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A journey upstream: Fluctuating platelet-specific genes in cell-free plasma as proof-of-concept for using ribonucleic acid sequencing to improve understanding of postinjury platelet biology. | LitMetric

A journey upstream: Fluctuating platelet-specific genes in cell-free plasma as proof-of-concept for using ribonucleic acid sequencing to improve understanding of postinjury platelet biology.

J Trauma Acute Care Surg

From the Department of Surgery (L.Z.K., A.T.F., Z.A.M., B.N.-G., R.A.C.), Department of Anesthesiology and Perioperative Care (C.M.V.B., N.T.M., A.P., P.A.K., R.J.B.), Zuckerberg San Francisco General Hospital and the University of California, San Francisco, San Francisco, California; and Department of Surgery (M.J.C.), Denver Health Medical Center and the University of Colorado, Denver, Colorado.

Published: June 2020

AI Article Synopsis

  • Researchers studied RNA in plasma from traumatic brain injury (TBI) patients to understand how platelets change after injury.
  • They used RNA sequencing to compare the platelet-specific RNA between severely injured patients and minimally injured controls.
  • They identified 42 different RNA transcripts that were significantly altered in severely injured patients, indicating active changes in platelet function post-injury.

Article Abstract

Background: The mechanisms of aberrant circulating platelet behavior following injury remain unclear. Platelets retain megakaryocyte immature ribonucleic acid (RNA) splicing and protein synthesis machinery to alter their functions based on physiologic signals. We sought to identify fluctuating platelet-specific RNA transcripts in cell-free plasma (CFP) from traumatic brain injury (TBI) patients as proof-of-concept for using RNA sequencing to improve our understanding of postinjury platelet behavior. We hypothesized that we could identify differential expression of activated platelet-specific spliced RNA transcripts from CFP of patients with isolated severe fatal TBI (fTBI) compared with minimally injured trauma controls (t-controls), filtered by healthy control (h-control) data sets.

Methods: High-read depth RNA sequencing was applied to CFP from 10 patients with fTBI (Abbreviated Injury Scale [AIS] for head ≥3, AIS for all other categories <3, and expired) and five t-controls (Injury Severity Score ≤1, and survived). A publicly available CFP RNA sequencing data set from 23 h-controls was used to determine the relative steady state of splice-form RNA transcripts discoverable in CFP. Activated platelet-specific spliced RNA transcripts were derived from studies of ex vivo platelet activation and identified by splice junction presence greater than 1.5-fold or less than 0.67-fold ex vivo nonactivated platelet-specific RNA transcripts.

Results: Forty-two differentially spliced activated platelet-specific RNA transcripts in 34 genes were altered in CFP from fTBI patients (both upregulated and downregulated).

Conclusion: We have discovered differentially expressed activated platelet-specific spliced RNA transcripts present in CFP from isolated severe fTBI patients that are upregulated or downregulated compared with minimally injured trauma controls. This proof-of-concept suggests that a pool of immature platelet RNAs undergo splicing events after injury for presumed modulation of platelet protein products involved in platelet function. This validates our exploration of injury-induced platelet RNA transcript modulation as an upstream "liquid biopsy" to identify novel postinjury platelet biology and treatment targets for aberrant platelet behavior.

Level Of Evidence: Diagnostic tests, level V.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7571783PMC
http://dx.doi.org/10.1097/TA.0000000000002681DOI Listing

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