Evidence map›Paper›PMID 35488146›Full record

ArticleMolecular and cellular biochemistry2022

HIF1A promotes miR-210/miR-424 transcription to modulate the angiogenesis in HUVECs and HDMECs via sFLT1 under hypoxic stress.

Haifu Zhao, Xiancheng Wang, Bairong Fang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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

3 authors at 1 institution in 1 country.

Haifu ZhaoDepartment of Plastic and Aesthetic (Burn) Surgery, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Road, Furong District, Changsha, 410011, Hunan, China.
Xiancheng WangDepartment of Plastic and Aesthetic (Burn) Surgery, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Road, Furong District, Changsha, 410011, Hunan, China.
Bairong FangDepartment of Plastic and Aesthetic (Burn) Surgery, The Second Xiangya Hospital, Central South University, 139 Renmin Middle Road, Furong District, Changsha, 410011, Hunan, China. fbrfbr2004@csu.edu.cn.ORCID http://orcid.org/0000-0001-7730-4238
Central South University · CN

Funding

National Natural Science Foundation of China 81501709Natural Science Foundation of Hunan Province 2021JJ30928
6 · The paper itself

Abstract

Angiogenesis is a critical process during human skin wound healing. However, hypoxia might lead to the dysfunction of the cellular interplay of endothelial cells and subcutaneous fibroblasts, resulting in the deregulation of angiogenesis. HIF1A is a key regulatory of the recovery of intracellular homeostasis under hypoxia. In the present study, the detailed role and mechanism of HIF1A in the angiogenesis under hypoxia were investigated. Via bioinformatic analyses on microarray profiles (GSE1041 and GSE17944), solube fms-related tyrosine kinase 1 (sFLT1, also known as sVEGFR1) and miR-210/miR-424 might be involved in HIF1A function on the angiogenesis under hypoxia in human umbilical vascular endothelium cells (HUVECs) and human dermal microvascular endothelial cells (HDMECs). In the present study, we identified sFLT1 as a downregulated gene in response to hypoxia and HIF1A overexpression in HUVECs and HDMECs. sFLT1 overexpression inhibited the capacity of migration and angiogenesis and significantly reversed the inducible effects of HIF1A on the migration and angiogenesis in both cell lines. miR-210 and miR-424 were upregulated by hypoxia and targeted sFLT1 3'-UTR to negatively modulate its expression. HIF1A modulated sFLT1 expression, VEGF signaling, and the migration and angiogenesis in HUVECs and HDMECs via miR-210/miR-424. Regarding the molecular mechanism, HIF1A bound the promoter region of miR-210 and miR-424 to activate their transcription, while miR-210/miR-424 bound sFLT1 3'-UTR to suppress its expression. In summary, HIF1A/miR-210/miR-424/sFLT1 axis modulates the angiogenesis in HUVECs and HDMECs upon hypoxic condition via VEGF signaling.

Indexed as

Endothelial CellsMicroRNAsHumansHuman Umbilical Vein Endothelial CellsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitNeovascularization, PathologicVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1FLT1 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN210 microRNA, humanMIRN424 microrna, humanVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1AngiogenesisHIF1AHypoxiamiR-210miR-424sFLT1VEGFR1

Identifiers

PMID35488146
OpenAlexW4225163121

What Socratic 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 Socratic graph.