Longitudinal variation of circulating Inc-ITSN1-2: A novel biomarker reflecting disease severity, inflammation, recurrence, and death risk in acute ischemic stroke patients.

Background: Long noncoding RNA intersectin 1-2 (lnc-ITSN1-2) regulates inflammation and neuronal apoptosis; meanwhile, the latter two factors participate in the pathogenesis of acute ischemic stroke (AIS). Therefore, this study detected lnc-ITSN1-2 at multiple time points, aiming to explore its longitudinal variation and clinical value in the management of AIS patients.

Methods: The current study enrolled 102 AIS patients, then detected their lnc-ITSN1-2 in peripheral blood mononuclear cell (PBMC) at baseline (D0), day (D)1, D3, D7, month (M)1, M3, M6, and year (Y)1 after admission using RT-qPCR. Additionally, lnc-ITSN1-2 in PBMC of 50 controls was also detected.

Results: Lnc-ITSN1-2 was up-regulated in AIS patients than that in controls (p < 0.001). Lnc-ITSN1-2 positively associated with NIHSS score, TNF-α, and IL-17A (all p < 0.050) but was not linked with IL-6 (p = 0.093) in AIS patients. Notably, lnc-ITSN1-2 was gradually increased from D0 to D3; while it switched to decrease from D3 to Y1 in AIS patients. Lnc-ITSN1-2 disclosed similar longitudinal variation during 1 year in non-recurrent (p < 0.001), recurrent (p = 0.001), and survived patients (p < 0.001), while the variation of lnc-ITSN1-2 in died patients was not obvious (p = 0.132). More importantly, lnc-ITSN1-2 at D0, D3, D7, M1, M3, M6, and Y1 was higher in recurrent AIS patients than that in non-recurrent AIS patients (all p < 0.050); moreover, lnc-ITSN1-2 at D3, D7, M1, M3, and M6 was up-regulated in died AIS patients than AIS survivors (all p < 0.050).

Conclusion: The dynamic variation of Inc-ITSN1-2 could serve as a biomarker reflecting disease severity, inflammatory cytokines, recurrence, and death risk in AIS patients.