Evidence map›Paper›PMID 34156983›Full record

ArticleThe Journal of clinical investigation2021

Extracellular matrix protein laminin β1 regulates pain sensitivity and anxiodepression-like behaviors in mice.

Zhen-Zhen Li, Wen-Juan Han, Zhi-Chuan Sun, Yun Chen, Jun-Yi Sun, Guo-Hong Cai, Wan-Neng Liu, Tao-Zhi Wang, Yang-Dan Xie, Hong-Hui Mao and 6 more

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In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. [Mechanistic role of spinal Lamb1 in negative emotionZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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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

16 authors at 5 institutions in 1 country.

Zhen-Zhen LiDepartment of Neurobiology, School of Basic Medicine.
Wen-Juan HanDepartment of Neurobiology, School of Basic Medicine.
Zhi-Chuan SunDepartment of Neurobiology, School of Basic Medicine.
Yun ChenThe Second Regiment, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Jun-Yi SunThe Second Regiment, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Guo-Hong CaiDepartment of Neurobiology, School of Basic Medicine.
Wan-Neng LiuDepartment of Neurobiology, School of Basic Medicine.
Tao-Zhi WangDepartment of Neurobiology, School of Basic Medicine.
Yang-Dan XieThe Second Regiment, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Hong-Hui MaoDepartment of Neurobiology, School of Basic Medicine.
Fei WangDepartment of Neurobiology, School of Basic Medicine.
Sui-Bin MaDepartment of Neurobiology, School of Basic Medicine.
Fu-Dong WangDepartment of Neurobiology, School of Basic Medicine.
Rou-Gang XieDepartment of Neurobiology, School of Basic Medicine.
Sheng-Xi WuDepartment of Neurobiology, School of Basic Medicine.
Ceng LuoDepartment of Neurobiology, School of Basic Medicine.
Air Force Medical University · CNShaanxi University of Chinese Medicine · CNNorthwest University · CNSecond Affiliated Hospital of Jilin University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with neuropathic pain often experience comorbid psychiatric disorders. Cellular plasticity in the anterior cingulate cortex (ACC) is assumed to be a critical interface for pain perception and emotion. However, substantial efforts have thus far been focused on the intracellular mechanisms of plasticity rather than the extracellular alterations that might trigger and facilitate intracellular changes. Laminin, a key element of the extracellular matrix (ECM), consists of one α-, one β-, and one γ-chain and is implicated in several pathophysiological processes. Here, we showed in mice that laminin β1 (LAMB1) in the ACC was significantly downregulated upon peripheral neuropathy. Knockdown of LAMB1 in the ACC exacerbated pain sensitivity and induced anxiety and depression. Mechanistic analysis revealed that loss of LAMB1 caused actin dysregulation via interaction with integrin β1 and the subsequent Src-dependent RhoA/LIMK/cofilin pathway, leading to increased presynaptic transmitter release probability and abnormal postsynaptic spine remodeling, which in turn orchestrated the structural and functional plasticity of pyramidal neurons and eventually resulted in pain hypersensitivity and anxiodepression. This study sheds new light on the functional capability of ECM LAMB1 in modulating pain plasticity and identifies a mechanism that conveys extracellular alterations to intracellular plasticity. Moreover, we identified cingulate LAMB1/integrin β1 signaling as a promising therapeutic target for the treatment of neuropathic pain and associated anxiodepression.

Indexed as

Behavior, AnimalAnimalsAnxietyDepressionFemaleGene Knockdown TechniquesGyrus CinguliLamininMiceNeuralgiaPeripheral Nervous System DiseasesLamb1 protein, mouseLamininDepressionLamininNeurosciencePain

Identifiers

PMID34156983
PMCPMC8321574
OpenAlexW3173195041

What OpenQuestion holds

Textmetadata
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.