Evidence map›Paper›PMID 21836138›Full record

ArticleAmerican journal of respiratory and critical care medicine2011

Identification of SPOCK2 as a susceptibility gene for bronchopulmonary dysplasia.

Alice Hadchouel, Xavier Durrmeyer, Emmanuelle Bouzigon, Roberto Incitti, Johanna Huusko, Pierre-Henri Jarreau, Richard Lenclen, Florence Demenais, Marie-Laure Franco-Montoya, Inès Layouni and 5 more

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 3 pooled it
6.2field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 3 syntheses or guidelines pooled it, 154 citations in OpenAlex.

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  5. Ancestry and genetic associations with bronchopulmonary dysplasia in preterm infants.American journal of physiology. Lung cellular and molecular physiology · 2018
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  6. Testican-2 (SPOCK2): A multifunctional matricellular regulator.Matrix biology : journal of the International Society for Matrix Biology · 2026
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12 more citing papers are in PubMed but not listed here.

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

15 authors at 6 institutions in 2 countries.

Alice HadchouelInserm, U955, Créteil, France. alice.hadchouel-duverge@nck.aphp.fr
Xavier Durrmeyer
Emmanuelle Bouzigon
Roberto Incitti
Johanna Huusko
Pierre-Henri Jarreau
Richard Lenclen
Florence Demenais
Marie-Laure Franco-Montoya
Inès Layouni
Juliana Patkai
Jacques Bourbon
Mikko Hallman
Claude Danan
Christophe Delacourt
Inserm · FRDélégation Paris 5 · FRHôpital Intercommunal de Créteil · FRUniversity of Oulu · FICentre Hospitalier Intercommunal de Poissy · FRMaternité Port Royal · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleBronchopulmonary dysplasia is the most common chronic respiratory disease in premature infants. Genetic factors might contribute to bronchopulmonary dysplasia susceptibility.

objectivesTo identify genetic variants involved in bronchopulmonary dysplasia through a genome-wide association study.

methodsWe prospectively evaluated 418 premature neonates (gestational age <28 wk), of whom 22% developed bronchopulmonary dysplasia. Two discovery series were created, using a DNA pooling strategy in neonates from white and African ancestry. Polymorphisms associated with the disease were confirmed in an independent replication population. Genes were then explored by fine mapping and associations were replicated in an external Finnish population of 213 neonates. Validated genes expression patterns were studied in rat lung, after air or hyperoxia exposure. MEASUREMENTS AND MAIN

resultsSPOCK2 gene was identified by both discovery series. The most significant polymorphism (rs1245560; P = 1.66 × 10(-7)) was confirmed by individual genotyping, and in the replication population (P = 0.002). Fine mapping confirmed the association of rs1245560 with bronchopulmonary dysplasia in both white and African populations with adjusted odds ratios of 2.96 (95% confidence interval [CI], 1.37-6.40) and 4.87 (95% CI, 1.88-12.63), respectively. In white neonates, rs1049269 was also associated with the disease (odds ratio, 3.21; 95% CI, 1.51-6.82). These associations were replicated in the Finnish population. In newborn rat lungs, SPOCK2 mRNA levels markedly increased during the alveolar stage of lung development. After rat exposure to hyperoxia, SPOCK2 expression increased relative to air-exposed controls.

conclusionsWe identified SPOCK2 as a new possible candidate susceptibility gene for bronchopulmonary dysplasia. Its lung expression pattern points toward a potential role in alveolarization.

Indexed as

AnimalsAnimals, NewbornBlack PeopleBronchopulmonary DysplasiaFemaleFinlandGene ExpressionGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansInfant, NewbornInfant, PrematureLungMalePolymorphism, Single NucleotideProteoglycansSPOCK2 protein, human

Identifiers

PMID21836138
PMCPMC4826668
OpenAlexW1972952097

What OpenQuestion holds

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Registered trials

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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.