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PEDF-34 attenuates neurological deficit and suppresses astrocyte-dependent neuroinflammation by modulating astrocyte polarization via 67LR/JNK/STAT1 signaling pathway after subarachnoid hemorrhage in rats.

Lei Wu | Yanchao Liu | Qiuguang He | Guangnan Ao | Ningbo Xu | Wangqing He | Xiao Liu | Lei Huang | Qian Yu | Hideki Kanamaru | Siyuan Dong | Shiyi Zhu | Ye Yuan | Mingyang Han | Yeping Ling | Lu Liu | Chenyu Wu | You Zhou | Prativa Sherchan | Jerry J Flores | Jiping Tang | Xionghui Chen | Xuying He | John H Zhang
Journal of neuroinflammation | 2024

Reactive astrocytes participate in various pathophysiology after subarachnoid hemorrhage (SAH), including neuroinflammation, glymphatic-lymphatic system dysfunction, brain edema, BBB disruption, and cell death. Astrocytes transform into two new reactive phenotypes with changed morphology, altered gene expression, and secretion profiles, termed detrimental A1 and beneficial A2. This study investigates the effect of 67LR activation by PEDF-34, a PEDF peptide, on neuroinflammation and astrocyte polarization after the experimental SAH.

Pubmed ID: 39034417

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Associated grants

  • Agency: NINDS NIH HHS, United States
    Id: P01 NS082184
  • Agency: NINDS NIH HHS, United States
    Id: R01 NS117179
  • Agency: Basic and Applied Basic Research Foundation of Guangdong Province,
    Id: 2021A1515010980
  • Agency: NIH HHS, United States
    Id: NS117179

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