Serum miR-329-3p is a potential diagnostic and prognostic biomarker for ischemic stroke and exerts in vitro neuroprotection by targeting PTPN1.
Key Findings
Results
Serum miR-329-3p was downregulated in acute ischemic stroke patients compared with healthy controls.
The study enrolled 126 acute ischemic stroke patients and 92 healthy controls.
Serum miR-329-3p was measured by qRT-PCR.
The abstract reports downregulation in patients but gives no fold-change or p-value.
Results
Serum miR-329-3p showed good diagnostic efficacy for distinguishing ischemic stroke patients from controls.
The abstract describes the diagnostic efficacy as 'good'.
No AUC, sensitivity or specificity values are given in the abstract.
Results
Serum miR-329-3p levels were negatively correlated with stroke severity and poor functional outcome.
Neurological function was evaluated using NIHSS and 3-month mRS scores.
miR-329-3p was negatively correlated with both NIHSS and mRS scores.
The abstract states miR-329-3p is 'significantly associated with the prognosis of patients'.
Results
Overexpressing miR-329-3p protected OGD/R-treated SH-SY5Y cells in vitro.
OGD/R-induced SH-SY5Y cells were used as the in vitro ischemia-reperfusion model.
Overexpression improved cell proliferation, reduced apoptosis, and alleviated oxidative stress and inflammation.
Overexpression also activated PI3K/Akt pathway activity.
Results
PTPN1 was validated as a direct target of miR-329-3p, and PTPN1 overexpression abolished miR-329-3p's neuroprotective effects.
The miR-329-3p-PTPN1 interaction was validated experimentally.
Rescue experiments showed that PTPN1 overexpression abolished the neuroprotective effects of miR-329-3p.
Serum PTPN1 mRNA was also measured by qRT-PCR in patients; the abstract does not report its result.
What This Means
This study looked at a small molecule called miR-329-3p, which helps regulate gene activity, in people who had an ischemic stroke (a stroke caused by a blocked blood vessel in the brain). Researchers compared blood levels in 126 stroke patients with those in 92 healthy people. Levels were lower in stroke patients. Lower levels were also linked to more severe stroke symptoms and worse recovery at 3 months.
The team also tested the molecule in nerve-like cells in the lab that were deprived of oxygen and glucose and then re-supplied, which mimics stroke injury. Raising miR-329-3p helped the cells grow, reduced cell death, and lowered oxidative stress and inflammation. It appeared to work by switching off a gene called PTPN1 and by activating a cell-survival pathway (PI3K/Akt). When PTPN1 was boosted, the protective effects disappeared.
This research suggests miR-329-3p might eventually serve as a blood marker to help detect stroke and predict outcomes, and that PTPN1 could be a target for study. The findings come from a single patient group and from cell experiments, so they do not show that changing this molecule would help actual stroke patients.
Fang H, Zhou Q, Wang H, Wang L, Li H. (2026). Serum miR-329-3p as a potential biomarker for ischemic stroke: clinical association and in vitro neuroprotection via PTPN1.. Metabolic brain disease. https://doi.org/10.1007/s11011-026-02005-5