ArticleMolecular neurobiology2020
Roles of Prokineticin 2 in Subarachnoid Hemorrhage-Induced Early Brain Injury via Regulation of Phenotype Polarization in Astrocytes.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- NEO1 modulates the A1 astrocyte polarization in subarachnoid hemorrhage through the cPLA2-MAVS signaling pathway.Journal of neuroinflammation · 2025Article
- Acupuncture regulates astrocyte neurotoxic polarization to protect blood-brain barrier integrity in delayed thrombolysis through mediating ERK1/2/Cx43 axis.IBRO neuroscience reports · 2025Article
- Evaluating the Evidence for Neuroprotective and Axonal Regenerative Activities of Different Inflammatory Cell Types After Optic Nerve Injury.Molecular neurobiology · 2025Review
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- Mechanisms and potential therapeutic molecular targets in blood-brain barrier disruption following subarachnoid hemorrhage: a review of early brain injury.Frontiers in neurology · 2025Review
- Advances in astrocytes in aneurysmal subarachnoid haemorrhage.Frontiers in surgery · 2025Review
- Update on Strategies to Reduce Early Brain Injury after Subarachnoid Hemorrhage.Current neurology and neuroscience reports · 2024Review
- Atractylenolide I Suppresses A1 Astrocyte Activation to Improve Depression in Mice.Molecular neurobiology · 2024Article
- Crosstalk Among Glial Cells in the Blood-Brain Barrier Injury After Ischemic Stroke.Molecular neurobiology · 2024Review
- 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.Journal of neuroinflammation · 2024Article
- Prokineticin-2 Participates in Chronic Constriction Injury-Triggered Neuropathic Pain and Anxiety via Regulated by NF-κB in Nucleus Accumbens Shell in Rats.Molecular neurobiology · 2024Article
- Targeting astrocytes polarization after spinal cord injury: a promising direction.Frontiers in cellular neuroscience · 2024Review
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
- NeuroD1 administration ameliorated neuroinflammation and boosted neurogenesis in a mouse model of subarachnoid hemorrhage.Journal of neuroinflammation · 2023Article
- Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- An in vitro study on the stimulatory effects of extracellular glutamate on astrocytes.Molecular biology reports · 2023Article
- Narrative review of roles of astrocytes in subarachnoid hemorrhage.Annals of translational medicine · 2023Review
- Astrocyte polarization in glaucoma: a new opportunity.Neural regeneration research · 2022Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have postulated that neuroinflammation can induce two different types of reactive astrocytes, A1 and A2. A1 astrocytes may be harmful, whereas A2 astrocytes may be protective. Specifically, prokineticin 2 (PK2) has been shown to regulate neuron-astrocyte signaling mechanism by promoting an alternative A2-protective phenotype in astrocytes. This study aimed to examine the role of PK2 in early brain injury (EBI) caused by subarachnoid hemorrhage (SAH). SAH-induced astrocytic activation was confirmed by Western blotting. We confirmed C3 and PTX3 as appropriate reactivity markers for discriminating A1 and A2 astrocytes, respectively. We also observed SAH-induced astrocytic activation in SAH patients. The increase of PK2 in neurons after SAH in both humans and rats suggested a possible relationship between PK2 and SAH pathology. PK2 knockdown promoted an A1 astrocytic phenotype with upregulation of neurodegenerative indicators, while intravascular injection of recombinant PK2 (rPK2) promoted A2 astrocytic phenotype and reduced SAH-induced neuronal injury and behavioral dysfunction. Finally, we identified that tumor necrosis factor alpha (TNF-α) was sufficient to elevate the protein level of PK2 in neurons and enhance astrocytic activation in vitro. Moreover, rPK2 selectively promoted astrocytic polarization to an A2 phenotype under a TNF-α stimulus and induced phosphorylation of signal transducer and activator of transcription 3 (STAT3), suggesting that SAH-induced increases in PK2 may function as an endogenous mechanism for self-repair. Collectively, our findings support that enhancing PK2 expression or administration of rPK2 may induce a selective modulation of astrocytic polarization to a protective phenotype following SAH-like stimuli.
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