After more than 15 years of research, these authors used a large number of donated human eye tissues and found that the HtrA1 protein usually increases with age at the retinal pigment epithelium (RPE)-Bruch's membrane interface of the eye. Help maintain the normal function of this area. The retinal pigment epithelium is a cell layer that transports nutrients and removes waste products to the light-sensitive light cells of the retina.
These new data show that this is not the case in individuals with AMD-related risk variants on chromosome 10. These mutations were found to impair the expression of the HTRA1 gene in the retinal pigment epithelium, resulting in a reduction of the HtrA1 protein level at the retinal pigment epithelium-Bruch membrane interface by about 50% during aging. Failure to produce sufficient levels of HtrA1 protein disrupts this critical area of the eye and is associated with AMD-related conditions, including abnormal deposits and abnormal blood vessels. These findings explain the important role of HtrA1 in maintaining eye health for the first time, and contradict previous literature published by others. They are expected to provide information for the development of new therapies for AMD related to chromosome 10.
Dr. Williams said that her team found that the levels of HTRA1 mRNA in the retinal pigment epithelium and the HtrA1 protein secreted at the retinal pigment epithelium-Bruch membrane interface were significantly reduced. It was found that the reduced expression of HTRA1 was specific to the risk allele, but only in the retinal pigment epithelium, not in the neural retina or choroid. It is worth noting that the team also narrowed a large genetic region of AMD-related chromosome 10 to a much smaller causal region, which may trigger a decrease in HTRA1 expression.
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