Evidence map›Paper›PMID 24633547›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

ZIPK is critical for the motility and contractility of VSMCs through the regulation of nonmuscle myosin II isoforms.

Satoshi Komatsu, Mitsuo Ikebe

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 19 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

2 authors at 1 institution in 1 country.

Satoshi KomatsuDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, Massachusetts.
Mitsuo Ikebe
University of Massachusetts Chan Medical School · US

Funding

Regulation of Myosin Phosphorylation in Smooth MuscleR01HL073050 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IKEBE, MITSUO · 2003 to 2013
$4.0M
Rac1 in Smooth MuscleR01HL111696 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IKEBE, MITSUO · 2012 to 2016
$1.7M
Regulation of Vascular Smooth Muscle Cell MigrationR21HL094983 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KOMATSU, SATOSHI · 2010 to 2011
$452k
NHLBI NIH HHS R01 HL073050NHLBI NIH HHS R01 HL111696NHLBI NIH HHS R21-HL-094983
6 · The paper itself

Abstract

Migration of medial vascular smooth muscle cells (VSMCs) into the intimal layer contributes to pathological remodeling of the blood vessel in arterial hypertension and atherosclerosis. It is well established that reorganization of cytoskeletal networks is an essential component of cellular motile events. However, there is currently a lack of insight into the cellular characteristics of VSMC migration under three-dimensional environments. Here, we investigated the mechanisms of VSMC migration and remodeling using two different collagen matrix assays as in vitro models: migration of VSMCs within a collagen matrix for VSMC invasion and contraction of a collagen gel by VSMCs for VSMC remodeling and contraction. We found that nonmuscle myosin IIA (NMIIA) and nonmuscle myosin IIB (NMIIB) differentially contribute to the migratory capacity of VSMCs via NMII isoform-dependent cytoskeletal reorganization. Depletion of NMIIA by short hairpin RNA revealed a unique interplay between actomyosin and microtubules during VSMC migration. On the other hand, NMIIB was required for the structural maintenance of migrating VSMC. Interestingly, there was a significant difference between NMIIA and NMIIB knockdown in the VSMC migration but not in the VSMC-mediated collagen gel contraction. Furthermore, depletion of zipper-interacting protein kinase by short hairpin RNA resulted in an impairment of VSMC migration and a substantial decrease of VSMC-mediated collagen gel contraction. These results suggest that NMIIA and NMIIB uniquely control VSMC migration and may contribute to vascular remodeling, which are both regulated by zipper-interacting protein kinase.

Indexed as

Cell MovementCells, CulturedCoronary VesselsDeath-Associated Protein KinasesHEK293 CellsHumansMicrotubulesMyocytes, Smooth MuscleNonmuscle Myosin Type IIANonmuscle Myosin Type IIBProtein IsoformsDAPK3 protein, humanDeath-Associated Protein KinasesNonmuscle Myosin Type IIANonmuscle Myosin Type IIBProtein Isoformscytoskeletonmigrationnonmuscle myosin IIthree-dimensionalvascular smooth muscle cellzipper-interacting protein kinase

Identifiers

PMID24633547
PMCPMC4010671
OpenAlexW2048268362

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.