Evidence map›Paper›PMID 31882811›Full record

ArticleScientific reports2019

Human β-defensin-3 reduces excessive autophagy in intestinal epithelial cells and in experimental necrotizing enterocolitis.

Liping Chen, Zhibao Lv, Zhimei Gao, Guijie Ge, Xueli Wang, Junmei Zhou, Qingfeng Sheng

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Mechanisms and regulation of defensins in host defense.Signal transduction and targeted therapy · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis.Journal of visualized experiments : JoVE · 2022
    Article
  13. Article
  14. Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  15. Article
  16. 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

7 authors at 2 institutions in 1 country.

Liping ChenDepartment of General Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Zhibao LvDepartment of General Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China. zhibao-lv@hotmail.com.
Zhimei GaoDepartment of Central Laboratory, Children's Hospital of Shanghai, Shanghai Jiao Tong University, Shanghai, 200062, China.
Guijie GeDepartment of General Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China.
Xueli WangDepartment of Pathology, Children's Hospital of Shanghai, Shanghai Jiao Tong University, Shanghai, 200062, China.
Junmei ZhouDepartment of Central Laboratory, Children's Hospital of Shanghai, Shanghai Jiao Tong University, Shanghai, 200062, China.
Qingfeng ShengDepartment of General Surgery, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062, China. shengqingfeng@hotmail.com.
Shanghai Children's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Necrotizing enterocolitis (NEC) is a leading cause of mortality in preterm newborns. Intestinal barrier dysfunction is one key event in NEC pathogenesis. Human β-defensin-3 (hBD3), one member of cationic host defence peptides, was reported to reduce the development of necrotizing enterocolitis in a neonatal rat model. And autophagy was induced in the intestine of human and animals with NEC. We hypothesized that regulation of autophagy might play a critical role in hBD3-mediated protection against NEC injury. Autophagy activity was evaluated both in intestinal epithelial cells and in NEC models. Newborn Sprague-Dawley rats were divided randomly into four groups: Control + NS, Control + rapamycin, NEC + NS, and NEC + hBD3. Body weight, histological score, survival time, enterocyte migration and mucosal barrier were recorded. Our results showed that hBD3 pretreatment could effectively inhibit autophagy activity in cultured IEC-6 and Caco2 enterocytes, and CXCR4 might be involved in hBD3-mediated autophagy suppression. Moreover, hBD3-induced inhibition of autophagy significantly promoted the intestinal epithelial cell migration by wound healing assay and transwell migration assay. In the rat model of NEC, hBD3 could noticeably reduce the expression of autophagy-activated proteins, down-regulate the expression of inflammatory mediators, and promote the mucosal integrity. Our data suggest an additional role of hBD3-mediated protection against intestinal mucosal injury: inhibition of over-activated autophagy in enterocytes.

Indexed as

AutophagyModels, BiologicalAnimalsbeta-DefensinsCaco-2 CellsEnterocolitis, NecrotizingEpithelial CellsHumansIntestinal MucosaRatsRats, Sprague-DawleyReceptors, CXCR4beta-DefensinsCXCR4 protein, humanDEFB103A protein, humanReceptors, CXCR4

Identifiers

PMID31882811
PMCPMC6934505
OpenAlexW2998675315

What OpenQuestion holds

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LicenceCC BY
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.