Evidence map›Paper›PMID 27130612›Full record

ArticleBMC cell biology2016

Matrix metalloproteinase 9 induces endothelial-mesenchymal transition via Notch activation in human kidney glomerular endothelial cells.

Ye Zhao, Xi Qiao, Lihua Wang, Tian Kui Tan, Hong Zhao, Yun Zhang, Jianlin Zhang, Padmashree Rao, Qi Cao, Yiping Wang and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 74 citations in OpenAlex.

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  5. Cancer-Associated Fibroblasts in Hepatocellular Carcinoma and Cholangiocarcinoma.Cellular and molecular gastroenterology and hepatology · 2023
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  13. The Role of Macrophages in Kidney Fibrosis.Frontiers in physiology · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 2 countries.

Ye ZhaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Xi QiaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Lihua WangDepartment of Nephrology, Second Hospital of Shanxi Medical University, Shanxi Kidney Disease Institute, WuYi Road 382, Taiyuan, 030001, Shanxi, PR China.
Tian Kui TanCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Hong ZhaoDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Xinjian Road 56, Taiyuan, 030001, Shanxi, PR China.
Yun ZhangExperimental Centre of Science and Research, the First Clinical Hospital of Shanxi Medical University, Xinjian Road 382, Taiyuan, 030001, Shanxi, PR China.
Jianlin ZhangDepartment of Biochemistry and Molecular Biology, Shanxi Medical University, Xinjian Road 56, Taiyuan, 030001, Shanxi, PR China.
Padmashree RaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Qi CaoCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Yiping WangCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Ya WangCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Yuan Min WangCentre for Kidney Research, Children's Hospital at Westmead, 212 Hawkesbury Road, Sydney, NSW, Australia.
Vincent W S LeeCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Stephen I AlexanderCentre for Kidney Research, Children's Hospital at Westmead, 212 Hawkesbury Road, Sydney, NSW, Australia.
David C H HarrisCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia.
Guoping ZhengCentre for Transplant and Renal Research, Westmead Institute for Medical Research, the University of Sydney, 176 Hawkesbury Road, Sydney, NSW, 2145, Australia. guoping.zheng@sydney.edu.au.
Westmead Institute for Medical Research · AUUniversity of Sydney · AUChildren's Hospital at Westmead · AUSecond Hospital of Shanxi Medical University · CNShanxi Medical University · CNChengdu Medical College · CNFirst Hospital of Shanxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial-mesenchymal transition (EndoMT) is a major source of myofibroblast formation in kidney fibrosis. Our previous study showed a profibrotic role for matrix metalloproteinase 9 (MMP-9) in kidney fibrosis via induction of epithelial-mesenchymal transition (EMT). Inhibition of MMP-9 activity reduced kidney fibrosis in murine unilateral ureteral obstruction. This study investigated whether MMP-9 also plays a role in EndoMT in human glomerular endothelial cells.

resultsTGF-β1 (10 or 20 ng/ml) induced EndoMT in HKGECs as shown by morphological changes. In addition, VE-cadherin and CD31 were significantly downregulated, whereas α-SMA, vimentin, and N-cadherin were upregulated. RT-PCR revealed that Snail, a known inducer of EMT, was upregulated. The MMP inhibitor GM6001 abrogated TGF-β1-induced EndoMT. Zymography indicated that MMP-9 was also upregulated in TGF-β1-treated HKGECs. Recombinant MMP-9 (2 μg/ml) induced EndoMT in HKGECs via Notch signaling, as evidenced by increased formation of the Notch intracellular domain (NICD) and decreased Notch 1. Inhibition of MMP-9 activity by its inhibitor showed a dose-dependent response in preventing TGF-β1-induced α-SMA and NICD in HKGECs, whereas inhibition of Notch signaling by γ-secretase inhibitor (GSI) blocked rMMP-9-induced EndoMT.

conclusionsTaken together, our results demonstrate that MMP-9 plays an important role in TGF-β1-induced EndoMT via upregulation of Notch signaling in HKGECs.

Indexed as

Amyloid Precursor Protein SecretasesDipeptidesEndothelial CellsHumansKidney GlomerulusMatrix Metalloproteinase 9Matrix Metalloproteinase InhibitorsMesodermReceptors, NotchRecombinant ProteinsSignal TransductionTransforming Growth Factor beta1Amyloid Precursor Protein SecretasesDipeptidesMatrix Metalloproteinase 9Matrix Metalloproteinase InhibitorsN-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamideReceptors, NotchRecombinant ProteinsTransforming Growth Factor beta1Endothelial-mesenchymal transitionHuman glomerular endothelial cellsMatrix metalloproteinase 9NotchTGF-β1

Identifiers

PMID27130612
PMCPMC4850690
OpenAlexW2342927726

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.