Figure 3.

Phase-contrast photomicrographs showing the process of wound repair by wild-type (upper panel) and SPARC-null (lower panel) fibroblasts cultured in the absence of SPARC (A) and in the presence of SPARC (B). In (A), wild-type (upper panel) and SPARC-null (lower panel) fibroblasts were grown to confluence in DMEM containing 10% FBS and then wounded (example shown at 0 hour). Wound closure was monitored at various time points. Wound healing is delayed in SPARC deficient fibroblasts. In (B), wounded monolayers of wild-type (upper panel) and SPARC-null (lower panel) fibroblasts were cultured in DMEM containing 10% FBS and SPARC protein purified from human platelets. Exogenous SPARC restores wound healing ability of SPARC-null cells to the level of wild-type cells. Scale bar, 62.5 μm.

Basu et al. BMC Cell Biology 2001 2:15   doi:10.1186/1471-2121-2-15
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