Evidence map›Paper›PMID 34290711›Full record

ArticleFrontiers in immunology2021

ST6GAL1 and α2-6 Sialylation Regulates IL-6 Expression and Secretion in Chronic Obstructive Pulmonary Disease.

Stefanie Krick, E Scott Helton, Molly Easter, Seth Bollenbecker, Rebecca Denson, Rennan Zaharias, Phillip Cochran, Shia Vang, Elex Harris, James M Wells and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. 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
1.7field-weighted citation impact, top 15% 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, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Chronic Kidney Disease-associated Lung Injury Is Mediated by Phosphate-induced MAPK/AKT Signaling.American journal of respiratory cell and molecular biology · 2024
    Article
  7. Review
  8. MCardiovascular diagnosis and therapy · 2024
    Article
  9. Frontiers in pharmacology · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. ST6Gal1: Oncogenic signaling pathways and targets.Frontiers in molecular biosciences · 2022
    Review
  19. 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

11 authors at 2 institutions in 1 country.

Stefanie KrickDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
E Scott HeltonDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Molly EasterDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Seth BollenbeckerDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Rebecca DensonDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Rennan ZahariasDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Phillip CochranDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Shia VangDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Elex HarrisDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
James M WellsDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
Jarrod W BarnesDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States.
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

UAB CF Research and Translation Core CenterP30DK072482 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Brian R. Davis · 2007 to 2026
$23.0M
A Novel Exosomal Inflammatory PathwayR35HL135710 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BLALOCK, J EDWIN · 2017 to 2023
$6.8M
Training Program in Cell, Molecular, and Developmental BiologyT32GM008111 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 1985 to 2022
$5.4M
Metabolic Landscape of the Aging LungR01HL152246 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNES, JARROD W., THANNICKAL, VICTOR J. · 2020 to 2023
$3.2M
Matrikines and COPD-PHR01HL148215 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WELLS, JAMES MICHAEL · 2019 to 2023
$2.4M
Metabolic drivers and sensors of cell proliferation in pulmonary hypertensionR00HL131866 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNES, JARROD W. · 2018 to 2020
$731k
Fibroblast Growth Factor 23/Klotho Crosstalk and Airway Epithelial Senescence in COPDR03AG059994 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KRICK, STEFANIE · 2018 to 2019
$223k
BLRD VA I01 BX003056NHLBI NIH HHS R00 HL131866NHLBI NIH HHS R01 HL148215NHLBI NIH HHS R01 HL152246NHLBI NIH HHS R35 HL135710NIA NIH HHS R03 AG059994NIDDK NIH HHS P30 DK072482NIGMS NIH HHS T32 GM008111
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a systemic disease strongly associated with cigarette smoking, airway inflammation, and acute disease exacerbations. Changes in terminal sialylation and fucosylation of asparagine (N)-linked glycans have been documented in COPD, but the role that glycosyltransferases may play in the regulation of N-linked glycans in COPD has not been fully elucidated. Recent studies suggest that modulation of ST6GAL1 (ST6 beta-galactoside alpha-2,6-sialyltransferase-1), which catalyzes terminal α2-6 sialylation of cellular proteins, may regulate inflammation and contribute to COPD phenotype(s). Interestingly, it has been previously demonstrated that ST6GAL1, a Golgi resident protein, can be proteolytically processed by BACE1 (beta-site amyloid precursor protein cleaving enzyme-1) to a circulating form that retains activity. In this study, we showed that loss of ST6GAL1 expression increased interleukin (IL)-6 expression and secretion in human bronchial epithelial cells (HBECs). Furthermore, exposure to cigarette smoke medium/extract (CSE) or BACE1 inhibition resulted in decreased ST6GAL1 secretion, reduced α2-6 sialylation, and increased IL-6 production in HBECs. Analysis of plasma ST6GAL1 levels in a small COPD patient cohort demonstrated an inverse association with prospective acute exacerbations of COPD (AECOPD), while IL-6 was positively associated. Altogether, these results suggest that reduced ST6GAL1 and α2-6 sialylation augments IL-6 expression/secretion in HBECs and is associated with poor clinical outcomes in COPD.

Indexed as

Protein Processing, Post-TranslationalAgedAntigens, CDbeta-D-Galactoside alpha 2-6-SialyltransferaseBiomarkersBronchiCell LineEpithelial CellsFemaleGlycosylationHumansInterleukin-6MaleMiddle AgedPulmonary Disease, Chronic ObstructiveSeverity of Illness IndexAntigens, CDbeta-D-Galactoside alpha 2-6-SialyltransferaseBiomarkersIL6 protein, humanInterleukin-6SialyltransferasesSmokeST6GAL1 protein, humanbronchial epitheliumcigarette smokeCOPDinflammationST6GAL1

Identifiers

PMID34290711
PMCPMC8287524
OpenAlexW3183884303

What Socratic 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 Socratic graph.