DOI 10.1016/j.joen.2019.09.006
Overexpression of Cyclophilin A in Human Periapical Lesions.
Аннотация
INTRODUCTION
Cyclophilin A (CypA) is a cytosolic protein involved in multiple biological functions, such as inflammation, tissue remodeling, tumorigenesis, and vascular diseases. Human periapical lesions are induced by bacterial infections. However, the expression of CypA in human periapical lesions remains unclear. This study aimed to investigate the presence of CypA in human periapical lesions and the possible association of CypA with angiogenesis, inflammatory cell infiltration, and alveolar bone degradation during inflammatory development.
METHODS
Fifty-eight human periapical tissues, including periapical granulomas (PGs, n = 28), radicular cysts (RCs, n = 24), and healthy control tissues (control group, n = 6) were collected. Samples were fixed and analyzed. CypA expression was detected and analyzed by immunohistochemistry in different cross sections. Double immunofluorescence was assessed to colocalize CypA with CD34, CypA with matrix metalloproteinase 9 (MMP-9), and CD147 with MMP-9.
RESULTS
CypA was significantly overexpressed in the RC and PG groups compared with the control group (P < .05), but the difference between the RC and PG groups was insignificant (P > .05). CypA-positive cells were mainly lymphocytes, endothelial cells, epithelial cells, and plasma cells. The double-labeling analysis of CypA with CD34 suggested that CypA expression was associated with angiogenesis during periapical lesions. MMP-9 colocalized with both CypA and CD147 indicated that CypA may colocalize with CD147 and may be associated with the degradation of soft and hard tissues around human periapical lesions.
CONCLUSIONS
CypA may be involved in the development of periapical lesions with an increase in inflammatory cell infiltration, angiogenesis acceleration, and alveolar bone degradation.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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