Evidence map›Paper›PMID 34915845›Full record

ArticleClinical proteomics2021

Proteomics and functional study reveal kallikrein-6 enhances communicating hydrocephalus.

Lei Yuan, Dongdong Zou, Xia Yang, Xin Chen, Youming Lu, Aijun Zhang, Pengqi Zhang, Fance Wei

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

Article in Clinical proteomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 50% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
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  7. Article
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

8 authors at 1 institution in 1 country.

Lei Yuan *Department of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Dongdong Zou *Department of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Xia Yang *Department of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Xin ChenDepartment of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China. masterchx@hotmail.com.ORCID http://orcid.org/0000-0002-6247-7862
Youming LuDepartment of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Aijun ZhangDepartment of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Pengqi ZhangDepartment of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Fance WeiDepartment of Neurosurgery, The Affiliated Sixth People's Hospital, Shanghai Jiaotong University, NO. 600 Yishan Road, Shanghai, 200233, China.
Shanghai Sixth People's Hospital · CN

Funding

National Natural Science Foundation of China 81671207
6 · The paper itself

Abstract

backgroundCommunicating hydrocephalus (CH) is a common neurological disorder caused by a blockage of cerebrospinal fluid. In this study, we aimed to explore the potential molecular mechanism underlying CH development.

methodsQuantitative proteomic analysis was performed to screen the differentially expressed proteins (DEPs) between patients with and without CH. A CH rat model was verified by Hoechst staining, and the co-localization of the target protein and neuron was detected using immunofluorescence staining. Loss-of-function experiments were performed to examine the effect of KLK6 on the synapse structure.

resultsA total of 11 DEPs were identified, and kallikrein 6 (KLK6) expression was found to be significantly upregulated in patients with CH compared with that in patients without CH. The CH rat model was successfully constructed, and KLK6 was found to be co-localized with neuronal nuclei in brain tissue. The expression level of IL-1β, TNF-α, and KLK6 in the CH group was higher than that in the control group. After knockdown of KLK6 expression using small-interfering RNA (siRNA), the expression levels of synapsin-1 and PSD95 in neuronal cells were increased, and the length, number, and structure of synapses were significantly improved. Following siRNA interference KLK6 expression, 5681 differentially expressed genes (DEGs) were identified in transcriptome profile. The upregulated DEGs of Appl2, Nav2, and Nrn1 may be involved in the recovery of synaptic structures after the interference of KLK6 expression.

conclusionsCollectively, KLK6 participates in the development of CH and might provide a new target for CH treatment.

Indexed as

Cerebrospinal fluidCommunicating hydrocephalusKallikrein-6Quantitative proteomic

Identifiers

PMID34915845
PMCPMC8903716
OpenAlexW4200035158

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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.