Abstract
The number of extremely low birth weight infants less than 1,000 gram of the weight is increasing year by year because of the development of perinatal and neonatal care, the increase of elderly birth, and the high rate of multiple pregnancy. Extremely low birth weight infants caused by organ dysfunction often involve various complications such as pulmonary dysplasia syndrome, anemia, and patent ductus arteriosus. Therefore, a high oxygen care is required to prevent them and save their lives. However, the exposure of extreme changes of an oxygen concentration during the intensive care leads to retinopathy of prematurity (ROP). Abnormal extension of the retinal vessels to avascular area is observed in the patients with ROP. In the case of severe patients, ROP is a leading cause of visual field defect or blindness by the tractional retinal detachment. For the treatment of ROP, laser photocoagulation, scleral buckle, and vitreous surgery are often performed in the early stage. The injection of anti-vascular endothelial growth factor (VEGF) antibody to the lesional site is effective to inhibit abnormal extension of the retinal vessels. However, the surgical treatment for ROP infants has the risk of sequela of the central nervous system caused by anesthesia-induced developmental neurotoxicity. Furthermore, treatment with anti-VEGF antibody requires careful consideration for using because of the diversity of a VEGF molecule.
The mast cell is one of the hematopoietic cells containing cytoplasmic granules that contain various kinds of cytokines, chemokines, and chondroitin sulfate proteoglycan, and these factors induce allergy and inflammation through degranulation process. Otherwise, mast cells also produce and release angiogenic factors.
Recently, our research group has demonstrated that the mast cells are activated by oxygen stress through the transient receptor potentially ankyrin 1 sensing. Moreover, abnormal retinal angiogenesis is sprout by mast cell tryptase in murine oxygen-induced retinopathy, a model for ROP. We mainly describe the novel pathogenesis of ROP via mast cell activation.
