Evidence map›Paper›PMID 27631350›Full record

ReviewCornea2016

Cell Therapy of Corneal Diseases.

Winston W-Y Kao, Vivien J Coulson-Thomas

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cornea, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Corneal stromal regeneration-keratoconus cell therapy: a review.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
    Review
  5. Article
  6. Three-dimensional bioprinting in ophthalmic care.International journal of ophthalmology · 2023
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
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

2 authors at 1 institution in 1 country.

Winston W-Y KaoEdith Crawley Vision Research Center, Department of Ophthalmology, University of Cincinnati, Cincinnati, OH.
Vivien J Coulson-Thomas
University of Cincinnati · US

Funding

Structure/Function Relationship of The Lumican GeneR01EY011845 · NEI · UNIVERSITY OF CINCINNATI · PI KAO, WINSTON W · 1999 to 2017
$5.2M
Cell Therapy of Corneal Diseases with Umbilical Mesenchymal Stem CellsR01EY021768 · NEI · UNIVERSITY OF CINCINNATI · PI KAO, WINSTON W · 2011 to 2014
$2.2M
NEI NIH HHS R01 EY011845NEI NIH HHS R01 EY021768
6 · The paper itself

Abstract

Mesenchymal stem cells isolated from connective tissues are pluripotent and differentiate into phenotypes of connective tissue cell lineages (osteoblasts, chondrocytes, and adipocytes) in vitro and in vivo. They have been used to treat mouse models of connective tissue disease such as lumican-null (Lum) and mucopolysaccharidosis (Gusb) mice. Mesenchymal stem cells have unique immunosuppressive properties allowing evasion of host rejection; thus, they are valuable tools for cell therapy of congenital and acquired diseases involving immune dysfunction of multiple tissues including ocular surface tissues (cornea). We previously showed that human umbilical mesenchymal stem cells (UMSCs) modulated host immune responses, enabling them to survive xenograft transplantation. In vitro, UMSCs modulated inflammatory cells by inhibiting adhesion and invasion, and inducing cell death. UMSCs also regulated M1/M2 macrophage polarization and induced T-regulatory cell maturation from naive intraperitoneal cavity lavage cells. UMSCs exposed to inflammatory cells synthesized a rich extracellular glycocalyx composed of hyaluronan (HA) bound to the heavy chains (HCs) of inter-alpha-trypsin inhibitor (HC-HA), which contains tumor necrosis factor-α-stimulated gene 6 (TSG6) that catalyzes the transfer of HCs to HA, versican, and pentraxin-3. Our in vivo and in vitro results showed that the glycocalyx regulated inflammatory cells, allowing UMSCs to survive host immune rejection. Administration of antibodies against glycocalyx constituents or digestion with hyaluronidase and chondroitinase ABC abolished the UMSCs' ability to modulate immune responses. Treatment with anti-CD44 antibodies also diminished modulation of M2 macrophages by UMSCs, indicating that cell surface CD44 is required for correct UMSC glycocalyx assembly to modulate inflammatory cells.

Indexed as

Cell- and Tissue-Based TherapyAnimalsCorneal DiseasesHumansHyaluronan ReceptorsMesenchymal Stem CellsUmbilical CordCD44 protein, humanHyaluronan Receptors

Identifiers

PMID27631350
PMCPMC5067970
OpenAlexW2520876997

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.