Evidence map›Paper›PMID 23844134›Full record

ArticlePloS one2013

Proteomic analysis reveals that proteasome subunit beta 6 is involved in hypoxia-induced pulmonary vascular remodeling in rats.

Jian Wang, Lei Xu, Xin Yun, Kai Yang, Dongjiang Liao, Lichun Tian, Haiyang Jiang, Wenju Lu

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

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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

8 authors.

Jian WangGuangzhou Institute of Respiratory Diseases, State Key Laboratory of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China.
Lei Xu
Xin Yun
Kai Yang
Dongjiang Liao
Lichun Tian
Haiyang Jiang
Wenju Lu

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

backgroundChronic hypoxia (CH) is known to be one of the major causes of pulmonary hypertension (PH), which is characterized by sustained elevation of pulmonary vascular resistance resulting from vascular remodeling. In this study, we investigated whether the ubiquitin proteasome system (UPS) was involved in the mechanism of hypoxia-induced pulmonary vascular remodeling. We isolated the distal pulmonary artery (PA) from a previously defined chronic hypoxic pulmonary hypertension (CHPH) rat model, performed proteomic analyses in search of differentially expressed proteins belonging to the UPS, and subsequently identified their roles in arterial remodeling.

resultsTwenty-two proteins were differently expressed between the CH and normoxic group. Among them, the expression of proteasome subunit beta (PSMB) 1 and PSMB6 increased after CH exposure. Given that PSMB1 is a well-known structural subunit and PSMB6 is a functional subunit, we sought to assess whether PSMB6 could be related to the multiple functional changes during the CHPH process. We confirmed the proteomic results by real-time PCR and Western blot. With the increase in quantity of the active subunit, proteasome activity in both cultured pulmonary artery smooth muscle cells (PASMCs) and isolated PA from the hypoxic group increased. An MTT assay revealed that the proteasome inhibitor MG132 was able to attenuate the hypoxia-induced proliferation of PASMC in a dose-dependent manner. Knockdown of PSMB6 using siRNA also prevented hypoxia-induced proliferation.

conclusionThe present study revealed the association between increased PSMB6 and CHPH. CH up-regulated proteasome activity and the proliferation of PASMCs, which may have been related to increased PSMB6 expression and the subsequently enhanced functional catalytic sites of the proteasome. These results suggested an essential role of the proteasome during CHPH development, a novel finding requiring further study.

Indexed as

ProteomicsAnimalsCell ProliferationComputational BiologyDisease Models, AnimalGene ExpressionGene Expression RegulationGene Knockdown TechniquesHypertension, PulmonaryHypoxiaMaleMyocytes, Smooth MuscleProteasome Endopeptidase ComplexPulmonary ArteryRatsRNA, MessengerProteasome Endopeptidase ComplexPSMB6 protein, ratRNA, Messenger

Identifiers

PMID23844134
PMCPMC3700908

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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.