Nanostring human miRNA panel: exosome fraction from peripheral blood of trauma patients versus healthy

ABSTRACT: 827 human miRNA standard human panel Plasma derived extracellular vesicles (EV)/exosomes can serve as markers of cell damage/disease but can also have therapeutic utility depending on the nature of their cargo, such as miRNA. Currently there are challenges and lack of innovations regarding early diagnosis and therapeutic options within different aspects of management of trauma patients. We characterized the miRNA cargo of exosomes purified from trauma patients, and compared it to those from healthy participants. Methods Plasma was collected from a prospective, cohort study of trauma patients (n = 15; 7 males, 8 females) with hip and/or femur fractures and an injury severity score (ISS) ≥ 15; elective total hip arthroplasty (THA) patients (n = 8; 4 males, 4 females) served as operative controls. Exosomes were isolated from plasma with the Invitrogen Total Exosome Isolation Kit and RNA was isolated using a miRNeasy Mini Kit. Direct quantification of miRNA copies was performed by NanoString Technologies on a human miRNA gene panel and analyzed with nSolver Results Trauma plasma-derived exosomes had 60 miRNA that were significantly downregulated and 3 miR upregulated when compared to THA (p<0.05). Thirteen miR have a direct role in hematopoiesis regulation, including miR-223 and miR-451a. Further, male trauma plasma-derived exosomes demonstrated downregulation of 150 miR compared to male THA (p<0.05). While female trauma plasma-derived exosomes demonstrated downregulation of only four miR and upregulation of 2 miR compared to female THA (p<0.05). Conclusions Sex-specific differences in the miR from plasma-derived exosomes occurred following severe trauma. These miR changes in plasma-derived exosomes likely contribute to postinjury systemic inflammation, immune system dysregulation, and bone marrow dysfunction and may merit consideration as future potential therapeutic targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE243485 | GEO | 2024/04/03

REPOSITORIES: GEO