Evidence map›Paper›PMID 31767169›Full record

ArticleMolecular metabolism2019

RGS2: A multifunctional signaling hub that balances brown adipose tissue function and differentiation.

Katarina Klepac, JuHee Yang, Staffan Hildebrand, Alexander Pfeifer

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2019. 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
1.3field-weighted citation impact, top 19% 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

7 citing papers in PubMed, 21 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Katarina KlepacInstitute of Pharmacology and Toxicology, University of Bonn, 53127 Bonn, Germany; Research Training Group 1873, University of Bonn, 53127 Bonn, Germany. Electronic address: katarina.klepac@helmholtz-muenchen.de.
JuHee YangInstitute of Pharmacology and Toxicology, University of Bonn, 53127 Bonn, Germany; Research Training Group 1873, University of Bonn, 53127 Bonn, Germany.
Staffan HildebrandInstitute of Pharmacology and Toxicology, University of Bonn, 53127 Bonn, Germany.
Alexander PfeiferInstitute of Pharmacology and Toxicology, University of Bonn, 53127 Bonn, Germany; Research Training Group 1873, University of Bonn, 53127 Bonn, Germany; PharmaCenter, University of Bonn, 53127 Bonn, Germany. Electronic address: alexander.pfeifer@uni-bonn.de.
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRecruitment of brown adipose tissue (BAT) is a potential new strategy for increasing energy expenditure (EE) to treat obesity. G protein-coupled receptors (GPCRs) represent promising targets to activate BAT, as they are the major regulators of BAT biological function. To identify new regulators of GPCR signaling in BAT, we studied the role of Regulator of G protein Signaling 2 (RGS2) in brown adipocytes and BAT.

methodsWe combined pharmacological and genetic tools to investigate the role of RGS2 in BAT in vitro and in vivo. Adipocyte progenitors were isolated from wild-type (WT) and RGS2 knockout (RGS2-/-) BAT and differentiated to brown adipocytes. This approach was complemented with knockdown of RGS2 using lentiviral shRNAs (shRGS2). Adipogenesis was analyzed by Oil Red O staining and by determining the expression of adipogenic and thermogenic markers. Pharmacological modulators and fluorescence staining of F-acting stress fibers were employed to identify the underlying signaling pathways. In vivo, the activity of BAT was assessed by ex vivo lipolysis and by measuring whole-body EE by indirect calorimetry in metabolic cages.

resultsRGS2 is highly expressed in BAT, and treatment with cGMP-an important enhancer of brown adipocyte differentiation-further increased RGS2 expression. Loss of RGS2 strongly suppressed adipogenesis and the expression of thermogenic genes in brown adipocytes. Mechanistically, we found increased Gq/Rho/Rho kinase (ROCK) signaling in the absence of RGS2. Surprisingly, in vivo analysis revealed elevated BAT activity in RGS2-deficient mice that was caused by enhanced Gs/cAMP signaling.

conclusionOverall, RGS2 regulates two major signaling pathways in BAT: Gq and Gs. On the one hand, RGS2 promotes brown adipogenesis by counteracting the inhibitory action of Gq/Rho/ROCK signaling. On the other hand, RGS2 decreases the activity of BAT through the inhibition of Gs signaling and cAMP production. Thus, RGS2 might represent a stress modulator that protects BAT from overstimulation.

Indexed as

Adipocytes, BrownAdipogenesisAdipose Tissue, BrownAnimalsCell DifferentiationEnergy MetabolismLipolysisMiceMice, Inbred C57BLMice, KnockoutObesityRGS ProteinsSignal TransductionThermogenesisRgs2 protein, mouseRGS ProteinsBrown adipose tissueG protein–coupled receptorsGqGsRegulator of G protein signaling 2

Identifiers

PMID31767169
PMCPMC6807268
OpenAlexW2977445203

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.