ABSTRACT
The immune function of HIV infected patients is severely damaged, which can cause a series of autoimmune related diseases including hyperthyroidism. Hyperthyroidism includes both primary and secondary hyperthyroidism. Graves' disease is the most common primary hyperthyroidism, and Graves' disease may occur in HIV patients during immune reconstitution after antiretroviral therapy A 47-year-old woman with a history of HIV presented with symptoms related to hyperthyroidism. After antithyroid drug therapy failed, the patient and her families opted for surgical treatment. Postoperative examination revealed papillary thyroid carcinoma.
ABSTRACT
tRNA-derived fragments (tRFs) and tRNA halves (tiRNAs) are originated from the specific cleavage of endogenous tRNAs or their precursors and regulate gene expression when the cells are in stressful circumstances. Here, we replicated the rat common carotid artery (CCA) intimal hyperplasia model and investigated the expression of tRFs/tiRNAs in the artery. The normal and the balloon-injured rat CCAs were subjected to small RNA sequencing, and then the differentially expressed tRFs/tiRNAs were identified and analyzed. The expression profiles of tRFs/tiRNAs in the healthy and injured CCAs were remarkably different. tRNAGlnCTG-derived fragments (tRFGlnCTG) were found to be overexpressed with a high abundance in the injured CCA. In in vitro experiments, the synthetic tRFGlnCTG mimetics elevated the proliferation and migration of rat vascular smooth muscle cells (VSMCs). Through bioinformatics analysis and an overexpression experiment, tRFGlnCTG was found to negatively regulate the expression of FAS cell surface death receptor (FAS). This study revealed that tRFGlnCTG is a crucial regulator in promoting VSMC proliferation. The investigation of the roles of tRFs/tiRNAs is of significance for understanding the mechanism, diagnosis, and treatment of intimal hyperplasia.
