Murine strain differences in inflammatory angiogenesis of internal wound in diabetes

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• 作者：Simone Aparecida de Almeida^a ; Laura Alejandra Ariza Orellano^a ; Luciana Xavier Pereira^a ; Celso Tarso Rodrigues Viana^a ; Paula Peixoto Campos^a ; ^{paulapc@icb.ufmg.br} ; Silvia Passos Andrade^b ; Monica Alves Neves Diniz Ferreira^a
• 关键词：Angiogenesis ; Diabetes ; Genetic background ; Internal wound
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：86
• 期：Complete
• 页码：715-724
• 全文大小：3397 K
• 卷排序：86

文摘

Genetic susceptibility is associated with inflammation, neovascularization, and diabetes phenotypes. However, to what extent this susceptibility influences inflammatory angiogenesis in internal injuries in diabetes has not been fully investigated. Using the subcutaneous implantation of a synthetic matrix as an internal wound model in Swiss, C57BL/6 and Balb/c mice, we have studied inflammation, angiogenesis, and cytokine production in the fibrovascular tissue induced by implants in diabetic animals. The hyperglycemic levels (mg/dl) after the diabetogenic treatment were 455.0 ± 15 in Swiss, 393.0 ± 22 in C57BL/6, and 190.0 ± 10 in Balb/c mice. Angiogenesis in Swiss implants from non-diabetic animals were higher than those in the implants from the other strains. However, the angiogenic inducers VEGF and nitric oxide (NO) were higher in implants from non-diabetic Swiss and Balb/c mice. Strain-related differences were also observed in the angiogenic parameters in implants from diabetic mice. Hb content and number of vessels decreased more than 40% in Swiss implants. In contrast, Hb content did not alter in implants from Balb/c diabetic mice and the number of vessels decreased. VEGF levels increased in implants from Swiss and C57BL/6 diabetic mice, but decreased in Balb/c implants. The levels of pro-inflammatory markers intra-implant also varied among the strains in both conditions. In the hyperglycemic environment, almost all inflammatory markers increased in implants from diabetic Swiss mice. These findings demonstrate the major contribution of genetic background in the pattern of inflammatory angiogenesis components of internal injury, in both normoglycemic and hyperglycemic animals.