Evidence map›Paper›PMID 19852957›Full record

ArticleExperimental eye research2010

Lymphocytic infiltration leads to degradation of lacrimal gland extracellular matrix structures in NOD mice exhibiting a Sjögren's syndrome-like exocrinopathy.

Katja Schenke-Layland, Jiansong Xie, Mattias Magnusson, Ekaterini Angelis, Xiaodong Li, Kaijin Wu, Dieter P Reinhardt, W Robb Maclellan, Sarah F Hamm-Alvarez

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  17. A thermo-responsive protein treatment for dry eyes.Journal of controlled release : official journal of the Controlled Release Society · 2015
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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 2 countries.

Katja Schenke-LaylandDepartment of Medicine/Cardiology, Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1760, USA. kschenkelayland@mednet.ucla.edu
Jiansong Xie
Mattias Magnusson
Ekaterini Angelis
Xiaodong Li
Kaijin Wu
Dieter P Reinhardt
W Robb Maclellan
Sarah F Hamm-Alvarez
LAC+USC Medical Center · USMcGill University · CAUCLA Health · USUniversity of California, Los Angeles · US

Funding

Research Supplements to Promote DiversityR01EY011386 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HAMM-ALVAREZ, SARAH F · 1996 to 2025
$9.3M
CARDIOVASCULAR SCIENTIST TRAINING PROGRAMT32HL007895 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM, WATSON, KAROL E · 1998 to 2023
$9.2M
CIHR 102821-1CIHR 106494-1CIHR MOP-68836NEI NIH HHS EY-11386NEI NIH HHS R01 EY011386NHLBI NIH HHS 5T32HL007895-10NHLBI NIH HHS T32 HL007895
6 · The paper itself

Abstract

We previously reported that lacrimal glands (LGs) of male non-obese diabetic (NOD) mice, an established mouse model of autoimmune inflammatory LG disease that displays many features of human LGs in patients afflicted with Sjögren's syndrome (SjS), exhibit significant degradation of extracellular matrix (ECM) structures as well as increased expression of matrix metalloproteinases (MMPs). The purpose of the current study was to expand the spectrum of proteases identified, to clarify their probable origin as well as to identify the contribution of these changes to disease pathogenesis. We explored in depth the changes in ECM structures and ECM protease expression at the onset of disease (6 weeks) versus late stage disease (18 weeks) in male NOD mouse LGs, relative to LGs of age-matched male NODscid, a severely immunocompromised congenic strain, and healthy BALB/c mice. LG tissues were examined using routine histological, immunohistochemical, Western Blot and gene expression analyses novel multiphoton imaging technologies. We further characterized the profile of infiltrating immune cells under each condition using flow cytometry. Our results show that the initial infiltrating cells at 6 weeks of age are responsible for increased MMP and cathepsin H expression and therefore initiate the LG ECM degradation in NOD mice. More importantly, NODscid mice exhibited normal LG ECM structures, indicating the lymphocytes seen in the LGs of NOD mice are responsible for the degradation of the LG ECM. The disease-related remodeling of LG ECM structures may play a crucial role in altering the acinar signaling environment, disrupting the signaling scaffolds within the cells, which are required to mobilize the exocytotic trafficking machinery, ultimately leading to a loss of LG function in patients afflicted with SjS.

Indexed as

AnimalsBlotting, WesternCathepsin HCell MovementDown-RegulationExtracellular MatrixExtracellular Matrix ProteinsFlow CytometryFluorescent Antibody Technique, IndirectLacrimal ApparatusLymphocytesMaleMatrix MetalloproteinasesMiceMice, Inbred BALB CMice, Inbred NODCathepsin HExtracellular Matrix ProteinsMatrix Metalloproteinases

Identifiers

PMID19852957
PMCPMC2821966
OpenAlexW2042963173

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.