Evidence map›Paper›PMID 22538237›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Reciprocal regulation controlling the expression of CPI-17, a specific inhibitor protein for the myosin light chain phosphatase in vascular smooth muscle cells.

Jee In Kim, Mark Urban, Garbo D Young, Masumi Eto

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 25 citations in OpenAlex.

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  18. A bioinformatic and computational study of myosin phosphatase subunit diversity.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
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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 2 institutions in 1 country.

Jee In KimDepartment of Molecular Physiology and Biophysics, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Mark Urban
Garbo D Young
Masumi Eto
Thomas Jefferson University · USSidney Kimmel Cancer Center · US

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI Andrew Chapman · 1995 to 2026
$94.8M
Regulation Vascular Smooth Muscle Myosin PhosphataseR01HL083261 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI ETO, MASUMI · 2006 to 2010
$1.3M
Myosin phosphatase autoinhibition in gastrointestinal smooth muscle contractionR01DK088905 · NIDDK · UNIVERSITY OF VIRGINIA · PI ETO, MASUMI, SOMLYO, AVRIL V. · 2010 to 2012
$1.1M
NCI NIH HHS P30-CA-56036NHLBI NIH HHS HL-083261NHLBI NIH HHS R01 HL083261NIDDK NIH HHS DK-088905NIDDK NIH HHS R01 DK088905
6 · The paper itself

Abstract

Cellular activity of the myosin light chain phosphatase (MLCP) determines agonist-induced force development of smooth muscle (SM). CPI-17 is an endogenous inhibitor protein for MLCP, responsible for mediating G-protein signaling into SM contraction. Fluctuations in CPI-17 expression occur in response to pathological stresses, altering excitation-contraction coupling in SM. Here, we determined the signaling pathways regulating CPI-17 expression in rat aorta tissues and the cell culture using a pharmacological approach. CPI-17 transcription was suppressed in response to the proliferative stimulus with platelet-derived growth factor (PDGF) through the ERK1/2 pathway, whereas it was elevated in response to inflammatory, stress-induced and excitatory stimuli with transforming growth factor-β, IL-1β, TNFα, sorbitol, and serotonin. CPI-17 transcription was repressed by inhibition of JNK, p38, PKC, and Rho-kinase (ROCK). The mouse and human CPI-17 gene promoters were governed by the proximal GC-boxes at the 5'-flanking region, where Sp1/Sp3 transcription factors bound. Sp1 binding to the region was more prominent in intact aorta tissues, compared with the SM cell culture, where the CPI-17 gene is repressed. The 173-bp proximal promoter activity was negatively and positively regulated through PDGF-induced ERK1/2 and sorbitol-induced p38/JNK pathways, respectively. By contrast, PKC and ROCK inhibitors failed to repress the 173-bp promoter activity, suggesting distal enhancer elements. CPI-17 transcription was insensitive to knockdown of myocardin/Kruppel-like factor 4 small interfering RNA or histone deacetylase inhibition. The reciprocal regulation of Sp1/Sp3-driven CPI-17 expression through multiple kinases may be responsible for the adaptation of MLCP signal and SM tone to environmental changes.

Indexed as

AnimalsAortaCells, CulturedHumansInterleukin-1betaJNK Mitogen-Activated Protein KinasesKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMAP Kinase Signaling SystemMiceMuscle ContractionMuscle ProteinsMuscle, Smooth, VascularMyocardinMyosin-Light-Chain PhosphataseInterleukin-1betaJNK Mitogen-Activated Protein KinasesKLF4 protein, humanKlf4 protein, mouseKlf4 protein, ratKruppel-Like Factor 4Kruppel-Like Transcription FactorsMuscle ProteinsMyocardinMyosin-Light-Chain PhosphataseNuclear Proteinsp38 Mitogen-Activated Protein KinasesPhosphoproteinsPlatelet-Derived Growth FactorPpp1r14a protein, ratProtein Kinase Crho-Associated KinasesRNA, Small InterferingSerotoninSorbitolSp1 Transcription FactorSp3 Transcription FactorTrans-ActivatorsTransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID22538237
PMCPMC3404528
OpenAlexW1974933319

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.