Evidence map›Paper›PMID 38532543›Full record

ArticleCNS neuroscience & therapeutics2024

RACK1 promotes autophagy via the PERK signaling pathway to protect against traumatic brain injury in rats.

Haibo Ni, Xugang Kan, Qin Rui, Yang Zhang, Weiwei Zhai, Baole Zhang, Zhengquan Yu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Haibo NiDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xugang KanDepartment of Neurobiology and Cell Biology, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, China.
Qin RuiDepartment of Center of Clinical Laboratory, The Fourth Affiliated Hospital of Soochow University, Suzhou, China.
Yang ZhangDepartment of Neurobiology and Cell Biology, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, China.
Weiwei ZhaiDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.
Baole ZhangDepartment of Neurobiology and Cell Biology, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou, China.
Zhengquan YuDepartment of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0009-0004-9398-7373
Soochow University · CNXuzhou Medical College · CN

Funding

National Natural Science Foundation of China 81901254National Natural Science Foundation of China 82201538Project of Suzhou Health Talent Training GSWS2020105Qing Lan Project in Jiangsu Province to BaoleZhangSix Talent Peaks in Jiangsu Province SWYY-088The 333 Project of Jiangsu Province to Baole Zhang
6 · The paper itself

Abstract

aimsNeuronal cell death is a primary factor that determines the outcome after traumatic brain injury (TBI). We previously revealed the importance of receptor for activated C kinase (RACK1), a multifunctional scaffold protein, in maintaining neuronal survival after TBI, but the specific mechanism remains unclear. The aim of this study was to explore the mechanism underlying RACK1-mediated neuroprotection in TBI.

methodsTBI model was established using controlled cortical impact injury in Sprague-Dawley rats. Genetic intervention and pharmacological inhibition of RACK1 and PERK-autophagy signaling were administrated by intracerebroventricular injection. Western blotting, coimmunoprecipitation, transmission electron microscopy, real-time PCR, immunofluorescence, TUNEL staining, Nissl staining, neurobehavioral tests, and contusion volume assessment were performed.

resultsEndogenous RACK1 was upregulated and correlated with autophagy induction after TBI. RACK1 knockdown markedly inhibited TBI-induced autophagy, whereas RACK1 overexpression exerted the opposite effects. Moreover, RACK1 overexpression ameliorated neuronal apoptosis, neurological deficits, and cortical tissue loss after TBI, and these effects were abrogated by the autophagy inhibitor 3-methyladenine or siRNAs targeting Beclin1 and Atg5. Mechanistically, RACK1 interacted with PERK and activated PERK signaling. Pharmacological and genetic inhibition of the PERK pathway abolished RACK1-induced autophagy after TBI.

conclusionOur findings indicate that RACK1 protected against TBI-induced neuronal damage partly through autophagy induction by regulating the PERK signaling pathway.

Indexed as

Brain Injuries, TraumaticSignal TransductionAnimalsApoptosisAutophagyNeuroprotectionRatsRats, Sprague-DawleyReceptors for Activated C KinaseRACK1 protein, ratReceptors for Activated C KinaseautophagyneuroprotectionPERKRACK1traumatic brain injury

Identifiers

PMID38532543
PMCPMC10966134
OpenAlexW4393228992

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Registered trials

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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.