Evidence map›Paper›PMID 22234512›Full record

ArticleHeart and vessels2012

Matrix metalloprotein-9 activation under cell-to-cell interaction between endothelial cells and monocytes: possible role of hypoxia and tumor necrosis factor-α.

Yuko Yamamoto, Tomohiro Osanai, Fumie Nishizaki, Takanori Sukekawa, Kei Izumiyama, Shigeki Sagara, Ken Okumura

Abstract read
PubMed Publisher
In one paragraph

Article in Heart and vessels, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. miR-378-3p alleviates contusion spinal cord injury by negatively regulating ATG12.International journal of experimental pathology · 2021
    Article
  17. Article
  18. Smoking and the Pathophysiology of Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2021
    Review
  19. Lymphocyte-to-monocyte ratio and risk of hemorrhagic transformation in patients with acute ischemic stroke.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020
    Article
  20. 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.

Yuko YamamotoDepartment of Cardiology, Hirosaki University Graduate School of Medicine, 5-Zaifu-cho, Hirosaki, 036-8562, Japan.
Tomohiro Osanai
Fumie Nishizaki
Takanori Sukekawa
Kei Izumiyama
Shigeki Sagara
Ken Okumura
Hirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Matrix metalloproteinase (MMP)-9 plays an important role in cardiovascular events. However, the mechanisms underlying in vivo activation of MMP-9 are largely unknown. We investigated the secretion and activation of MMP-9 under a cell-to-cell interaction, and the effects of hypoxia and cytokine. Human umbilical vein endothelial cell (HUVEC) and THP-1 (human monocyte cell line) were cultured individually, or cocultured under normoxic and hypoxic conditions. In a coculture of HUVEC and THP-1, proMMP-9 secretion was increased twofold compared with individual culture of HUVEC and THP-1, whereas MMP-2 secretion was unchanged. The increase in proMMP-9 secretion was suppressed by antiadhesion molecule antibodies and mitogen-activated protein kinase inhibitors, PD98059 (MAPK/ERK kinase1 inhibitor) and SP600125 (Jun N-terminal kinase inhibitor). ProMMP-9 secretion was increased by tumor necrosis factor (TNF)-α at 50 ng/ml (P < 0.05) but was not activated under normoxic (20%) conditions. ProMMP-9 in coculture was activated under hypoxic (<1%) conditions, and was potentiated by TNF-α (both P < 0.05). To further investigate the mechanism of hypoxia-induced MMP-9 activation, heat shock protein (Hsp)90, which was suggested to be related to MMP-9 activation, was measured by Western blot analysis. The ratio of Hsp90 to glyceraldehyde-3-phosphate dehydrogenase was increased in hypoxic (<1%) coculture conditions with TNF-α (P < 0.05). Treatment with geldanamycin and 17-DMAG (Hsp90 inhibitor) suppressed the active form of MMP-9. Cell-to-cell interaction between endothelial cells and monocytes promotes proMMP-9 synthesis and secretion. Hypoxia and inflammation are suggested to play an important role in activating proMMP-9, presumably via Hsp90.

Indexed as

Cell CommunicationCell HypoxiaCoculture TechniquesEnzyme ActivationEnzyme PrecursorsHSP90 Heat-Shock ProteinsHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1Matrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein KinasesMonocytesProtein Kinase InhibitorsP-SelectinTime FactorsEnzyme PrecursorsHSP90 Heat-Shock ProteinsIntercellular Adhesion Molecule-1Matrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein KinasesMMP2 protein, humanMMP9 protein, humanpro-matrix metalloproteinase 9Protein Kinase InhibitorsP-SelectinSELP protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID22234512
OpenAlexW1971191283

What OpenQuestion holds

Textmetadata
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.