Evidence map›Paper›PMID 29101035›Full record

ArticleBiochemical and biophysical research communications2018

Surfactant protein D attenuates nitric oxide-stimulated apoptosis in rat chondrocyte by suppressing p38 MAPK signaling.

Yan Zhou, Jianghua Ming, Yaming Li, Xianjin Du, Ming Deng, Bin He, Jianlin Zhou, Guirong Wang, Shiqing Liu

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2018. 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
3.3field-weighted citation impact, top 8% 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, 30 citations in OpenAlex.

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  6. Immunologic mechanism of fungal keratitis.International journal of ophthalmology · 2021
    Review
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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 3 institutions in 2 countries.

Yan ZhouDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Jianghua MingDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Yaming LiDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Xianjin DuDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Ming DengDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Bin HeDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Jianlin ZhouDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Guirong WangDepartment of Surgery, SUNY Upstate Medical University, Syracuse, NY 13210, USA. Electronic address: Wangg@upstate.edu.
Shiqing LiuDepartment of Orthopedics, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China. Electronic address: liusqrm@163.com.
Renmin Hospital of Wuhan University · CNWuhan University · CNSUNY Upstate Medical University · US

Funding

Mechanisms of differential susceptibility of human SP-B genetic variants to pneumonia and lung injuryR01HL136706 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI WANG, GUIRONG · 2017 to 2020
$1.6M
NHLBI NIH HHS R01 HL136706
6 · The paper itself

Abstract

Innate immune molecule surfactant protein D (SP-D), a member of the C-type lectin protein family, plays an indispensable role in host defense and the regulation of inflammation in the lung and other tissues. Osteoarthritis (OA) is a degenerative disease of cartilage, with inflammation that causes pathologic changes and tissue damage. However, it is unknown whether there exist SP-D expression and its potential role in the pathogenesis of OA. In this study, we examined SP-D expression and explored its biological function in a sodium nitroprusside (SNP)-stimulated rat chondrocytes and surgically-induced rat OA model. We found SP-D expression in both human and rat articular chondrocytes, with higher level in normal chondrocytes compared to in OA chondrocytes. Furthermore, In vivo study demonstrated that recombinant human SP-D (rhSP-D) ameliorated cartilage degeneration in surgically-induced rat OA model. In vitro cell culture study showed that rhSP-D markedly inhibited the expression of caspase-3 as an apoptosis biomarker, and decreased phosphorylation of p38 mitogen-activated protein kinase (MAPK), which resulted in maintaining normal nuclear morphology and increasing mitochondrial membrane potential in SNP-stimulated rat chondrocytes. Collectively, these findings indicate that SP-D expresses in articular chondrocytes and suppresses SNP-stimulated chondrocyte apoptosis and ameliorates cartilage degeneration via suppressing p38 MAPK activity.

Indexed as

Nitric OxideAnimalsApoptosisCells, CulturedChondrocytesDown-RegulationHumansMAP Kinase Signaling SystemOsteoarthritisPulmonary Surfactant-Associated Protein DRatsRats, Sprague-DawleyNitric OxidePulmonary Surfactant-Associated Protein DApoptosisChondrocyteOsteoarthritisSodium nitroprussideSurfactant protein D

Identifiers

PMID29101035
PMCPMC6421565
OpenAlexW2765491693

What OpenQuestion holds

Textmetadata
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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.