Evidence map›Paper›PMID 35603939›Full record

ArticleEuropean journal of histochemistry : EJH2022

Endoplasmic reticulum stress contributed to inflammatory bowel disease by activating p38 MAPK pathway.

Yan Long, Yan Zhao, Xiaoqing Ma, Ya Zeng, Tian Hu, Weijie Wu, Chongtian Deng, Jinyue Hu, Yueming Shen

Open access · goldAbstract read
In one paragraph

Article in European journal of histochemistry : EJH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Endoplasmic Reticular Stress and Pathogenesis of Experimental Colitis: Mechanism of Action of 5-Amino Salicylic Acid.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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 2 institutions in 1 country.

Yan LongDepartment of Digestive Diseases, Changsha Central Hospital, Changsha. jenny199301@163.com.
Yan ZhaoDepartment of Pathology, Changsha Central Hospital, Changsha. xxwn716@163.com.
Xiaoqing MaZhongshan City People Hospital, Zhongshan, Guangdong. YITONG20201020@163.com.
Ya ZengDepartment of Digestive Diseases, Changsha Central Hospital, Changsha. Zengya2010@126.com.
Tian HuDepartment of Digestive Diseases, Changsha Central Hospital, Changsha. 853520998@qq.com.
Weijie WuDepartment of Digestive Diseases, Changsha Central Hospital, Changsha. Wuweijie1995@yeah.net.
Chongtian DengDepartment of Digestive Diseases, Changsha Central Hospital, Changsha. dengchongtian@163.com.
Jinyue HuCentral Laboratory, Changsha Central Hospital, Changsha. hjyzxyy@126.com.
Yueming ShenDepartment of Digestive Diseases, Changsha Central Hospital, Changsha. 2018050504@usc.edu.cn.
Changsha Central Hospital · CNZhongshan People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence suggests that endoplasmic reticulum (ER) stress plays a vital role in inflammatory bowel disease (IBD). Therefore, the aim of this study was to investigate the mechanism by which ER stress promotes inflammatory response in IBD. The expression of Gro-α, IL-8 and ER stress indicator Grp78 in colon tissues from patients with Crohn's disease (CD) and colonic carcinoma was analyzed by immunohistochemistry staining. Colitis mouse model was established by the induction of trinitrobenzene sulphonic acid (TNBS), and the mice were treated with ER stress inhibitor tauroursodeoxycholic acid (TUDCA). Then the body weight, colon length and colon inflammation were evaluated, and Grp78 and Gro-α in colon tissues were detected by immunohistochemistry. Epithelial cells of colon cancer HCT116 cells were treated with tunicamycin to induce ER stress. Grp78 was detected by Western blot, and chemokines were measured by PCR and ELISA. The expression levels of Grp78, Gro-α and IL-8 were significantly upregulated in intestinal tissues of CD patients. Mice with TNBS induced colitis had increased expression of Grp78 and Gro-α in colonic epithelia. TUDCA reduced the severity of TNBS-induced colitis. In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-α and IL-8 in a concentration-dependent manner. Furthermore, p38 MAPK inhibitor significantly inhibited the upregulation of Gro-α and IL-8 induced by tunicamycin. In conclusion, ER stress promotes inflammatory response in IBD, and the effects may be mediated by the activation of p38 MAPK signaling pathway.

Indexed as

ColitisInflammatory Bowel DiseasesAnimalsEndoplasmic Reticulum StressHumansInterleukin-8Micep38 Mitogen-Activated Protein KinasesTrinitrobenzenesulfonic AcidTunicamycinInterleukin-8p38 Mitogen-Activated Protein KinasesTrinitrobenzenesulfonic AcidTunicamycin

Identifiers

PMID35603939
PMCPMC9178311
OpenAlexW4281790073

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.