Evidence map›Paper›PMID 28170292›Full record

ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2017

Heparanase Mediates Intestinal Inflammation and Injury in a Mouse Model of Sepsis.

Song Chen, Ying He, Ziwei Hu, Siyu Lu, Xiaohan Yin, Xiaochun Ma, Chuanzhu Lv, Guiyun Jin

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

Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

40 citing papers in PubMed, 56 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

8 authors at 5 institutions in 1 country.

Song ChenDepartment of Emergency Medicine (SC, CL), The First Affiliated Hospital of Hainan Medical College, Haikou, People's Republic of China.
Ying HeDepartment of Geratology (YH), The First Affiliated Hospital of Hainan Medical College, Haikou, People's Republic of China.
Ziwei HuDepartment of Critical Care Medicine, The First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China (ZH, XY, XM).
Siyu LuDepartment of Critical Care Medicine, Peking University Cancer Hospital, Beijing, People's Republic of China (SL).
Xiaohan YinDepartment of Critical Care Medicine, The First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China (ZH, XY, XM).
Xiaochun MaDepartment of Critical Care Medicine, The First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China (ZH, XY, XM).
Chuanzhu LvDepartment of Emergency Medicine (SC, CL), The First Affiliated Hospital of Hainan Medical College, Haikou, People's Republic of China.
Guiyun JinDepartment of Intervention Therapy (GJ), The First Affiliated Hospital of Hainan Medical College, Haikou, People's Republic of China.
Peking University Cancer Hospital · CNChina Medical University · CNFirst Hospital of China Medical University · CNHainan Medical College Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heparanase, a heparan sulfate (HS)-specific endoglycosidase, plays an important role in inflammation and mediates acute pulmonary and renal injuries during sepsis. To explore its role in septic intestinal injury, a non-anticoagulant heparanase inhibitor, N-desulfated/re- N-acetylated heparin (NAH), was administrated to a mouse sepsis model induced by cecal ligation and puncture (CLP). Immunohistochemical staining revealed massive shedding of HS from the intestinal mucosal surfaces after CLP, and effective inhibition of heparanase by NAH was confirmed by markedly reduced HS shedding. Following CLP, intestinal expression of heparanase was increased, whereas pretreatment with NAH reduced the sepsis-induced upregulation of heparanase expression. Meanwhile, CLP led to shedding of syndecan-1 and upregulated expression of proteases such as matrix metalloprotease-9 and urokinase-type plasminogen activator in the intestine, whereas NAH markedly suppressed syndecan-1 shedding and protease upregulation following CLP. In addition, pretreatment with NAH attenuated intestinal injury, inhibited neutrophil infiltration and suppressed the production of inflammatory cytokines (tumor necrosis factor-α, interleukin-1β, and interleukin-6) in the intestine during sepsis, and it also significantly reduced the elevation of inflammatory cytokines in the serum 24 hr after CLP. Our findings demonstrate that the activation of intestinal heparanase contributes to intestinal injury during early sepsis by facilitating the destruction of mucosal epithelial glycocalyx and promoting inflammatory responses.

Indexed as

AnimalsCytokinesGlucuronidaseHeparanaseHeparan SulfateHeparinInterleukin-1betaInterleukin-6Intestinal MucosaIntestinesMaleMice, Inbred C57BLNeutrophil InfiltrationSepsisSyndecan-1Tumor Necrosis Factor-alphaCytokinesGlucuronidaseHeparanaseHeparan SulfateHeparinheparin, N-desulfatedInterleukin-1betaInterleukin-6Syndecan-1Tumor Necrosis Factor-alphaheparanaseheparan sulfateintestinal injurymucosal epithelial glycocalyxsepsissyndecan-1

Identifiers

PMID28170292
PMCPMC5407566
OpenAlexW2587617526

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.