated in the control of wound healing. Here we examined the function of SPARC in cutaneous wound healing using SPARC-null mice and dermal fibroblasts derived from them.
Results:
In large (25 mm) wounds, SPARC-null mice showed a significant delay in healing as compared to wild-type mice (31 days versus 24 days). Granulation tissue formation and extracellular matrix protein production were delayed in small 6 mm SPARC-null wounds initially but were resolved by day 6. In in vitro wound-healing assays, while wild-type primary dermal fibroblasts showed essentially complete wound closure at 11 hours, wound closure of SPARC-null cells was incomplete even at 31 hours. Addition of purified SPARC restored the normal time course of wound closure. Treatment of SPARC-null cells with mitomycin C to analyze cell migration without cell proliferation showed that wound repair remained incomplete after 31 hours. Cell proliferation as measured by 3H-thymidine incorporation and collagen gel contraction by SPARC-null cells were not compromised.
Conclusions:
A significant delay in healing large excisional wounds and setback in granulation tissue formation and extracellular matrix protein production in small wounds establish that SPARC is required for granulation tissue formation during normal repair of skin wounds in mice. A defect in wound closure in vitro indicates that SPARC regulates cell migration. We conclude that SPARC plays a role in wound repair by promoting fibroblast migration and thus granulation tissue formation.
Insights
SPARC protein is crucial for effective skin wound healing. SPARC-null mice exhibited delayed healing, indicating SPARC promotes fibroblast migration and granulation tissue formation.
Area of Science:
- Biochemistry
- Dermatology
- Cell Biology
Background:
- SPARC is a matricellular protein regulating cell-matrix interactions.
- Expression patterns suggest SPARC influences wound healing.
- This study investigates SPARC's role in cutaneous wound repair.
Purpose of the Study:
- To determine the function of SPARC in cutaneous wound healing.
- To analyze the impact of SPARC deficiency on fibroblast behavior in vitro and in vivo.
Main Methods:
- Utilized SPARC-null mice and derived dermal fibroblasts.
- Assessed wound closure in vivo (large and small excisional wounds).
- Performed in vitro wound-healing assays with fibroblasts, including migration and proliferation assessments.
Main Results:
- SPARC-null mice showed significantly delayed healing in large wounds (31 vs. 24 days).
- Granulation tissue formation and extracellular matrix production were initially delayed in small wounds.
- In vitro, SPARC-null fibroblasts exhibited impaired wound closure, which was restored by adding purified SPARC.
Conclusions:
- SPARC is essential for granulation tissue formation during skin wound repair in mice.
- SPARC regulates fibroblast migration, a key process in wound closure.
- The findings establish SPARC's critical role in promoting fibroblast migration and subsequent granulation tissue formation for effective wound repair.
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