Background
Jun N‐terminal kinase pathway‐associated phosphatase (JKAP) regulates neuronal function, T helper (Th) 1/2/17 cell differentiation, and inflammatory process, but its clinical role in acute ischemic stroke (AIS) patients remains unclear. Hence, this study intended to evaluate JKAP level and its relationship with disease severity, Th1, 2, 17 secreted cytokines, adhesion molecules, and prognosis of AIS patients.
Methods
Serum JKAP of 122 AIS patients and 50 controls was detected by ELISA. For AIS patients only, Th1, 2, 17 secreted cytokines IFN‐γ, IL‐4, IL‐17; TNF‐α, ICAM‐1, and VCAM‐1 were also detected by ELISA.
Results
JKAP was decreased in AIS patients compared with controls (46.350 (interquartile range (IQR): 34.250–59.875) pg/ml vs. 84.500 (IQR: 63.175–113.275) pg/ml, p < 0.001), which could distinguish AIS patients from controls (area under curve (AUC): 0.810, 95% confidence interval (CI): 0.732–0.888). In AIS patients, JKAP negatively linked with the National Institutes of Health Stroke Scale (NIHSS) score (rs = −0.342, p < 0.001); besides, it was positively related to IL‐4 (rs = 0.213, p = 0.018) and negatively associated with IL‐17 (rs = −0.270, p = 0.003) but not related to IFN‐γ (rs = −0.146, p = 0.109). Furthermore, elevated JKAP associated with declined TNF‐α (rs = −0.219, p = 0.015) and ICAM‐1 (rs = −0.235, p = 0.009) but not related to VCAM‐1 (rs = −0.156, p = 0.085). Besides, declined JKAP was linked with 2‐year recurrence (p = 0.027) and 3‐year recurrence (p = 0.010) in AIS patients; while JKAP was not related to 1‐year recurrence or death risk (both p > 0.050).
Conclusion
JKAP may sever as a candidate prognostic biomarker in AIS patients, indicating its potency for AIS management.
