Evidence map›Paper›PMID 27783995›Full record

ArticleOncotarget2016

MKP-1 attenuates LPS-induced blood-testis barrier dysfunction and inflammatory response through p38 and IκBα pathways.

Yiqing Pan, Yue Liu, Li Wang, Feng Xue, Yanqin Hu, Ran Hu, Chen Xu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
0.5field-weighted citation impact, top 28% 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, 15 citations in OpenAlex.

  1. Microorganisms · 2026
    Article
  2. Review
  3. Review
  4. MyD88 Signaling in Sertoli Cells Mediates LPS-Induced Orchitis in Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. UropathogenicFrontiers in immunology · 2021
    Article
  11. Article
  12. Review
  13. 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 1 institution in 1 country.

Yiqing PanDepartment of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Key Laboratory of Reproductive Medicine, Shanghai 200025, China.
Yue LiuDepartment of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Key Laboratory of Reproductive Medicine, Shanghai 200025, China.
Li WangDepartment of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Key Laboratory of Reproductive Medicine, Shanghai 200025, China.
Feng XueDepartment of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Key Laboratory of Reproductive Medicine, Shanghai 200025, China.
Yanqin HuDepartment of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Key Laboratory of Reproductive Medicine, Shanghai 200025, China.
Ran HuShanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Chen XuDepartment of Anatomy, Histology and Embryology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; Shanghai Key Laboratory of Reproductive Medicine, Shanghai 200025, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sertoli cells create a local tolerogenic microenvironment to maintain testicular immune privilege especially through the formation of a blood-testis barrier (BTB). However, the molecular mechanisms underlying the immune modulation function and BTB dynamics of Sertoli cells remained elusive. MAP phosphatase (MKP)-1 acts as a crucial negative regulator of the inflammatory response. Nevertheless, the role of MKP-1 in regulating Sertoli cells has not been elucidated. In this study, we have for the first time uncovered distinct cellular localization of MKP-1 in the cells at different stages of mouse testis, and the level of MKP-1 expression was significantly up-regulated by LPS-induced acute testis inflammation. In addition, MKP-1 staining was strongly detected in nuclei and peri-nuclear regions of cytoplasm in the Sertoli cells, and it was presented at Sertoli cell tight junctions (TJs) at stages VII-VIII after LPS treatment. Moreover, we demonstrated that MKP-1 was capable of attenuating LPS-induced decrease of occludin by interaction with p38 MAP kinase and IκBα molecules. Taken together, our data highlight that MKP-1 was an important endogenous suppressor of innate immune responses involved in the regulation of BTB barrier dynamic. This study thus might offer novel targets for treating inflammatory diseases in the testis.

Indexed as

AnimalsBlood-Testis BarrierCell NucleusCells, CulturedCellular MicroenvironmentDual Specificity Phosphatase 1Immune PrivilegeInflammationLipopolysaccharidesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLNF-KappaB Inhibitor alphaOccludinProtein TransportDual Specificity Phosphatase 1LipopolysaccharidesNF-KappaB Inhibitor alphaOccludininflammationMAP phosphatase-1occludinsignaling transductiontesticular immune privilege

Identifiers

PMID27783995
PMCPMC5356708
OpenAlexW2532501998

What OpenQuestion holds

Textmetadata
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.