Evidence map›Paper›PMID 29062612›Full record

ArticlePeerJ2017

lncRNA H19 is involved in TGF-

Wei Yang, Xuezhong Li, Shaopei Qi, Xueru Li, Kun Zhou, Suzhu Qing, Yong Zhang, Ming-Qing Gao

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Hemin attenuates bleomycin-induced lung fibrosis in mice by regulating the TGF-β1/MAPK and AMPK/SIRT1/PGC-1α/HO-1/NF-κB pathways.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  5. Article
  6. Staphylococcal mastitis in dairy cows.Frontiers in veterinary science · 2024
    Review
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  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
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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 2 institutions in 2 countries.

Wei YangCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Xuezhong LiCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Shaopei QiCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Xueru LiCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Kun ZhouInnovation Experimental College, Northwest A&F University, Yangling, Shaanxi, China.
Suzhu QingCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Yong ZhangCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Ming-Qing GaoCollege of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Northwest A&F University · CNMinistry of Agriculture · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased levels of long noncoding RNA H19 (H19) have been observed in many inflammatory and organ fibrosis diseases including ulcerative colitis, osteoarthritis, liver fibrosis, renal fibrosis and pulmonary fibrosis. However, the role of H19 in bovine mastitis and mastitis-caused fibrosis is still unclear. In our study, H19 was characterized as a novel regulator of EMT induced by transforming growth factor-β1 (TGF-β1) in bovine mammary alveolar cell-T (MAC-T) cell line. We found that H19 was highly expressed in bovine mastitis tissues and inflammatory MAC-T cells induced by virulence factors of pathogens. TGF-β1 was also highly expressed in inflammatory MAC-T cells, and exogenous TGF-β1 could induce EMT, enhance extracellular matrix protein expression, and upregulate H19 expression in epithelial cells. Stable expression of H19 significantly promotes EMT progression and expression of ECM protein induced by TGF-β1 in MAC-T cells. Furthermore, by using a specific inhibitor of the PI3K/AKT pathway, we demonstrated that TGF-β1 upregulated H19 expression through PI3K/AKT pathway. All these observations imply that the lncRNA H19 modulated TGF-β1-induced epithelial to mesenchymal transition in bovine epithelial cells through PI3K/AKT signaling pathway, which suggests that mammary epithelial cells might be one source for myofibroblasts

Indexed as

BovineEpithelial cellsH19MAC-TMastitisTGF-β1

Identifiers

PMID29062612
PMCPMC5649593
OpenAlexW2737832093

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.