Evidence map›Paper›PMID 26151598›Full record

ArticleNature communications2015

Pirt reduces bladder overactivity by inhibiting purinergic receptor P2X3.

Xiao-Fei Gao, Ji-Feng Feng, Wei Wang, Zheng-Hua Xiang, Xiu-Jie Liu, Chan Zhu, Zong-Xiang Tang, Xin-Zhong Dong, Cheng He

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Xiao-Fei GaoInstitute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China.
Ji-Feng FengInstitute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China.
Wei WangInstitute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China.
Zheng-Hua XiangInstitute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China.
Xiu-Jie LiuInstitute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China.
Chan ZhuNanjing University of Chinese Medicine, 138 Xianlin Road, Nanjing 210046, China.
Zong-Xiang TangNanjing University of Chinese Medicine, 138 Xianlin Road, Nanjing 210046, China.
Xin-Zhong Dong1] The Solomon H. Snyder Department of Neuroscience, Center for Sensory Biology, School of Medicine, Johns Hopkins University, 725N Wolfe Street, Baltimore, Maryland 21205, USA. [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA.
Cheng HeInstitute of Neuroscience, Key Laboratory of Molecular Neurobiology of Ministry of Education and the Collaborative Innovation Center for Brain Science, Second Military Medical University, Shanghai 200433, China.
Second Military Medical University · CNNanjing University of Chinese Medicine · CNJohns Hopkins University · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Pirt is a transmembrane protein predominantly expressed in peripheral neurons. However, the physiological and pathological roles of Pirt in hollow viscus are largely unknown. Here we show that Pirt deficiency in mice causes bladder overactivity. The density of α,β-meATP-induced currents is significantly reinforced in Pirt-deficient dorsal root ganglion (DRG) neurons. Pirt and P2X3 receptor co-localize in bladder nerve fibres and heterologous Pirt expression significantly reduces P2X3-mediated currents. Pirt interacts with P2X3 through the N-terminal 14 amino-acid residues. TAT-conjugated Pirt(N14) peptide (Pirt(N14)) is sufficient to inhibit P2X3 activation in bladder DRG neurons and to alleviate bladder overactivity in Pirt(-/-) mice. Pirt expression is decreased in the bladder of cyclophosphamide (CYP)-treated mice, a commonly used model of bladder overactivity. Importantly, Pirt(N14) administration reduces the frequency of bladder voiding and restores the voided volume of CYP-treated mice. Therefore, our results demonstrate that Pirt is an endogenous regulator of P2X3 in bladder function.

Indexed as

AnimalsCarrier ProteinsCyclophosphamideDNA, ComplementaryFemaleGene Expression RegulationHEK293 CellsHumansImmunosuppressive AgentsMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMutationPurinergic P2X Receptor AntagonistsReceptors, Purinergic P2X3Carrier ProteinsCyclophosphamideDNA, ComplementaryImmunosuppressive AgentsMembrane ProteinsPirt protein, mousePurinergic P2X Receptor AntagonistsReceptors, Purinergic P2X3

Identifiers

PMID26151598
OpenAlexW801751564

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.