Evidence map›Paper›PMID 34336553›Full record

ArticleAnalytical cellular pathology (Amsterdam)2021

Pannexin1: Role as a Sensor to Injury Is Attenuated in Pretype 2 Corneal Diabetic Epithelium.

Garrett Rhodes, Kristen L Segars, Yoonjoo K Lee, Audrey E K Hutcheon, Celeste B Rich, Vickery Trinkaus-Randall

Open access · goldAbstract read
In one paragraph

Article in Analytical cellular pathology (Amsterdam), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Age Dependent Changes in Corneal Epithelial Cell Signaling.Frontiers in cell and developmental biology · 2022
    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

6 authors at 2 institutions in 1 country.

Garrett RhodesDepartment of Ophthalmology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Kristen L SegarsDepartment of Pharmacology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Yoonjoo K LeeDepartment of Pharmacology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Audrey E K HutcheonSchepens Eye Research Institute of Mass Eye and Ear, Department of Ophthalmology, Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.
Celeste B RichDepartment of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
Vickery Trinkaus-RandallDepartment of Ophthalmology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.ORCID https://orcid.org/0000-0002-8573-9108
Boston University · USMassachusetts Eye and Ear Infirmary · US

Funding

Molecular Mechanisms of corneal wound repairR01EY006000 · NEI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TRINKAUS-RANDALL, VICKERY E · 1986 to 2018
$6.8M
Calcium oscillations and cell motility with corneal injuryR21EY029097 · NEI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TRINKAUS-RANDALL, VICKERY E · 2019 to 2020
$454k
NEI NIH HHS R01 EY006000NEI NIH HHS R21 EY029097
6 · The paper itself

Abstract

Epithelial wound healing is essential to repair the corneal barrier function after injury and requires coordinated epithelial sheet movement over the wounded region. The presence and role of pannexin1 on multilayered epithelial sheet migration was examined in unwounded and wounded corneal epithelium from C57BL/6J (B6) control and diet-induced obese (DiO) mice, a pretype 2 diabetic model. We hypothesize that pannexin1 is dysregulated, and the interaction of two ion-channel proteins (P2X7 and pannexin1) is altered in pretype 2 diabetic tissue. Pannexin1 was found to be present along cell borders in unwounded tissue, and no significant difference was observed between DiO and B6 control. However, an epithelial debridement induced a striking difference in pannexin1 localization. The B6 control epithelium displayed intense staining near the leading edge, which is the region where calcium mobilization was detected, whereas the staining in the DiO corneal epithelium was diffuse and lacked distinct gradation in intensity back from the leading edge. Cells distal to the wound in the DiO tissue were irregular in shape, and the morphology was similar to that of epithelium inhibited with 10Panx, a pannexin1 inhibitor. Pannexin1 inhibition reduced mobilization of calcium between cells near the leading edge, and MATLAB scripts revealed a reduction in cell-cell communication that was also detected in cultured cells. Proximity ligation was performed to determine if P2X7 and pannexin1 interaction was a necessary component of motility and communication. While there was no significant difference in the interaction in unwounded DiO and B6 control corneal epithelium, there was significantly less interaction in the wounded DiO corneas both near the wound and back from the edge. The results demonstrate that pannexin1 contributes to the healing response, and P2X7 and pannexin1 coordination may be a required component of cell-cell communication and an underlying reason for the lack of pathologic tissue migration.

Indexed as

Diabetes MellitusEpithelium, CornealAnimalsMiceMice, Inbred C57BLSignal TransductionWound Healing

Identifiers

PMID34336553
PMCPMC8295002
OpenAlexW3179621048

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.