ALBERT

Description: Diabetic retinopathy (DR) is the leading cause of legal blindness in working age adults in the United States with about 18 thousand new cases of blindness each year. Approximately 75% of patients with type-2 diabetes will develop some sign of retinopathy after 15 years. The healthcare costs associated with diabetes related vision loss has been estimated at $500 million annually and the cost rises significantly with the severity of DR. Therefore, preventing the progression of DR from mild non-progressive diabetic retinopathy (NPDR) to progressive diabetic retinopathy (PDR) could ameliorate the economic burden related to diabetes and vision loss. Our laboratory has focused on a pro-inflammatory axis comprised by thrombospondin-1 (TSP1), transforming growth factor β (TGFb) and connective tissue growth factor (CTGF/CCN2) in the pathophysiology of DR. Furthermore, the regulation of this pro-inflammatory axis during disease states in humans associated with acute and chronic inflammation such as type-2 diabetes has not been elucidated. The current prospective study documents a potential regulatory mechanism, namely a microRNA associated with the up-regulation of the pro-inflammatory axis. Patients were recruited between February 2013 to May 2014. In May of 2015 it was determined by this research team that the data was mature for final analysis and, thus the results are the topic of this abstract. The participants were patients with type-2 diabetes (n=36) with either evidence of non-proliferative diabetic retinopathy (NPDR Group, n=16), or with evidence of proliferative diabetic retinopathy (PDR Group, n=20) as well as non-diabetic human subjects (Control Group, n=21). Each patient's history and duration of diabetes was obtained from the medical electronic records. TSP1 was found significantly increased in the NPDR (502±145.03 ng/ml, p