Evidence mapPaperPMID 26202084Full record

ArticleCurrent vascular pharmacology2016

MiR-135a Suppresses Calcification in Senescent VSMCs by Regulating KLF4/STAT3 Pathway.

Lin Lin, Yue He, Bei-Li Xi, Hong-Chao Zheng, Qian Chen, Jun Li, Ying Hu, Ming-Hao Ye, Ping Chen, Yi Qu

Open access · bronzeAbstract read
In one paragraph

Article in Current vascular pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  4. Review
  5. Curcumin attenuates vascular calcification via the exosomal miR-92b-3p/KLF4 axis.Experimental biology and medicine (Maywood, N.J.) · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Noncoding RNAs in Vascular Aging.Oxidative medicine and cellular longevity · 2020
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Lin Lin
Yue He
Bei-Li XiDepartment of Geriatrics, Xuhui Central hospital, Shanghai Clinical Center, Chinese Academy of Science, No.966 Middle Huaihai Road, Shanghai, 200031, China. believexi@126.com.
Hong-Chao Zheng
Qian Chen
Jun Li
Ying Hu
Ming-Hao Ye
Ping Chen
Yi QuDepartment of Geriatrics, Xuhui Central hospital, Shanghai Clinical Center, Chinese Academy of Science, No.966 Middle Huaihai Road, Shanghai, 200031, China. quyi2014xk@163.com.
Shanghai Xuhui Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular function phenotype is regulated by various microRNAs (miRs), including miR-135a. However, how miR-135a is involved in the calcification in senescent vascular smooth muscle cells (VSMCs) is not clear yet. In the present study, we first identified the significantly altered miRNAs in VSMCs, then performed consecutive passage culture of VSMCs and analyzed the expression of miR- 135a and calcification genes in the senescent phase. Next, the effects of the miR-135a inhibition on calcification and calcification genes were analyzed. The luciferase assay was used to validate the target protein of miR-135a. The western blotting was used to determine the effects of miR-135a on Krüppel-like factor 4 (KLF4) and signal transducer and activator of transcription 3 protein (STAT3) expression, as well as the relationship between KLF4 and STAT3. Finally, the quantified cellular calcification was measured to examine the involvement of miR-135a, KLF4 and STAT3 in VSMCs calcification. Our results showed that miR-135a was significantly altered in VSMCs. Cell calcification and calcification genes were greatly altered by miR-135a inhibition. KLF4 was validated as the target RNA of miR-135a. Expression of KLF4 and STAT3 were both significantly decreased by over expressed miR-135a, while the inhibition of miR-135a and KLF4 siRNA both decreased the STAT3 protein levels. Moreover, the inhibition of miR-135a dramatically increased the calcium concentration, but co-treatment with KLF4 or STAT3 siRNA both decreased the calcium concentration. The present study identified miR-135a as a potential osteogenic differentiation suppressor in senescent VSMCs and revealed that KLF4/STAT3 pathway, at least partially, was involved in the mechanism.

Indexed as

AnimalsCells, CulturedCellular SenescenceKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleRatsRats, Sprague-DawleySignal TransductionSTAT3 Transcription FactorVascular CalcificationKlf4 protein, ratKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN135 microRNA, ratStat3 protein, ratSTAT3 Transcription Factor

Identifiers

PMID26202084
PMCPMC5403971
OpenAlexW1169947809

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.