Differences in PVAT mRNA profiles of recipient mice transplanted with splenocytes
Recent investigations raise the possibility that senescent immune cells may fuel vascular damage by perivascular adipose tissue (PVAT) dysfunction, as immune cell infiltration in PVAT increases substantially in the development of vascular disease compared to the healthy state and leads to changes in PVAT-derived effector cytokine levels that comprise vascular biology.Though evidence revealed possible cross-talk among immune cells, PVAT and vasculature, it is less clear if senescent immune cells or a particular cell subset may induce PVAT dysfunction and further impair vascular biology during type 2 diabtes (T2DM). NLRP3 inflammasome plays a critical role in inflammatory response as a major component of innate immunity, it provides a molecular platform that responds to a variety of stimuli, initiating sterile in?ammation cascade.Furthermore, there is evidence that NLRP3 inflammasome can be activated by sensing danger-associated molecular patterns (DAMPs), which in turn promotes age-related thymic demise and T cell senescence, implicating its potential role in immunosenescence. Here, we employed WT and Nlrp3 KO mice to develop T2DM, and implanted the splenocytes isolated from WT, Nlrp3 KO, WT-T2DM, Nlrp3 KO-T2DM mice that were modeled for 4 months to 3-month-old WT mice. Then, we explored the differentially expressed genes of PVAT in recipient mice implanted with splenocytes and evaluate immune infiltration of PVAT. Overall design: To investigate the immune infiltration profiles of PVAT among recipient mice and explore the impacts of diabetic immune cells on PVAT function.(WTS-R: recipient for splenocyte from WT mice; NS-R: recipient for splenocyte from Nlrp3 KO mice; TS-R: recipient for splenocyte from T2DM mice; NTS-R:recipient for splenocyte from Nlrp3 KO T2DM mice )