Evidence map›Paper›PMID 25461595›Full record

ArticlePloS one2014

BMP4 increases the expression of TRPC and basal [Ca2+]i via the p38MAPK and ERK1/2 pathways independent of BMPRII in PASMCs.

Yi Zhang, Yingfeng Wang, Kai Yang, Lichun Tian, Xin Fu, Yan Wang, Yueqian Sun, Qian Jiang, Wenju Lu, Jian Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
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  8. Article
  9. TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020
    Review
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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

10 authors at 4 institutions in 3 countries.

Yi ZhangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China; The 2nd Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China; Division of Pulmonary & Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Yingfeng WangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
Kai YangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China; Division of Pulmonary & Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Lichun TianState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
Xin FuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yan WangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yueqian SunDepartment of Arts and Science, University of Toronto, Toronto, Ontario, Canada.
Qian JiangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
Wenju LuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China; Department of Laboratory Medicine, The 1st Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Jian WangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China; Division of Pulmonary & Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America; Department of Pulmonary, Inner Mongolia People's Hospital, Hohhot, Inner Mongolia, China.
State Key Laboratory of Respiratory Disease · CNGuangzhou Medical University · CNJohns Hopkins University · USUniversity of Toronto · CA

Funding

Role of Bone Morphogenetic Protein 4 in Hypoxic Pulmomary HypertensionR01HL093020 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI WANG, JIAN · 2010 to 2014
$1.8M
NHLBI NIH HHS R01 HL093020NHLBI NIH HHS R01HL093020
6 · The paper itself

Abstract

Multiple abnormalities of bone morphogenetic protein (BMPs) signaling are implicated in the process of pulmonary arterial hypertension (PAH). BMP4 plays an important role during the process of pulmonary arterial remodeling and mutant of the principle BMP4 receptor, BMP receptors II (BMPRII), is found to associate with the development of PAH. However, the likely mechanism defining the contribution of BMPRII to BMP4 mediated signaling in pulmonary arterial smooth muscle cells (PASMCs) remains comprehensively unclear. We previously found that enhanced store operated calcium entry (SOCE) and basal intracellular calcium concentration [Ca2+]i were induced by BMP4 via upregulation of TRPC1, 4 and 6 expression in PASMCs, and that BMP4 modulated TRPC channel expression through activating p38MAPK and ERK1/2 signaling pathways. In this study, BMPRII siRNA was used to knockdown BMPRII expression to investigate whether BMP4 upregulates the expression of TRPC and activating Smad1/5/8, ERK1/2 and p38MAPK pathway via BMPRII in distal PASMCs. Our results showed that knockdown of BMPRII: 1) attenuated BMP4 induced activation of P-Smad1/5/8, without altering BMP4 induced P-p38MAPK and P-ERK1/2 activation in PASMCs; 2) did not attenuate the BMP4-induced TRPC1, 4 and 6 expression; 3) did not affect BMP4-enhanced SOCE and basal [Ca2+]i. Thus, we concluded that BMP4 activated Smad1/5/8 pathway is BMPRII-dependent, while the BMP4 - ERK/p-P38 - TRPC - SOCE signaling axis are likely mediated through other receptor rather than BMPRII.

Indexed as

AnimalsApoptosis Regulatory ProteinsBone Morphogenetic Protein 4Bone Morphogenetic Protein Receptors, Type IICalcium SignalingCarrier ProteinsCell ProliferationGene Expression RegulationHumansMAP Kinase Signaling SystemMitochondrial ProteinsMyocytes, Smooth Musclep38 Mitogen-Activated Protein KinasesPulmonary ArteryRatsRNA, Small InterferingApoptosis Regulatory ProteinsBMP4 protein, humanBMPR2 protein, humanBone Morphogenetic Protein 4Bone Morphogenetic Protein Receptors, Type IICarrier ProteinsDIABLO protein, ratMitochondrial Proteinsp38 Mitogen-Activated Protein KinasesRNA, Small InterferingTRPC Cation Channels

Identifiers

PMID25461595
PMCPMC4251900
OpenAlexW2074695080

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.