Evidence map›Paper›PMID 26811058›Full record

ArticlePhysiological reports2016

RGS2 squelches vascular Gi/o and Gq signaling to modulate myogenic tone and promote uterine blood flow.

Li Jie, Elizabeth A Owens, Lauren A Plante, Zhuyuan Fang, Derek T Rensing, Kevin D Moeller, Patrick Osei-Owusu

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Anti-angiogenic mechanisms and serotonergic dysfunction in the Rgs2 knockout model for the study of psycho-obstetric risk.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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  6. Associations ofPharmaceutics · 2022
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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

7 authors at 4 institutions in 2 countries.

Li JieDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu, China.
Elizabeth A OwensDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Lauren A PlanteDepartment of Obstetrics & Gynecology, Drexel University College of Medicine, Philadelphia, Pennsylvania.
Zhuyuan FangJiangsu Hospital of Traditional Chinese Medicine, Nanjing, Jiangsu, China.
Derek T RensingDepartment of Chemistry, Washington University, St. Louis, Missouri.
Kevin D MoellerDepartment of Chemistry, Washington University, St. Louis, Missouri.
Patrick Osei-OwusuDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, Pennsylvania patrick.osei-owusu@drexelmed.edu.
Drexel University · USWashington University in St. Louis · USJiangsu Provincial Hospital of Traditional Chinese Medicine · CNNanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uterine artery blood flow (UABF) is critical to maintaining uterine perfusion in nonpregnant states and for uteroplacental delivery of nutrients and oxygen to the fetus during pregnancy. Impaired UABF is implicated in infertility and several pregnancy complications including fetal growth restriction, small for gestational age, and preeclampsia. The etiology of abnormal UABF is not known. Here, we determined whether deficiency or loss of RGS2, a GTPase-activating protein for Gq/11 and Gi/o class G proteins, affects UABF in nonpregnant mice. We used Doppler ultrasonography to assess UABF in wild type (WT), Rgs2 heterozygous (Rgs2+/-), and homozygous knockout (Rgs2-/-) mice. Video microscopy was used for ex vivo examination of uterine artery myogenic tone and fura-2 imaging for in vitro assessment of internal stores Ca(2+) release. We found that baseline UABF velocity was markedly decreased while impedance measured as resistive index (WT = 0.58 ± 0.04 vs. Rgs2-/- = 0.71 ± 0.03, P < 0.01) and pulsatile index (WT = 0.90 ± 0.06 vs. Rgs2-/- = 1.25 ± 0.11, P < 0.01) was increased in Rgs2-/- mice. Uterine artery tone was augmented in Rgs2+/- and Rgs2-/- mice, which was normalized to WT levels following Gi/o and Gq inactivation. Conversely, blockade of ryanodine receptors increased WT myogenic tone to RGS2 mutant levels. The data together indicate that RGS2 deficiency decreases UABF by increasing myogenic tone at least partly through prolonged G protein activation. Mutations that decrease vascular RGS2 expression may be a predisposition to decreased uterine blood flow. Targeting G protein signaling therefore might improve uterine and uteroplacental underperfusion disorders.

Indexed as

AnimalsDisease Models, AnimalFemaleFetal Growth RetardationGTP-Binding ProteinsMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMuscle TonusPregnancyRGS ProteinsUltrasonography, DopplerUterine ArteryUterusGTP-Binding ProteinsRgs2 protein, mouseRGS ProteinsG protein signalingmyogenic tone, calciumRGS2uterine blood flow

Identifiers

PMID26811058
PMCPMC4760385
OpenAlexW2305038069

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LicenceCC BY
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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.