Evidence map›Paper›PMID 27235450›Full record

ArticlePhysiological genomics2016

Loss of bone marrow adrenergic beta 1 and 2 receptors modifies transcriptional networks, reduces circulating inflammatory factors, and regulates blood pressure.

Niousha Ahmari, Jordan T Schmidt, Gregory A Krane, Wendi Malphurs, Bruce E Cunningham, Jennifer L Owen, Christopher J Martyniuk, Jasenka Zubcevic

Open access · greenAbstract read
In one paragraph

Article in Physiological genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  13. Immune cell βAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
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  17. Elevated bone marrow sympathetic drive precedes systemic inflammation in angiotensin II hypertension.American journal of physiology. Heart and circulatory physiology · 2019
    Article
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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

8 authors at 1 institution in 1 country.

Niousha AhmariDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida;
Jordan T SchmidtDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida;
Gregory A KraneDepartment of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, Florida; and.
Wendi MalphursDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida;
Bruce E CunninghamDepartment of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, Florida.
Jennifer L OwenDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida;
Christopher J MartyniukDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida;
Jasenka ZubcevicDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida; jasenkaz@ufl.edu.
University of Florida · US

Funding

Gut-brain axis: functional link between microbial metabolites and neurogenic hypertensionR21AT010192 · NCCIH · UNIVERSITY OF FLORIDA · PI MARTYNIUK, CHRISTOPHER JOSEPH · 2019 to 2020
$419k
High salt diet potentiation of AngII HTN : Novel role for Th17 cell infiltration into the PVNR56HL136692 · NHLBI · UNIVERSITY OF FLORIDA · PI MARTYNIUK, CHRISTOPHER JOSEPH, ZUBCEVIC, JASENKA · 2017 to 2017
$370k
NCCIH NIH HHS R21 AT010192NHLBI NIH HHS R56 HL136692
6 · The paper itself

Abstract

Hypertension (HTN) is a prevalent condition with complex etiology and pathophysiology. Evidence exists of significant communication between the nervous system and the immune system (IS), and there appears to be a direct role for inflammatory bone marrow (BM) cells in the pathophysiology of hypertension. However, the molecular and neural mechanisms underlying this interaction have not been characterized. Here, we transplanted whole BM cells from the beta 1 and 2 adrenergic receptor (AdrB1(tm1Bkk)AdrB2(tm1Bkk)/J) knockout (KO) mice into near lethally irradiated C57BL/6J mice to generate a BM AdrB1.B2 KO chimera. This allowed us to evaluate the role of the BM beta 1 and beta 2 adrenergic receptors in mediating BM IS homeostasis and regulating blood pressure (BP) in an otherwise intact physiological setting. Fluorescence-activated cell sorting demonstrated that a decrease in systolic and mean BP in the AdrB1.B2 KO chimera is associated with a decrease in circulating inflammatory T cells, macrophage/monocytes, and neutrophils. Transcriptomics in the BM identified 7,419 differentially expressed transcripts between the C57 and AdrB1.B2 KO chimera. Pathway analysis revealed differentially expressed transcripts related to several cell processes in the BM of C57 compared with AdrB1.B2 KO chimera, including processes related to immunity (e.g., T-cell activation, T-cell recruitment, cytokine production, leukocyte migration and function), the cardiovascular system (e.g., blood vessel development, peripheral nerve blood flow), and the brain (e.g., central nervous system development, neurite development) among others. This study generates new insight into the molecular events that underlie the interaction between the sympathetic drive and IS in modulation of BP.

Indexed as

AnimalsBlood PressureBone MarrowBone Marrow CellsBone Marrow TransplantationDisease Models, AnimalGene Regulatory NetworksHypertensionInflammationMacrophagesMiceMice, Inbred C57BLMice, KnockoutMonocytesNeutrophilsReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2adrenergic receptorsbone marrowchimeraimmune systemsympathetic drive

Identifiers

PMID27235450
PMCPMC11735009
OpenAlexW2405716852

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.