Macrophage 11β-HSD-1 deficiency promotes inflammatory angiogenesis

• DOI: 10.1530/joe-17-0223
• Publication Date: 2017-07-05T00:20:18Z
• Authors: Zhenguang Zhang; Agnes E Coutinho; Tak Yung Man; Tiina M J Kipari; Patrick W F Hadoke; Donald M Salter; Jonathan R Seckl; Karen E Chapman
• Keywords: Inflammation; Mice; Neovascularization, Pathologic; Research; Macrophages; 11-beta-Hydroxysteroid Dehydrogenase Type 1; Journal Article; Animals; Humans; 3. Good health

11β-Hydroxysteroid dehydrogenase-1 (11β-HSD1) predominantly converts inert glucocorticoids into active forms, thereby contributing to intracellular glucocorticoid levels. 11β-HSD1 is dynamically regulated during inflammation, including in macrophages where it regulates phagocytic capacity. The resolution of inflammation some disease models inflammatory arthritis impaired by deficiency or inhibition. However, deficiency/inhibition also promotes angiogenesis, which beneficial mouse surgical wound healing, myocardial infarction obesity. cell types responsible for the anti-inflammatory and anti-angiogenic roles have not been characterised. Here, we generated Hsd11b1MKO mice with LysM-Cre mediated deletion Hsd11b1 investigate whether myeloid phagocytes pro-angiogenic and/or affects inflammation. Resolution K/BxN-induced was a similar extent as globally deficient 11β-HSD1. This associated >2-fold elevation levels endothelial marker Cdh5 mRNA, suggesting increased angiogenesis joints following arthritis. A phenotype confirmed measuring subcutaneously implanted polyurethane sponges, showed 20% greater vessel density than their littermate controls, higher expression Thus, angiogenesis. Targeting may be tissue repair.