Evidence map›Paper›PMID 26342724›Full record

ArticleThe American journal of pathology2015

TMIGD1 is a novel adhesion molecule that protects epithelial cells from oxidative cell injury.

Emad Arafa, Philip A Bondzie, Kobra Rezazadeh, Rosana D Meyer, Edward Hartsough, Joel M Henderson, John H Schwartz, Vipul Chitalia, Nader Rahimi

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2015. 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
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

19 citing papers in PubMed, 45 citations in OpenAlex.

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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 2 institutions in 1 country.

Emad ArafaDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts.
Philip A BondzieDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts.
Kobra RezazadehDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts.
Rosana D MeyerDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts.
Edward HartsoughDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts.
Joel M HendersonDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts.
John H SchwartzRenal Section, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts.
Vipul ChitaliaRenal Section, Department of Medicine, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts.
Nader RahimiDepartment of Pathology, Boston University Medical Campus, Boston, Massachusetts; Department of Ophthalmology, School of Medicine, Boston University Medical Campus, Boston, Massachusetts. Electronic address: nrahimi@bu.edu.
Boston Medical Center · USBoston University · US

Funding

Role of c-Cbl in Colon cancerR01CA175382 · NCI · BOSTON MEDICAL CENTER · PI CHITALIA, VIPUL C · 2014 to 2018
$1.8M
Role of Protein Ubiquitination in AngiogenesisR01EY017955 · NEI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAHIMI, NADER · 2008 to 2010
$1.2M
Overcoming the resistance to anti-angiogenesis therapyR21CA191970 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAHIMI, NADER · 2015 to 2016
$392k
IGPR-1 in colon cancer chemotherapyR21CA193958 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAHIMI, NADER · 2015 to 2016
$392k
NCI NIH HHS R01 CA175382NCI NIH HHS R21 CA191970NCI NIH HHS R21 CA193958NEI NIH HHS R01 EY017955
6 · The paper itself

Abstract

Oxidative damage to renal tubular epithelial cells is a fundamental pathogenic mechanism implicated in both acute kidney injury and chronic kidney diseases. Because epithelial cell survival influences the outcome of acute kidney injury and chronic kidney diseases, identifying its molecular regulators could provide new insight into pathobiology and possible new therapeutic strategies for these diseases. We have identified transmembrane and immunoglobulin domain-containing 1 (TMIGD1) as a novel adhesion molecule, which is highly conserved in humans and other species. TMIGD1 is expressed in renal tubular epithelial cells and promotes cell survival. The extracellular domain of TMIGD1 contains two putative immunoglobulin domains and mediates self-dimerization. Our data suggest that TMIGD1 regulates transepithelial electric resistance and permeability of renal epithelial cells. TMIGD1 controls cell migration, cell morphology, and protects renal epithelial cells from oxidative- and nutrient-deprivation-induced cell injury. Hydrogen peroxide-induced oxidative cell injury downregulates TMIGD1 expression and targets it for ubiquitination. Moreover, TMIGD1 expression is significantly affected in both acute kidney injury and in deoxy-corticosterone acetate and sodium chloride (deoxy-corticosterone acetate salt)-induced chronic hypertensive kidney disease mouse models. Taken together, we have identified TMIGD1 as a novel cell adhesion molecule expressed in kidney epithelial cells that protects kidney epithelial cells from oxidative cell injury to promote cell survival.

Indexed as

Acute Kidney InjuryAnimalsCell Adhesion MoleculesEpithelial CellsHumansHydrogen PeroxideImmunoglobulinsKidney Tubules, ProximalMembrane GlycoproteinsMice, 129 StrainOxidative StressRNA, MessengerCell Adhesion MoleculesHydrogen PeroxideImmunoglobulinsMembrane GlycoproteinsRNA, MessengerTMIGD1 protein, human

Identifiers

PMID26342724
PMCPMC4607757
OpenAlexW2103101389

What OpenQuestion holds

Textmetadata
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.