Evidence map›Paper›PMID 27612459›Full record

ArticleStem cell research & therapy2016

Adipose-derived mesenchymal stem cells from patients with atherosclerotic renovascular disease have increased DNA damage and reduced angiogenesis that can be modified by hypoxia.

Ahmed Saad, Xiang-Yang Zhu, Sandra Herrmann, LaTonya Hickson, Hui Tang, Allan B Dietz, Andre J van Wijnen, Lilach Lerman, Stephen Textor

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Renovascular Disease and Mitochondrial Dysfunction in Human Mesenchymal Stem Cells.Journal of the American Society of Nephrology : JASN · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Extracellular Vesicles in Cardiovascular Diseases: Diagnosis and Therapy.Frontiers in cell and developmental biology · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
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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

9 authors at 1 institution in 1 country.

Ahmed SaadDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.ORCID 0000-0003-1861-4521
Xiang-Yang ZhuDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
Sandra HerrmannDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
LaTonya HicksonDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
Hui TangDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
Allan B DietzDivision of Transfusion Medicine, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
Andre J van WijnenDepartment of Orthopedic Surgery, Biochemistry and Molecular Biology, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
Lilach LermanDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA.
Stephen TextorDivision of Nephrology and Hypertension, Mayo Clinic, Rochester Minnesota, 200 First Street SW, Rochester, MN, USA. stextor@mayo.edu.
Mayo Clinic · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
Tissue Oxygenation in Human Renovascular HypertensionP01HL085307 · NHLBI · MAYO CLINIC ROCHESTER · PI ROMERO, JUAN C · 2007 to 2011
$10.4M
CT imaging for the assessment of kidney injury distal to renal artery stenosisR01DK073608 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2006 to 2015
$3.1M
Hypoxia and inflammatory injury in human renovascular hypertensionR01DK100081 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O, TEXTOR, STEPHEN C · 2014 to 2018
$2.8M
Mesenchymal stem cell senescence in diabetic nephropathy (K23 COVID Admin Supplement)K23DK109134 · NIDDK · MAYO CLINIC ROCHESTER · PI HICKSON, LATONYA J · 2016 to 2021
$1.0M
NCRR NIH HHS UL1 RR024150NHLBI NIH HHS P01 HL085307NIDDK NIH HHS K23 DK109134NIDDK NIH HHS R01 DK073608NIDDK NIH HHS R01 DK100081
6 · The paper itself

Abstract

backgroundAdipose-derived MSC (AMSCs) possess angiogenic and immunomodulatory properties that may modulate kidney regeneration. Whether these properties are retained in older patients with atherosclerotic vascular disease is poorly understood. Hypoxic conditions are known to modify properties and growth characteristics of AMSCs. We tested the hypothesis that AMSCs from older patients with atherosclerotic renovascular disease (RVD) differ from normal kidney donors, and whether hypoxia changes their functional and molecular properties to promote angiogenesis.

methodsAMSCs from 11 patients with RVD (mean age =74.5 years) and 10 healthy kidney donors (mean age = 51.2 years) were cultured under normoxia (20 % O2) and hypoxia (1 % O2) for 3-4 days until they reached 80 % confluency. We analyzed expression of genes and microRNAs using RNA sequencing and real-time quantitative rt-PCR. Protein expression of selected angiogenic factors (VEGF, IGF, HGF and EGF) were quantified in conditioned media using ELISAs. Apoptosis was tested using Annexin IV staining.

resultsNormoxic AMSC from RVD patients grew normally, but exhibited increased DNA damage and reduced migration. VEGF protein secretion was significantly lower in the RVD AMSCs (0.08 vs 2.4 ng/mL/ cell, p <0.05) while HGF was higher. Both trends were reversed during growth under hypoxic conditions. Hypoxia upregulated pro-angiogenic mRNAs expression in AMSCs (VEGF, FGF, STC and ANGPTL4), and downregulated expression of many miRNAs (e.g., miR-15a, miR-16, miR-93, miR-424, 126, 132, 221) except miR-210.

conclusionsThus, although AMSC from patients with RVD had increased DNA damage and reduced migration, hypoxia stimulated pro-angiogenic responses via increased expression of angiogenic genes, VEGF secretion and induction of the hypoxia-inducible miR-210, while downregulating angiogenesis-related miRNAs.

Indexed as

Adipose TissueAdiposityAgedAngiogenesis Inducing AgentsApoptosisCell HypoxiaCells, CulturedCerebrovascular DisordersCulture Media, ConditionedDNA DamageFemaleHumansMaleMesenchymal Stem CellsMicroRNAsMiddle AgedAngiogenesis Inducing AgentsCulture Media, ConditionedMicroRNAsVascular Endothelial Growth Factor AAngiogenesisHypoxiaMesenchymal stem cellsRenovascular diseaseVEGF and MicroRNAs

Identifiers

PMID27612459
PMCPMC5016873
OpenAlexW2511197848

What OpenQuestion holds

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Registered trials

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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.