# Clinical Characteristics and Gene Expression of JAK2, STAT3, miRNA-155, and miRNA-216a in Young Adults with Acute Ischemic Stroke

**Authors:** David Vidal-González, Jazmin Marquez-Pedroza, Betsabé Contreras-Haro, Ana Miriam Saldaña-Cruz, Carlos Fernando Godínez-González, Antonio Kobayashi-Gutiérrez, Nayeli Alejandra Sánchez-Rosales, Edgar Ricardo Valdivia-Tangarife, José de Jesús García-Rivera, Idarmis Brisseida Reyes-Cortés, Blanca Miriam Torres-Mendoza, Martha Rocio Hernández-Preciado

PMC · DOI: 10.3390/ijms27041991 · 2026-02-19

## TL;DR

This study explores gene expression patterns in young adults with acute ischemic stroke, identifying potential biomarkers for the condition.

## Contribution

The study identifies JAK2, STAT3, and miR-155 as potential biomarkers for acute ischemic stroke in young adults.

## Key findings

- Stroke patients showed overexpression of JAK2, STAT3, and miR-155 compared to healthy controls.
- miR-216a was not significantly overexpressed in stroke patients.
- These findings suggest potential biomarkers for acute ischemic stroke.

## Abstract

Acute ischemic stroke (AIS) is a leading cause of long-term disability and death. The genetic, epigenetic, and molecular mechanisms underlying AIS in young adults require further investigation. Inflammatory pathways, such as the programmed death-ligand 1 (PD-L1) and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway, are implicated in promoting post-ischemic neuroinflammation and neuronal apoptosis. While miR-155 and miR-216a are mediators of inflammation, apoptosis, and tissue repair following AIS. This exploratory study aimed to analyze the expression of the JAK2/STAT3, miR-155, and miR-216a genes in young AIS patients (mean age: 39.4 ± 11.9 years) versus the healthy population (HP). Peripheral blood samples were collected, and gene and miRNA expressions were measured using quantitative real-time PCR. Our results showed that stroke patients exhibited overexpression of all genes (p < 0.001), except for miRNA-216a (p = 0.061), compared to HP. These findings suggest that JAK2, STAT3, and miR-155 could be potential biomarkers for patients with AIS.

## Linked entities

- **Genes:** JAK2 (Janus kinase 2) [NCBI Gene 3717], STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774], MIR155 (microRNA 155) [NCBI Gene 406947], MIR216A (microRNA 216a) [NCBI Gene 406998]
- **Proteins:** CD274 (CD274 molecule)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, MIR216A (microRNA 216a) [NCBI Gene 406998] {aka MIR216, MIRN216, MIRN216A, miRNA216, mir-216, mir-216a}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, Stat3 (signal transducer and activator of transcription 3) [NCBI Gene 20848] {aka 1110034C02Rik, Aprf}, CD274 (CD274 molecule) [NCBI Gene 29126] {aka ADMIO5, B7-H, B7H1, PD-L1, PDCD1L1, PDCD1LG1}, PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}, MIR155 (microRNA 155) [NCBI Gene 406947] {aka MIRN155, miRNA155, mir-155}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}, GDE1 (glycerophosphodiester phosphodiesterase 1) [NCBI Gene 51573] {aka 363E6.2, MIR16}
- **Diseases:** thrombosis (MESH:D013927), neurodegenerative diseases (MESH:D019636), injury to (MESH:D014947), headache (MESH:D006261), Inflammatory (MESH:D007249), brain damage (MESH:D001925), Atherosclerosis (MESH:D050197), Hypertension (MESH:D006973), ataxia (MESH:D001259), HP (MESH:D000067329), dyslipidemia (MESH:D050171), death (MESH:D003643), diabetes (MESH:D003920), sensory deficits (MESH:D012678), ischemic injury (MESH:D017202), muscle weakness (MESH:D018908), cerebral ischemia (MESH:D002545), Posterior circulation infarction (MESH:D020520), cerebral infarction (MESH:D002544), aphasia (MESH:D001037), neuroinflammation (MESH:D000090862), circulation (MESH:D009360), cardioembolic (MESH:D000083262), Infarction (MESH:D007238), nausea (MESH:D009325), type 2 diabetes (MESH:D003924), Stroke (MESH:D020521), oculomotor nerve palsy (MESH:D015840), paralysis (MESH:D010243), vertigo (MESH:D014717), posterior and anterior infarction (MESH:D056988), dysarthria (MESH:D004401), AIS (MESH:D000083242), visual field deficits (MESH:D005128), immune dysregulation (OMIM:614878), vomiting (MESH:D014839), facial paralysis (MESH:D005158), anterior or posterior cerebral infarction (MESH:D020243), neurological disability (MESH:D009069)
- **Chemicals:** EDTA (MESH:D004492), agarose (MESH:D012685), alcohol (MESH:D000438)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Nicotiana tabacum (American tobacco, species) [taxon 4097]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12940177/full.md

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Source: https://tomesphere.com/paper/PMC12940177