Evidence map›Paper›PMID 10432321›Full record

ArticleThe Biochemical journal1999

Role of the Janus kinase (JAK)/signal transducters and activators of transcription (STAT) cascade in advanced glycation end-product-induced cellular mitogenesis in NRK-49F cells.

J S Huang, J Y Guh, W C Hung, M L Yang, Y H Lai, H C Chen, L Y Chuang

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 1999. 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
2.8field-weighted citation impact, top 10% 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, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Signaling Pathways Involved in Diabetic Renal Fibrosis.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. DJC Suppresses Advanced Glycation End Products-Induced JAK-STAT Signaling and ROS in Mesangial Cells.Evidence-based complementary and alternative medicine : eCAM · 2017
    Article
  11. Article
  12. Protective Effects of Luteolin on Lipopolysaccharide-Induced Acute Renal Injury in Mice.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

J S HuangDepartment of Biochemistry, Kaohsiung Medical College, Kaohsiung, Taiwan, R.O.C.
J Y Guh
W C Hung
M L Yang
Y H Lai
H C Chen
L Y Chuang
Kaohsiung Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Advanced glycation end product (AGE) is important in the pathogenesis of diabetic nephropathy, which is characterized by cellular hypertrophy/hyperplasia leading to renal fibrosis. However, the signal transduction pathways of AGE remain poorly understood. The Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway has been associated with cellular proliferation in some extra-renal cells. Because interstitial fibroblast proliferation might be important in renal fibrosis, we studied the role of the JAK/STAT pathway in NRK-49F (normal rat kidney fibroblast) cells cultured in AGE/BSA and non-glycated BSA. We showed that AGE dose-dependently (10-200 microgram/ml) increased cellular mitogenesis in NRK-49F cells at 5 and 7 days. However, cellular mitogenesis was unaffected by the simultaneous presence of BSA. Regarding the JAK/STAT pathway, AGE (100 microgram/ml) induced tyrosine phosphorylation of JAK2 (but not JAK1, JAK3 or TYK2) at 15-60 min; it also induced the tyrosine phosphorylation of STAT1 and STAT3 at 1-2 h and 0.5-4 h respectively. Being a transcription factor, AGE also increased the DNA-binding activities of STAT1 and STAT3 AG-490 (a specific JAK2 inhibitor) (5 microM) inhibited tyrosine phosphorylation of JAK2 and the DNA-binding activities of STAT1 and STAT3. The same results were obtained by using specific 'decoy' oligodeoxynucleotides (ODNs) that prevented STAT1 and STAT3 from binding to DNA. Meanwhile, the STAT1 or STAT3 decoy ODN and AG-490 were effective in reversing AGE-induced cellular mitogenesis. We concluded that the JAK2-STAT1/STAT3 signal transduction pathway is necessary for AGE-induced cellular mitogenesis in NRK-49F cells.

Indexed as

Proto-Oncogene ProteinsAnimalsCell DivisionCell LineDNADNA-Binding ProteinsDose-Response Relationship, DrugFibroblastsGlycation End Products, AdvancedJanus Kinase 1Janus Kinase 2Janus Kinase 3KidneyMitogensOligodeoxyribonucleotidesPhosphorylationalpha-cyano-(3,4-dihydroxy)-N-benzylcinnamideDNADNA-Binding ProteinsGlycation End Products, AdvancedJak1 protein, ratJak2 protein, ratJak3 protein, ratJanus Kinase 1Janus Kinase 2Janus Kinase 3MitogensOligodeoxyribonucleotidesPhosphotyrosineProtein-Tyrosine KinasesProto-Oncogene ProteinsSerum Albumin, BovineStat1 protein, ratSTAT1 Transcription FactorStat3 protein, ratSTAT3 Transcription FactorTrans-ActivatorsTyrphostins

Identifiers

PMID10432321
PMCPMC1220457
OpenAlexW1975405608

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.