Evidence map›Paper›PMID 34380908›Full record

ArticleNeural regeneration research2022

Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury.

Wen-Yuan Li, Xiu-Mei Fu, Zhen-Dong Wang, Zhi-Gang Li, Duo Ma, Ping Sun, Gui-Bo Liu, Xiao-Feng Zhu, Ying Wang

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 29 citations in OpenAlex.

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  11. Molecular function of Krüppel-like factor 7 in biology.Acta biochimica et biophysica Sinica · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Wen-Yuan LiInstitute of Neural Tissue Engineering, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Xiu-Mei FuDepartment of Anatomy, College of Basic Medical Sciences; Hebei Key Laboratory of Nerve Injury and Repair, Chengde Medical University, Chengde, Hebei Province, China.
Zhen-Dong WangDepartment of Otorhinolaryngology, Mudanjiang City Second People's Hospital, Mudanjiang, Heilongjiang Province, China.
Zhi-Gang LiThe First Department of General Surgery, Hongqi Hospital, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Duo MaInstitute of Neural Tissue Engineering, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Ping SunInstitute of Neural Tissue Engineering, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Gui-Bo LiuInstitute of Neural Tissue Engineering, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Xiao-Feng ZhuInstitute of Neural Tissue Engineering, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Ying WangInstitute of Neural Tissue Engineering, Mudanjiang Medical University, Mudanjiang, Heilongjiang Province, China.
Mudanjiang Medical University · CNChengde Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous study has shown that the transcription factor Krüppel-like factor 7 (KLF7) promotes peripheral nerve regeneration and motor function recovery after spinal cord injury. KLF7 also participates in traumatic brain injury, but its regulatory mechanisms remain poorly understood. In the present study, an HT22 cell model of traumatic brain injury was established by stretch injury and oxygen-glucose deprivation. These cells were then transfected with an adeno-associated virus carrying KLF7 (AAV-KLF7). The results revealed that, after stretch injury and oxygen-glucose deprivation, KLF7 greatly reduced apoptosis, activated caspase-3 and lactate dehydrogenase, downregulated the expression of the apoptotic markers B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) and cleaved caspase-3, and increased the expression of βIII-tubulin and the antiapoptotic marker Bcl-2. Furthermore, KLF7 overexpression upregulated Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) phosphorylation in HT22 cells treated by stretch injury and oxygen-glucose deprivation. Immunoprecipitation assays revealed that KLF7 directly participated in the phosphorylation of STAT3. In addition, treatment with AG490, a selective inhibitor of JAK2/STAT3, weakened the protective effects of KLF7. A mouse controlled cortical impact model of traumatic brain injury was then established. At 30 minutes before modeling, AAV-KLF7 was injected into the ipsilateral lateral ventricle. The protein and mRNA levels of KLF7 in the hippocampus were increased at 1 day after injury and recovered to normal levels at 3 days after injury. KLF7 reduced ipsilateral hippocampal atrophy, decreased the injured cortex volume, downregulated Bax and cleaved caspase-3 expression, and increased the number of 5-bromo-2'-deoxyuridine-positive neurons and Bcl-2 protein expression. Moreover, KLF7 transfection greatly enhanced the phosphorylation of JAK2 and STAT3 in the ipsilateral hippocampus. These results suggest that KLF7 may protect hippocampal neurons after traumatic brain injury through activation of the JAK2/STAT3 signaling pathway. The study was approved by the Institutional Review Board of Mudanjiang Medical University, China (approval No. mdjyxy-2018-0012) on March 6, 2018.

Indexed as

apoptosishippocampusJAK2/STAT3Kruppel-like factor 7neuroprotectionoxygen-glucose deprivationstretchtraumatic brain injury

Identifiers

PMID34380908
PMCPMC8504401
OpenAlexW3188264794

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.