Evidence map›Paper›PMID 26760976›Full record

ArticlePloS one2016

Imbalances in Mobilization and Activation of Pro-Inflammatory and Vascular Reparative Bone Marrow-Derived Cells in Diabetic Retinopathy.

Harshini Chakravarthy, Eleni Beli, Svetlana Navitskaya, Sandra O'Reilly, Qi Wang, Nermin Kady, Chao Huang, Maria B Grant, Julia V Busik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Article
  3. Resilient Calvarial Bone Marrow Supports Retinal Repair in Type 2 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Adult Stem Cell Therapeutics in Diabetic Retinopathy.International journal of molecular sciences · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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 4 institutions in 1 country.

Harshini ChakravarthyDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Eleni BeliDepartment of Ophthalmology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Svetlana NavitskayaDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Sandra O'ReillyDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Qi WangDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Nermin KadyDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Chao HuangDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Maria B GrantDepartment of Ophthalmology, Indiana University School of Medicine, Indianapolis, Indiana, United States of America.
Julia V BusikDepartment of Physiology, Michigan State University, East Lansing, Michigan, United States of America.
Michigan United · USMichigan State University · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON · 2013 to 2026
$24.3M
NITRIC OXIDE IN THE PATHOGENESIS OF DIABETIC RETINOPATHYR01EY012601 · NEI · UNIVERSITY OF FLORIDA · PI Julia V Busik, Maria Bartolomeo Grant · 1998 to 2026
$9.6M
Dyslipidemia and Diabetic RetinopathyR01EY016077 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI BUSIK, JULIA V · 2005 to 2025
$6.3M
Targeting the IGF-1 System in Retinal AngiogenesisR01EY007739 · NEI · UNIVERSITY OF FLORIDA · PI ABCOUWER, STEVEN F, GRANT, MARIA BARTOLOMEO · 1995 to 2015
$5.4M
LXR as a Novel Therapeutic Target in Diabetic RetinopathyR01EY025383 · NEI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BUSIK, JULIA V, GRANT, MARIA BARTOLOMEO · 2015 to 2024
$4.2M
NO Dysregulation of the Peripheral Clock in Diabetic ComplicationsR01DK090730 · NIDDK · UNIVERSITY OF FLORIDA · PI GRANT, MARIA BARTOLOMEO · 2010 to 2013
$1.3M
HORMONES &NEOVASCULARIZATION IN DIABETIC RETINOPATHYR29EY007739 · NEI · UNIVERSITY OF FLORIDA · PI GRANT, MARIA B · 1989 to 1993
–
NEI NIH HHS EY-01-6077NEI NIH HHS EY-07739NEI NIH HHS EY-12601NEI NIH HHS R01 EY007739NEI NIH HHS R01 EY012601NEI NIH HHS R01 EY016077NEI NIH HHS R01 EY025383NIDDK NIH HHS DK-09-0730NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

Diabetic retinopathy is a sight-threatening complication of diabetes, affecting 65% of patients after 10 years of the disease. Diabetic metabolic insult leads to chronic low-grade inflammation, retinal endothelial cell loss and inadequate vascular repair. This is partly due to bone marrow (BM) pathology leading to increased activity of BM-derived pro-inflammatory monocytes and impaired function of BM-derived reparative circulating angiogenic cells (CACs). We propose that diabetes has a significant long-term effect on the nature and proportion of BM-derived cells that circulate in the blood, localize to the retina and home back to their BM niche. Using a streptozotocin mouse model of diabetic retinopathy with GFP BM-transplantation, we have demonstrated that BM-derived circulating pro-inflammatory monocytes are increased in diabetes while reparative CACs are trapped in the BM and spleen, with impaired release into circulation. Diabetes also alters activation of splenocytes and BM-derived dendritic cells in response to LPS stimulation. A majority of the BM-derived GFP cells that migrate to the retina express microglial markers, while others express endothelial, pericyte and Müller cell markers. Diabetes significantly increases infiltration of BM-derived microglia in an activated state, while reducing infiltration of BM-derived endothelial progenitor cells in the retina. Further, control CACs injected into the vitreous are very efficient at migrating back to their BM niche, whereas diabetic CACs have lost this ability, indicating that the in vivo homing efficiency of diabetic CACs is dramatically decreased. Moreover, diabetes causes a significant reduction in expression of specific integrins regulating CAC migration. Collectively, these findings indicate that BM pathology in diabetes could play a role in both increased pro-inflammatory state and inadequate vascular repair contributing to diabetic retinopathy.

Indexed as

AnimalsBone Marrow CellsBone Marrow TransplantationCell CountChimeraDendritic CellsDiabetic RetinopathyEndothelial CellsGreen Fluorescent ProteinsInflammationLipopolysaccharidesMaleMice, Inbred C57BLMicrogliaMicrovesselsMonocytesGreen Fluorescent ProteinsLipopolysaccharides

Identifiers

PMID26760976
PMCPMC4711951
OpenAlexW2237584729

What OpenQuestion holds

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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.