Evidence map›Paper›PMID 28570277›Full record

ArticleJCI insight2017

Epithelial Gpr116 regulates pulmonary alveolar homeostasis via Gq/11 signaling.

Kari Brown, Alyssa Filuta, Marie-Gabrielle Ludwig, Klaus Seuwen, Julian Jaros, Solange Vidal, Kavisha Arora, Anjaparavanda P Naren, Kathirvel Kandasamy, Kaushik Parthasarathi and 5 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 66 citations in OpenAlex.

  1. Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

15 authors at 6 institutions in 4 countries.

Kari BrownDepartment of Pediatrics, Perinatal Institute, Section of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Alyssa FilutaDepartment of Pediatrics, Perinatal Institute, Section of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Marie-Gabrielle LudwigNovartis Institutes for Biomedical Research, Basel, Switzerland.
Klaus SeuwenNovartis Institutes for Biomedical Research, Basel, Switzerland.
Julian JarosNovartis Institutes for Biomedical Research, Basel, Switzerland.
Solange VidalNovartis Institutes for Biomedical Research, Basel, Switzerland.
Kavisha AroraDepartment of Pediatrics, Division of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Anjaparavanda P NarenDepartment of Pediatrics, Division of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Kathirvel KandasamyDepartment of Physiology, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA.
Kaushik ParthasarathiDepartment of Physiology, University of Tennessee Health Sciences Center, Memphis, Tennessee, USA.
Stefan OffermannsDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Robert J MasonDepartment of Medicine, National Jewish Health, Denver, Colorado, USA.
William E MillerDepartment of Molecular Genetics, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.
Jeffrey A WhitsettDepartment of Pediatrics, Perinatal Institute, Section of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
James P BridgesDepartment of Pediatrics, Perinatal Institute, Section of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Cincinnati Children's Hospital Medical Center · USNovartis (Switzerland) · CHUniversity of Tennessee Health Science Center · USMax Planck Institute for Heart and Lung Research · DENational Jewish Health · USUniversity of Cincinnati Medical Center · US

Funding

LPA2 receptor-containing complexes in regulating secretory diarrheaR01DK093045 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI NAREN, ANJAPARAVANDA P · 2011 to 2019
$3.0M
Role of EMC3/TMEM111 in Alveolar Epithelial Cell FunctionR01HL136722 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI LIN, XINHUA, WHITSETT, JEFFREY A · 2017 to 2020
$2.1M
Role of GPR116 in Alveolar HomeostasisR01HL131634 · NHLBI · NATIONAL JEWISH HEALTH · PI BRIDGES, JAMES PATRICK · 2016 to 2020
$2.0M
NHLBI NIH HHS R01 HL131634NHLBI NIH HHS R01 HL136722NIDDK NIH HHS R01 DK093045
6 · The paper itself

Abstract

Pulmonary function is dependent upon the precise regulation of alveolar surfactant. Alterations in pulmonary surfactant concentrations or function impair ventilation and cause tissue injury. Identification of the molecular pathways that sense and regulate endogenous alveolar surfactant concentrations, coupled with the ability to pharmacologically modulate them both positively and negatively, would be a major therapeutic advance for patients with acute and chronic lung diseases caused by disruption of surfactant homeostasis. The orphan adhesion GPCR GPR116 (also known as Adgrf5) is a critical regulator of alveolar surfactant concentrations. Here, we show that human and mouse GPR116 control surfactant secretion and reuptake in alveolar type II (AT2) cells by regulating guanine nucleotide-binding domain α q and 11 (Gq/11) signaling. Synthetic peptides derived from the ectodomain of GPR116 activated Gq/11-dependent inositol phosphate conversion, calcium mobilization, and cortical F-actin stabilization to inhibit surfactant secretion. AT2 cell-specific deletion of Gnaq and Gna11 phenocopied the accumulation of surfactant observed in Gpr116-/- mice. These data provide proof of concept that GPR116 is a plausible therapeutic target to modulate endogenous alveolar surfactant pools to treat pulmonary diseases associated with surfactant dysfunction.

Indexed as

Cell BiologyPulmonology

Identifiers

PMID28570277
PMCPMC5453702
OpenAlexW2621261983

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.