Evidence map›Paper›PMID 24043632›Full record

ArticleThe Journal of biological chemistry2013

Implications of a vasodilatory human monoclonal autoantibody in postural hypotension.

Hongliang Li, Jonathan Zuccolo, David C Kem, Caitlin Zillner, Jiyeon Lee, Kenneth Smith, Judith A James, Madeleine W Cunningham, Xichun Yu

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Autoantibodies as Endogenous Modulators of GPCR Signaling.Trends in pharmacological sciences · 2021
    Review
  5. Article
  6. Increased circulating βScientific reports · 2017
    Article
  7. 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

9 authors.

Hongliang LiFrom the Departments of Medicine and; the Oklahoma City Veterans Affairs Medical Center, and.
Jonathan ZuccoloMicrobiology and Immunology, University of Oklahoma Health Sciences Center.
David C KemFrom the Departments of Medicine and; the Oklahoma City Veterans Affairs Medical Center, and.
Caitlin ZillnerFrom the Departments of Medicine and; the Oklahoma City Veterans Affairs Medical Center, and.
Jiyeon LeeFrom the Departments of Medicine and.
Kenneth Smiththe Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104.
Judith A JamesFrom the Departments of Medicine and; Microbiology and Immunology, University of Oklahoma Health Sciences Center,; the Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104.
Madeleine W CunninghamMicrobiology and Immunology, University of Oklahoma Health Sciences Center.
Xichun YuFrom the Departments of Medicine and; the Oklahoma City Veterans Affairs Medical Center, and. Electronic address: xichun-yu@ouhsc.edu.

Funding

AUTOIMMUNE DETERMINANTS OF HUMAN CARDIAC MYOSINR01HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 1997 to 2013
$4.7M
Science in a Culture of MentoringP30GM103510 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JAMES, JUDITH A · 2012 to 2016
$3.9M
Autoimmune Determinants of Human Cardiac MyosinR56HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 2008 to 2015
$933k
NHLBI NIH HHS R01 HL056267NHLBI NIH HHS R56 HL056267NIGMS NIH HHS P30 GM103510
6 · The paper itself

Abstract

Functional autoantibodies to the autonomic receptors are increasingly recognized in the pathophysiology of cardiovascular diseases. To date, no human activating monoclonal autoantibodies to these receptors have been available. In this study, we describe for the first time a β2-adrenergic receptor (β2AR)-activating monoclonal autoantibody (C5F2) produced from the lymphocytes of a patient with idiopathic postural hypotension. C5F2, an IgG3 isotype, recognizes an epitope in the N terminus of the second extracellular loop (ECL2) of β2AR. Surface plasmon resonance analysis revealed high binding affinity for the β2AR ECL2 peptide. Immunoblotting and immunofluorescence demonstrated specific binding to β2AR in H9c2 cardiomyocytes, CHO cells expressing human β2AR, and rat aorta. C5F2 stimulated cyclic AMP production in β2AR-transfected CHO cells and induced potent dilation of isolated rat cremaster arterioles, both of which were specifically blocked by the β2AR-selective antagonist ICI-118551 and by the β2AR ECL2 peptide. This monoclonal antibody demonstrated sufficient activity to produce postural hypotension in its host. Its availability provides a unique opportunity to identify previously unrecognized causes and new pharmacological management of postural hypotension and other cardiovascular diseases.

Indexed as

Adrenergic beta-AntagonistsAnimalsAntibodies, MonoclonalAortaArteriolesAutoantibodiesCHO CellsCricetinaeCricetulusHumansHypotension, OrthostaticImmunoglobulin GMaleMyocytes, CardiacPeptidesPropanolaminesAdrenergic beta-AntagonistsAntibodies, MonoclonalAutoantibodiesICI 118551Immunoglobulin GPeptidesPropanolaminesReceptors, Adrenergic, beta-2Vasodilator AgentsAdrenergic ReceptorAutoimmunityCardiovascular DiseaseHuman Monoclonal AutoantibodyPathogenesisPostural HypotensionVascularVasodilatory

Identifiers

PMID24043632
PMCPMC3798543

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.