Stroke· 2026Q1
Endotel Hücre Yüzeyinde Bulunan Prion Proteini Prnd/Doppel, İskemik İnme Sonrası Uzun Süreli İyileşmeyi Destekler
Endothelial Cell-Expressed Prion Protein Prnd/Doppel Promotes Long-Term Recovery After Ischemic Stroke
- 2atıf
- Q1SCImago
- 2026yıl
Kısa özet
Endotelde ifade edilen Prnd (Prion Protein-like protein 2), akut hasar boyutunu etkilemeden vasküler onarımı, kan-beyin bariyeri bütünlüğünü ve yeniden yapılanmayı artırarak iskemik inme sonrası uzun süreli fonksiyonel iyileşmeyi destekler.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Ana noktalar
- Endotel Prnd, iskemik inme sonrası akut enfarktüs hacmini etkilemez.
- Prnd-null farelerde iyileşme sürecinde serebrovasküler mimari bozukluğu, kan-beyin bariyeri bütünlüğünde azalma ve artmış beyin atrofisi görülür.
- Endotel Prnd aşırı ifadesi uzun süreli fonksiyonel iyileşmeyi ve vasküler onarımı iyileştirir.
- Prnd'nin mekanizması, gelişmiş VEGF-A sinyalizasyonunu ve artmış endotel sıkı kavşak proteinlerini içerir.
Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.
Özet (abstract)
BACKGROUND: Recovery after ischemic stroke is limited by persistent cerebrovascular dysfunction, but the mechanisms regulating vascular repair remain poorly understood. Prnd (Prnd/Doppel) is a prion family protein expressed in the cerebrovascular endothelium during development. We tested the hypothesis that endothelial Prnd promotes vascular repair and functional recovery in the adult brain after stroke. METHODS: Using middle cerebral artery occlusion in mice, we compared wild-type and Prnd-null mice and evaluated endothelial-specific Prnd overexpression. Functional recovery was assessed by behavioral testing, while infarct volume, brain atrophy, vascular architecture, blood-brain barrier integrity, and macrophage/microglia infiltration were evaluated histologically. Vascular signaling and endothelial cell junctional proteins were examined mechanistically. RESULTS: Acute infarct volumes were comparable between wild-type and Prnd-null mice, indicating that Prnd does not substantially affect initial ischemic injury. During recovery, however, Prnd-null mice exhibited disrupted cerebrovascular architecture, increased blood-brain barrier disruption, greater brain atrophy, and increased macrophage/microglial infiltration. Conversely, endothelial Prnd overexpression improved long-term functional recovery without altering acute infarct size and was associated with enhanced blood-brain barrier integrity and vascular remodeling. Mechanistically, Prnd manipulation was associated with enhanced VEGF-A (vascular endothelial growth factor-A) signaling and increased endothelial cell tight junction protein expression. CONCLUSIONS: Prnd is dispensable for acute ischemic injury but promotes cerebrovascular remodeling, blood-brain barrier restoration, and functional recovery after stroke. These findings identify endothelial Prnd as a regulator of poststroke vascular repair and a potential therapeutic target for enhancing long-term recovery.
Yazarların özeti; kaynağından alınmıştır. Stroke, 2026 · DOI ↗
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Alan: Epidemiyoloji
EpidemiologyMedicine