Evidence map›Paper›PMID 27247942›Full record

ArticleBioMed research international2016

Histone Lysine Methylation in TGF-β1 Mediated p21 Gene Expression in Rat Mesangial Cells.

Qiaoyan Guo, Xiaoxia Li, Hongbo Han, Chaoyuan Li, Shujun Liu, Wenhui Gao, Guangdong Sun

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Role of Histone Modifications in Kidney Fibrosis.Medicina (Kaunas, Lithuania) · 2024
    Review
  5. Review
  6. Epigenetics in the pathogenesis of diabetic nephropathy.Acta biochimica et biophysica Sinica · 2022
    Review
  7. Review
  8. Review
  9. The Role of Histone H3 Methylation in Acute Kidney Injury.Drug design, development and therapy · 2022
    Review
  10. Epigenetic Histone Modifications in the Pathogenesis of Diabetic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021
    Review
  11. Accelerated Kidney Aging in Diabetes Mellitus.Oxidative medicine and cellular longevity · 2020
    Review
  12. Review
  13. Review
  14. Article
  15. 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 2 institutions in 1 country.

Qiaoyan GuoDepartment of Nephrology, 2nd Hospital of Jilin University, Changchun 130041, China.
Xiaoxia LiDepartment of Nephrology, 2nd Hospital of Jilin University, Changchun 130041, China.
Hongbo HanDepartment of Endocrinology, 208th Hospital of Chinese PLA, Changchun 130062, China.
Chaoyuan LiDepartment of Nephrology, 2nd Hospital of Jilin University, Changchun 130041, China.
Shujun LiuDepartment of Nephrology, 2nd Hospital of Jilin University, Changchun 130041, China.
Wenhui GaoDepartment of Neonatology, 2nd Hospital of Jilin University, Changchun 130041, China.
Guangdong SunDepartment of Nephrology, 2nd Hospital of Jilin University, Changchun 130041, China.ORCID 0000-0002-2899-7899
Jilin University · CNChangchun 208 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor beta1- (TGF-β1-) induced p21-dependent mesangial cell (MC) hypertrophy plays a key role in the pathogenesis of chronic renal diseases including diabetic nephropathy (DN). Increasing evidence demonstrated the role of posttranscriptional modifications (PTMs) in the event; however, the precise regulatory mechanism of histone lysine methylation remains largely unknown. Here, we examined the roles of both histone H3 lysine 4 and lysine 9 methylations (H3K4me/H3K9me) in TGF-β1 induced p21 gene expression in rat mesangial cells (RMCs). Our results indicated that TGF-β1 upregulated the expression of p21 gene in RMCs, which was positively correlated with the increased chromatin marks associated with active genes (H3K4me1/H3K4me2/H3K4me3) and negatively correlated with the decreased levels of repressive marks (H3K9me2/H3K9me3) at p21 gene promoter. TGF-β1 also elevated the recruitment of the H3K4 methyltransferase (HMT) SET7/9 to the p21 gene promoter. SET7/9 gene silencing with small interfering RNAs (siRNAs) significantly abolished the TGF-β1 induced p21 gene expression. Taken together, these results reveal the key role of histone H3Kme in TGF-β1 mediated p21 gene expression in RMC, partly through HMT SET7/9 occupancy, suggesting H3Kme and SET7/9 may be potential renoprotective agents in managing chronic renal diseases.

Indexed as

AnimalsCells, CulturedCyclin-Dependent Kinase Inhibitor p21DNA MethylationGene Expression RegulationHistone-Lysine N-MethyltransferaseHistonesLysineMaleMesangial CellsRatsRats, Sprague-DawleyTransforming Growth Factor beta1Cdkn1a protein, ratCyclin-Dependent Kinase Inhibitor p21Histone-Lysine N-MethyltransferaseHistonesLysineTransforming Growth Factor beta1

Identifiers

PMID27247942
PMCPMC4876202
OpenAlexW2347067993

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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.