Evidence map›Paper›PMID 21562308›Full record

ArticleAmerican journal of physiology. Cell physiology2011

Hypoxic preconditioning enhances bone marrow mesenchymal stem cell migration via Kv2.1 channel and FAK activation.

Xinyang Hu, Ling Wei, Tammi M Taylor, Jianfeng Wei, Xin Zhou, Jian-An Wang, Shan Ping Yu

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 117 citations in OpenAlex.

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  9. Antagonistic roles of Ras-MAPK and Akt signaling in integrin-KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Xinyang HuDepartment of Cardiology, Second Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, China.
Ling Wei
Tammi M Taylor
Jianfeng Wei
Xin Zhou
Jian-An Wang
Shan Ping Yu
Medical University of South Carolina · USEmory University · USSecond Affiliated Hospital of Zhejiang University · CN

Funding

Angiogenesis, Functional Recovery and TNF-alpha after StrokeR01NS045810 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI WEI, LING · 2004 to 2008
$1.3M
FUNCTION RESTORATION BY ES CELL IMPLANT AFTER ISCHEMIAR01NS045155 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI WEI, LING · 2003 to 2006
$1.2M
NEURAL PLASTICITY/VASCULAR REMODELING AFTER MINISTROKER01NS037372 · NINDS · WASHINGTON UNIVERSITY · PI WEI, LING · 1999 to 2002
$731k
NINDS NIH HHS NS-045155NINDS NIH HHS NS-045810NINDS NIH HHS NS-37372NINDS NIH HHS R01 NS045810
6 · The paper itself

Abstract

Transplantation using stem cells including bone marrow mesenchymal stem cells (BMSCs) is emerging as a potential regenerative therapy after ischemic attacks in the heart and brain. The migration capability of transplanted cells is a critical cellular function for tissue repair. Based on our recent observations that hypoxic preconditioning (HP) has multiple benefits in improving stem cell therapy and that the potassium Kv2.1 channel acts as a promoter for focal adhesion kinase (FAK) activation and cell motility, the present investigation tested the hypothesis that HP treatment can increase BMSC migration via the mechanism of increased Kv2.1 expression and FAK activities. BMSCs derived from green fluorescent protein-transgenic mice were treated under either normoxic (N-BMSC) or hypoxic (0.5% O(2)) (HP-BMSC) conditions for 24 h. Western blot analysis showed HP selectively upregulated Kv2.1 expression while leaving other K(+) channels, such as Kv1.5 and Kv1.4, unaffected. Compared with normoxic controls, significantly larger outward delayed rectifier K(+) currents were recorded in HP-BMSCs. HP enhanced BMSC migration/homing activities in vitro and after intravenous transplantation into rats subjected to permanent myocardial infarction (MI). The HP-promoted BMSC migration was inhibited by either blocking K(+) channels or knocking down Kv2.1. Supporting a relationship among HP, Kv2.1, and FAK activation, HP increased phosphorylation of FAK(397) and FAK(576/577), and this effect was antagonized by blocking K(+) channels. These findings provide novel evidence that HP enhances the ability of BMSCs to migrate and home to the injured region; this effect is mediated through a regulatory role of Kv2.1 on FAK phosphorylation/activation.

Indexed as

Cell HypoxiaCell MovementAnimalsBlotting, WesternCells, CulturedDisease Models, AnimalEnzyme ActivationFlow CytometryFocal Adhesion Kinase 1Green Fluorescent ProteinsMembrane PotentialsMesenchymal Stem CellsMesenchymal Stem Cell TransplantationMiceMice, TransgenicMicroscopy, FluorescenceFocal Adhesion Kinase 1Green Fluorescent ProteinsKcnb1 protein, mouseKcnb1 protein, ratPotassium Channel BlockersPtk2 protein, mousePtk2 protein, ratShab Potassium Channels

Identifiers

PMID21562308
PMCPMC3154562
OpenAlexW2035426530

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.