HuR coordinates systemic aging through platelet infiltration
Aging involves morphological and functional changes across different organs, but how these changes are linked among the different organs remains to be elucidated. Here, we uncover a central role of platelets in sys temic aging. In aged mice, the levels of platelet secreted pro inflammatory factors (PSPF) increased greatly in the serum and platelets, leading to a diffuse increase of platelet infiltration in brain, liver, lung, kidney, and aortic root. The RNA binding protein HuR/ELAVL1, a major regulator of R NA metabolism, promoted the production of PSPF in platelets. Platelet specific deletion of HuR reduced the expression of PSPF in platelets, alleviated platelet infiltration in brain, liver, lung, kidney, and aortic root, and delayed systemic aging. Our findings highlight a role of platelets in coordinating aging traits across organs. Overall design: To investigate the function of platelet HuR in systemic aging, we generated a conditional platelet-specific HuR knockout (cKO) mouse. We collected three 25 month-old wild type(WT) and cKO mice liver, lung and brain for single-nucleus RNA sequencing. We then performed gene expression profiling analysis using data obtained from sn-RNA-seq of 3 WT and cKO mice. Comparative gene expression profiling analysis of different cell type from different tissue of sn-RNA-seq data for cKO mice and its WT littermates.