KLF 4 Knockdown Attenuates TBI ‐Induced Neuronal Damage through p53 and JAK ‐ STAT 3 Signaling
Open accessAbstract
AIMS: Traumatic brain injury (TBI) is induced by complex primary and secondary mechanisms that give rise to cell death, inflammation, and neurological dysfunction. Understanding the mechanisms that drive neurological damage as well as those that promote repair can guide the development of therapeutic drugs for TBI. Kruppel-like factor 4 (KLF4) has been reported to negatively regulate axon regeneration of injured retinal ganglion cells (RGCs) through inhibition of JAK-STAT3 signaling. However, the role of KLF4 in TBI remains unreported. Reactive oxygen species (ROS)-induced neuronal death is a pathophysiological hallmark of TBI. METHODS: -treated RGCs in vitro and the optic nerve crush model in vivo to simulate neuronal damage in TBI. The function of KLF4 in RGC survival and axon regeneration in these models was investigated. In addition, the effects of KLF4 knockdown on neuronal damage after a brain impact that mimics moderate TBI were studied. RESULTS: induces p53-dependent apoptosis of RGCs in vitro through upregulation of KLF4. Additionally, KLF4 knockdown in vivo significantly enhances CNTF-induced axon regeneration of RGCs after optic nerve crush, and more importantly, prevents neuronal damage after a moderate brain impact in rats. Our Western blot analysis and immunoprecipitation assay results indicate that these effects of KLF4 knockdown are mediated by the p53 and JAK-STAT3 pathways. CONCLUSION: These findings provide evidence that KLF4 plays an important role in the pathophysiology of TBI. Blocking KLF4 may be a potential therapeutic strategy for the treatment of TBI, either alone or in combination with agents that target complementary mechanisms.
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KLF4 is expressed in neuronal stem cells and regulates neuronal differentiation and migration in the brain.
“One eukaryotic transcription factor, which is expressed in neuronal stem cells (NSCs) and regulates neuronal differentiation and migration in the brain, is that of KLF4.28”
From Microglia secrete miR-146a-5p-containing exosomes to regulate neurogenesis in depression (2022) · cites this paper as [28]
The expression of KLF4 in neural stem cells can regulate the differentiation and migration of neurons in the developing cerebral cortex.
“It has been reported that the expression of KLF4 in neural stem cells can regulate the differentiation and migration of neurons in the developing cerebral cortex.28”
From Microglia secrete miR-146a-5p-containing exosomes to regulate neurogenesis in depression (2022) · cites this paper as [28]
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- Authors
- Cui, D., Zeng, T., Ren, J., Wang, K., Jin, Y., Zhou, L., & Gao, L.
- Affiliations
- Department of Neurosurgery Shanghai Tenth People's Hospital Tongji University School of Medicine Shanghai China
- Tongji University (CN)
- Corresponding author
- Gao, Liang
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2016-09-27
- Volume
- 23
- Issue
- 2
- Pages
- 106-118
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- PMC
- PMC6492741
- OpenAlex
- W2524928277
- Cited by
- 51
- References
- 32
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 10 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 3 · 2019: 1 · 2018: 6 · 2017: 1
- FWCI
- 2.01
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- CNS Neuroscience & Therapeutics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81201979)
- Topics
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Kruppel-like factors research
- Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
- Keywords
- traumatic brain injury, KLF4, p53, JAK/STAT3 signaling, retinal ganglion cells, axon regeneration, optic nerve crush, reactive oxygen species, neuronal apoptosis, ciliary neurotrophic factor, neuroprotection
- MeSH terms
- Brain Injuries, Traumatic, Kruppel-Like Factor 4, Animals, Cerebral Cortex, Disease Models, Animal, Enzyme Inhibitors, Gene Expression Regulation, Hydrogen Peroxide, Nerve Regeneration, Retinal Ganglion Cells, Signal Transduction, Tumor Suppressor Protein p53, Rats, Sprague-Dawley, Apoptosis, Cyclin D1, Tyrphostins, Optic Nerve Injuries, STAT3 Transcription Factor, Rats, Kruppel-Like Transcription Factors, Janus Kinases
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