Evidence map›Paper›PMID 33416101›Full record

ArticleInternational journal of molecular medicine2021

EpCAM is essential for maintenance of the small intestinal epithelium architecture via regulation of the expression and localization of proteins that compose adherens junctions.

Guibin Chen, Yanhong Yang, Wanwan Liu, Li Huang, Lanxiang Yang, Yuting Lei, Huijuan Wu, Zili Lei, Jiao Guo

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Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

9 citing papers in PubMed, 16 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

9 authors at 1 institution in 1 country.

Guibin Chen *Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Yanhong Yang *The First Affiliated Hospital (School of Clinical Medicine), Guangdong Pharmaceutical University, Guangzhou, Guangdong 510080, P.R. China.
Wanwan Liu *Guangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Li HuangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Lanxiang YangGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Yuting LeiGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Huijuan WuGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Zili LeiGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Jiao GuoGuangdong Metabolic Diseases Research Center of Integrated Chinese and Western Medicine and Key Laboratory of Glucolipid Metabolic Disorder, Ministry of Education of China and Institute of Chinese Medicine, Guangdong Pharmaceutical University and Guangdong TCM Key Laboratory for Metabolic Diseases, Guangzhou, Guangdong 510006, P.R. China.
Guangdong Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial cell adhesion molecule (EpCAM) is highly expressed in mammalian intestines, and is essential for maintaining the homeostasis of the intestinal epithelium. EpCAM protein is localized at tight junctions and the basolateral membrane of the intestinal epithelium, where it interacts with many cell adhesion molecules. To explore the molecular functions of EpCAM in regulating adherens junctions in the intestinal epithelium, EpCAM knockout embryos and newborn pups were analyzed. Hematoxylin and eosin staining was used to assess the histology of the duodenum, jejunum, ileum and colon from wild-type and EpCAM‑/‑ mice at E18.5, P0 and P3. The expression and localization of adherens junction‑associated genes and genes that encode the proteins that participate in the assembly of adherens junctions were measured at the mRNA and protein levels using qPCR, western blot analysis and immunofluorescence staining. The results showed that although there was no significant damage to the intestines of EpCAM‑/‑ mice at E18.5 and P0, they were significantly damaged at P3 in mutant mice. The expression of adherens junction‑associated genes in EpCAM mutant mice was normal at the mRNA level from E18.5 to P3, but their protein levels were gradually reduced and mislocalized from E18.5 to P3. The expression of nectin 1, which can regulate the assembly and adhesion activity of E‑cadherin, was also gradually reduced at both the mRNA and protein levels in the intestinal epithelium of EpCAM mutant mice from E18.5 to P3. In summary, the loss of EpCAM may cause the reduction and mislocalization of proteins that compose adherens junctions partly via the downregulation of nectin 1 in the intestines.

Indexed as

Gene Expression RegulationAdherens JunctionsAnimalsEpithelial Cell Adhesion MoleculeIntestinal MucosaIntestine, SmallMiceMice, KnockoutEpithelial Cell Adhesion Moleculeadherens junctionEpCAMintestinal epitheliumnectin 1

Identifiers

PMID33416101
PMCPMC7797445
OpenAlexW3113145792

What OpenQuestion holds

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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.