Saaristo Anne, Tammela Tuomas, Farkkilā Anniina, Kärkkäinen Marika, Suominen Erkki, Yla-Herttuala Seppo, Alitalo Kari
Molecular/Cancer Biology Laboratory, Ludwig Institute for Cancer Research, Biomedicum Helsinki and Helsinki University Hospital, Finland.
Am J Pathol. 2006 Sep;169(3):1080-7. doi: 10.2353/ajpath.2006.051251.
Diabetes impairs numerous aspects of tissue repair. Failure of wound angiogenesis is known to delay diabetic wound healing, whereas the importance of lymphangiogenesis for wound healing is unclear. We have examined whether overexpression of vascular endothelial growth factor (VEGF)-C via an adenoviral vector could improve the healing of full-thickness punch biopsy wounds in genetically diabetic (db/db) mice. We found that VEGF-C enhanced angiogenesis and lymphangiogenesis in the wound and significantly accelerated wound healing in comparison to the control wounds. VEGF-C also recruited inflammatory cells, some of which expressed VEGFR-3. On the other hand, when the function of endogenous VEGF-C/VEGF-D was blocked with a specific inhibitor, wound closure was delayed even further. These results suggest a function for VEGF-C in wound healing and demonstrate the therapeutic potential of VEGF-C in the treatment of diabetic wounds.
糖尿病会损害组织修复的多个方面。已知伤口血管生成失败会延迟糖尿病伤口愈合，而淋巴管生成对伤口愈合的重要性尚不清楚。我们研究了通过腺病毒载体过表达血管内皮生长因子（VEGF）-C是否能改善遗传性糖尿病（db/db）小鼠全层打孔活检伤口的愈合情况。我们发现，与对照伤口相比，VEGF-C可增强伤口的血管生成和淋巴管生成，并显著加速伤口愈合。VEGF-C还招募了炎症细胞，其中一些表达VEGFR-3。另一方面，当用特异性抑制剂阻断内源性VEGF-C/VEGF-D的功能时，伤口闭合会进一步延迟。这些结果表明VEGF-C在伤口愈合中具有作用，并证明了VEGF-C在治疗糖尿病伤口方面的治疗潜力。
