Evidence map›Paper›PMID 25309796›Full record

ArticleEndocrinology and metabolism (Seoul, Korea)2014

Vav3, a GEF for RhoA, Plays a Critical Role under High Glucose Conditions.

Jie Sha, Jungsik Na, Jung Ok Lee, Nami Kim, Soo Kyung Lee, Ji Hae Kim, Ji Wook Moon, Su Jin Kim, Hye Jeong Lee, Jong-Il Choi and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Endocrinology and metabolism (Seoul, Korea), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

6 citing papers in PubMed, 9 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

12 authors at 1 institution in 1 country.

Jie ShaDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Jungsik NaBando Hospital, Korea.
Jung Ok LeeDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Nami KimDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Soo Kyung LeeDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Ji Hae KimDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Ji Wook MoonDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Su Jin KimDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Hye Jeong LeeDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Jong-Il ChoiDivision of Cardiology, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, Seoul, Korea.
Sun Hwa ParkDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Hyeon Soo KimDepartment of Anatomy, Korea University College of Medicine, Seoul, Korea.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of small GTPase molecules is poorly understood under high glucose conditions.

methodsWe analyzed the expression pattern of Vav3 in skeletal muscle C2C12 cells under high glucose culture condition with reverse transcription-polymerase chain reaction and Western blot analysis. We also measured glucose uptake using isotope-labelled glucose.

resultsWe showed that expression of Vav3 (a guanine nucleotide exchange factor for RhoA) increased. mRNA and protein levels in skeletal muscle C2C12 cells under high glucose conditions. The AMP-activated protein kinase (AMPK) activator AMPK agonist 5-aminoimidazole-4-carboxy-amide-1-d-ribofuranoside (AICAR) suppressed high glucose-induced Vav3 induction. In addition, exposure of cells to high glucose concentration increased the phosphorylation of PAK-1, a molecule downstream of RhoA. The phosphorylation of paxillin, a downstream molecule of PAK-1, was also increased by exposure to high glucose. Phosphorylation of these molecules was not observed in the presence of AICAR, indicating that AMPK is involved in the RhoA signal pathway under high glucose conditions. Knock down of Vav3 enhances metformin-mediated glucose uptake. Inhibition of AMPK blocked the increases of Vav3 knock down-induced glucose uptake. Metformin-mediated Glut4 translocation was also increased by Vav3 knock-down, suggesting that Vav3 is involved in metformin-mediated glucose uptake.

conclusionThese results demonstrate that Vav3 is involved in the process of metformin-mediated glucose regulation.

Indexed as

AMP-activated protein kinasesDiabetesHigh glucoseMetforminVav3

Identifiers

PMID25309796
PMCPMC4192823
OpenAlexW2131752015

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.