Evidence map›Paper›PMID 29378858›Full record

ArticleHypertension (Dallas, Tex. : 1979)2018

Plasma Cell Depletion Attenuates Hypertension in an Experimental Model of Autoimmune Disease.

Erin B Taylor, Michelle T Barati, David W Powell, Hannah R Turbeville, Michael J Ryan

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

36 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Revisiting sex as a biological variable in hypertension research.The Journal of clinical investigation · 2024
    Review
  5. Review
  6. Immune cells and hypertension.Immunologic research · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Update on Immune Mechanisms in Hypertension.American journal of hypertension · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  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

5 authors at 1 institution in 1 country.

Erin B TaylorFrom the Department of Physiology and Biophysics (E.B.T., M.J.R.) and Department of Pharmacology & Toxicology (H.R.T.), University of Mississippi Medical Center, Jackson; Department of Medicine, University of Louisville School of Medicine, KY (M.T.B., D.W.P.); and G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS (M.J.R.).
Michelle T BaratiFrom the Department of Physiology and Biophysics (E.B.T., M.J.R.) and Department of Pharmacology & Toxicology (H.R.T.), University of Mississippi Medical Center, Jackson; Department of Medicine, University of Louisville School of Medicine, KY (M.T.B., D.W.P.); and G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS (M.J.R.).
David W PowellFrom the Department of Physiology and Biophysics (E.B.T., M.J.R.) and Department of Pharmacology & Toxicology (H.R.T.), University of Mississippi Medical Center, Jackson; Department of Medicine, University of Louisville School of Medicine, KY (M.T.B., D.W.P.); and G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS (M.J.R.).
Hannah R TurbevilleFrom the Department of Physiology and Biophysics (E.B.T., M.J.R.) and Department of Pharmacology & Toxicology (H.R.T.), University of Mississippi Medical Center, Jackson; Department of Medicine, University of Louisville School of Medicine, KY (M.T.B., D.W.P.); and G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS (M.J.R.).
Michael J RyanFrom the Department of Physiology and Biophysics (E.B.T., M.J.R.) and Department of Pharmacology & Toxicology (H.R.T.), University of Mississippi Medical Center, Jackson; Department of Medicine, University of Louisville School of Medicine, KY (M.T.B., D.W.P.); and G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS (M.J.R.). mjryan@umc.edu.
University of Louisville · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI RECKELHOFF, JANE F · 1993 to 2018
$39.4M
Tracking and Evaluation CoreU54GM115428 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI COMPRETTA, CAROLINE E. · 2016 to 2025
$38.2M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Functional Mechanisms of Causal Variants in Systemic Lupus ErythematosusR01AR063124 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GAFFNEY, PATRICK M · 2012 to 2016
$2.0M
Autoantibodies and the pathogenesis of hypertension in systemic lupus erythematosusF32HL137393 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2017 to 2018
$118k
Renal mechanisms of hypertension in autoimmune disease I01BX002604 · VA · VETERANS HEALTH ADMINISTRATION · PI MICHAEL RYAN · 2015 to 2026
–
BLRD VA I01 BX002604NHLBI NIH HHS F32 HL137393NHLBI NIH HHS P01 HL051971NHLBI NIH HHS T32 HL105324NIAMS NIH HHS R01 AR063124NIGMS NIH HHS P20 GM104357NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

Numerous studies show a direct relation between circulating autoantibodies, characteristic of systemic autoimmune disorders, and primary hypertension in humans. Whether these autoantibodies mechanistically contribute to the development of hypertension remains unclear. Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by aberrant immunoglobulin production, notably pathogenic autoantibodies, and is associated with prevalent hypertension, renal injury, and cardiovascular disease. Because plasma cells produce the majority of serum immunoglobulins and are the primary source of autoantibodies in SLE, we hypothesized that plasma cell depletion using the proteasome inhibitor bortezomib would lower autoantibody production and attenuate hypertension. Thirty-week-old female SLE (NZBWF1) and control (NZW [New Zealand White]) mice were injected IV with vehicle (0.9% saline) or bortezomib (0.75 mg/kg) twice weekly for 4 weeks. Bortezomib treatment significantly lowered the percentage of bone marrow plasma cells in SLE mice. Total plasma IgG and anti-dsDNA IgG levels were higher in SLE mice compared with control mice but were lowered by bortezomib treatment. Mean arterial pressure (mm Hg) measured in conscious mice by carotid artery catheter was higher in SLE mice than in control mice, but mean arterial pressure was significantly lower in bortezomib-treated SLE mice. Bortezomib also attenuated renal injury, as assessed by albuminuria and glomerulosclerosis, and reduced glomerular immunoglobulin deposition and B and T lymphocytes infiltration into the kidneys. Taken together, these data show that the production of autoantibodies by plasma cells mechanistically contributes to autoimmune-associated hypertension and suggests a potential role for patients with primary hypertension who have increased circulating immunoglobulins.

Indexed as

Bone MarrowGlomerulosclerosis, Focal SegmentalKidneyLupus Erythematosus, SystemicAnimalsAntibodies, AntinuclearBlood PressureBortezomibDisease Models, AnimalDisease ProgressionFemaleHypertensionMiceMice, Inbred NZBPlasma CellsProteasome InhibitorsAntibodies, AntinuclearBortezomibProteasome Inhibitorsautoantibodiesautoimmunityhypertensionlupus erythematosus, systemicplasma cells

Identifiers

PMID29378858
PMCPMC5843526
OpenAlexW2789954624

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.