CD93 是一個表現在血管內皮細胞、單核球細胞、以及幹細胞表面的高度醣基化蛋白質。CD93　具有五個功能區域，分別為類凝集素區、五個重複的表皮生長因子區、黏液素區、穿膜區以及細胞內尾端。序列比對顯示CD93與凝血酶調節素 (thrombomodulin) 在老鼠與人類中皆有很高的結構同源性。先前研究已經證明在血液中可偵測到可溶性CD93，暗示可溶性CD93參與調控某些生理作用。本實驗室先前研究發現，CD93蛋白的第二及第三功能區(CD93D23)可誘發人類臍靜脈內皮細胞的爬行及增生，而在小鼠血管新生實驗中發現CD93D23可促進活體中的血管新生，暗示CD93是促進血管生長的因子。血管新生在傷口癒合的過程中扮演著支持細胞增生的重要角色，而糖尿病患者因血管新生作用異常導致創傷處的傷口癒合減弱。最近研究發現，在非肥胖型糖尿病小鼠血液內的可溶性CD93較正常小鼠低，然而CD93在糖尿病患者血管新生以及傷口癒合的角色並不清楚。為了進一步探討CD93在糖尿病患者血管新生以及傷口癒合扮演的角色，本論文首先製備了不同功能區域的CD93重組蛋白，包含CD93D23以及CD93D123。在細胞實驗中CD93D23及CD93蛋白的第一,二,三功能區(CD93D123)能促進人類臍靜脈內皮細胞在高血糖濃度環境下的增生以及爬行的能力，另外CD93D23以及CD93D123也可促進A7r5平滑肌細胞增生。在小鼠血管新生實驗中，CD93D23可在糖尿病小鼠中引起血管新生。另外，當外加CD93D23以及CD93D123可顯著改善糖尿病小鼠的傷口癒合。由以上結果可知CD93重組蛋白可藉由促進高血糖濃度下的血管新生而改善糖尿病小鼠的傷口癒合。

CD93 is a transmebmrane protein expressed on endothelial cells, monocytes, neutrophils and stem cells. CD93 has five domains: N-terminal lectin-like domain (D1), repetitive epidermal growth factor (EGF)-like domain (D2), mucin-like domain (D3), transmembrane domain (D4) and cytoplasmic domain (D5). The result of sequence alignment shows high homology between CD93 and thrombomodulin, and both of them are conserved in human and mice. In previous study, soluble form of CD93 (sCD93) was found in human blood indicating that sCD93 might participate in some physiological processes. Our previous results showed that CD93 domain 2 and 3 (CD93D23) induced human umbilical vein endothelial cells migration and proliferation. In murine angiogenesis assay, CD93D23 stimulated angiogenesis in vivo. Wound angiogenesis is an important part of the proliferative phase of healing; diabetic patients display aberrant angiogenesis in various organs, with insufficient activity occurring in impaired wound healing including ulcers. Recent study has indicated that non-obese diabetic sera contained measurable levels of sCD93 at a slightly lower concentration compared to sera of B6 mice. However, the function of CD93 in wound healing process of diabetes is mostly unknown. To further investigate the role of CD93 in wound healing and angiogenesis of diabetic patient, we constructed different domains of CD93, including CD93D23 and CD93 domain 1, 2 and 3 (CD93D123). In vitro study showed that CD93D123 and CD93D23 had a significant enhancing effect on proliferation and migration of human umbilical vein endothelial cells under high glucose concentration. CD93D123 and CD93D23 could also enhance the proliferation of smooth muscle cell (A7r5) under normal glucose concentration. In murine angiogenesis assay, CD93D23 stimulated angiogenesis in diabetic mice. Besides, we demonstrated that treatment of CD93D123 and CD93D23 could significantly promote wound closure and recover wound contraction in the diabetic mice. Based on these observations, we concluded that CD93 recombinant proteins could improve wound healing processes of the diabetic mice by enhancing angiogenesis under high-glucose concentration.　

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