ArticleNeural regeneration research2023
Poly(ADP-ribose) polymerase family member 14 promotes functional recovery after spinal cord injury through regulating microglia M1/M2 polarization via STAT1/6 pathway.
Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Microglia and neuroinflammation: An in-depth analysis from functional diversity to disease mechanisms.Clinical and translational medicine · 2026Review
- An inflammation-targeted lipid nanoparticle inhibiting ferroptosis for spinal cord injury repair.Materials today. Bio · 2026Article
- Syndecan-4 in microglia mediates ischemic stroke-induced mitochondrial dysfunction and blood-brain barrier damage by interacting with Dishevelled.Scientific reports · 2026Article
- Exosomal Circ_STAT1-AS Delivery Induced by Dexmedetomidine Modulates Microglial Polarization to Alleviate Diabetic Peripheral Neuropathy by Inhibiting JAK/STAT1 Pathway.Diabetes & metabolism journal · 2026Article
- Microglial polarization in retinal neovascularization: Friend or foe?Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- The emerging role of ubiquitin-proteasome system dysfunction in the pathogenesis of perioperative neurocognitive disorders: a narrative review.Frontiers in behavioral neuroscience · 2026Review
- Regulation of microglial polarization via notch signaling pathway by intrathecal administration of tanshinone IIA-PLGA sustained-release microspheres to promote neurological recovery after spinal cord injury.Frontiers in bioengineering and biotechnology · 2026Article
- Probenecid relieves LPS-induced neuroinflammation by modulating the NLRP1 inflammasome pathway in BV2 cells.Scientific reports · 2025Article
- Remote Ischemic Post-conditioning Reduces Cognitive Impairment in Rats Following Subarachnoid Hemorrhage: Possible Involvement in STAT3/STAT5 Phosphorylation and Th17/Treg Cell Homeostasis.Translational stroke research · 2025Article
- Temporal changes of spinal microglia in murine models of neuropathic pain: a scoping review.Frontiers in immunology · 2024Article
- Myricetin suppresses traumatic brain injury-induced inflammatory response via EGFR/AKT/STAT pathway.Scientific reports · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose)polymerase family member 14 (PARP14), which is an intracellular mono(ADP-ribosyl) transferase, has been reported to promote post-stroke functional recovery, but its role in spinal cord injury (SCI) remains unclear. To investigate this, a T10 spinal cord contusion model was established in C57BL/6 mice, and immediately after the injury PARP14 shRNA-carrying lentivirus was injected 1 mm from the injury site to silence PARP14 expression. We found that PARP14 was up-regulated in the injured spinal cord and that lentivirus-mediated downregulation of PARP14 aggravated functional impairment after injury, accompanied by obvious neuronal apoptosis, severe neuroinflammation, and slight bone loss. Furthermore, PARP14 levels were elevated in microglia after SCI, PARP14 knockdown activated microglia in the spinal cord and promoted a shift from M2-polarized microglia (anti-inflammatory phenotype) to M1-polarized microglia (pro-inflammatory phenotype) that may have been mediated by the signal transducers and activators of transcription (STAT) 1/6 pathway. Next, microglia M1 and M2 polarization were induced in vitro using lipopolysaccharide/interferon-γ and interleukin-4, respectively. The results showed that PARP14 knockdown promoted microglia M1 polarization, accompanied by activation of the STAT1 pathway. In addition, PARP14 overexpression made microglia more prone to M2 polarization and further activated the STAT6 pathway. In conclusion, these findings suggest that PARP14 may improve functional recovery after SCI by regulating the phenotypic transformation of microglia via the STAT1/6 pathway.
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