CD34⁺ PI16⁺ fibroblast progenitors aggravate neointimal lesions of allograft arteries via CCL11/CCR3-PI3K/AKT pathway.

ABSTRACT: Rationale: Transplant-accelerated arteriosclerosis is a common complication that limits the long-term survival of organ transplant recipients. While previous studies have indicated the involvement of CD34⁺ stem/progenitor cells (SPCs) in this process, their heterogeneity and potential adverse effects remains incompletely understood. Methods: To investigate the role of CD34⁺ SPCs in transplant arteriosclerosis, we used various genetically modified mouse models, including BALB/c, C57BL/6J, CD34-CreER^T2, Rosa26-tdTomato, Rosa26-iDTR, CD34-Dre, PI16-CreER^T2, and CAG-LSL-RSR-tdTomato-2A-DTR mice. Single-cell RNA sequencing (scRNA-seq), chemokine antibody microarrays, ELISA assays, and immunohistochemistry were employed to identify fibrob

SUBMITTER: Xu X 

PROVIDER: S-EPMC11840720 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature