Evidence map›Paper›PMID 35051185›Full record

ArticlePloS one

Enhanced β-adrenergic response in mice with dominant-negative expression of the PKD2L1 channel.

Manabu Murakami, Agnieszka M Murakami, Takayuki Nemoto, Takayoshi Ohba, Manabu Yonekura, Yuichi Toyama, Hirofumi Tomita, Yasushi Matsuzaki, Daisuke Sawamura, Kazuyoshi Hirota and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 100% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

13 authors at 5 institutions in 1 country.

Manabu MurakamiDepartment of Pharmacology, Faculty of Medicine, University of Miyazaki, Miyazaki, Miyazaki, Japan.ORCID https://orcid.org/0000-0001-6704-1796
Agnieszka M MurakamiDepartment of Pharmacology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Takayuki NemotoDepartment of Pharmacology, Faculty of Medicine, University of Miyazaki, Miyazaki, Miyazaki, Japan.
Takayoshi OhbaDepartment of Cell Physiology, Akita University School of Medicine, Akita, Akita, Japan.
Manabu YonekuraDepartment of Cardiology and Nephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Yuichi ToyamaDepartment of Cardiology and Nephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Hirofumi TomitaDepartment of Cardiology and Nephrology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Yasushi MatsuzakiDepartment of Dermatology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Daisuke SawamuraDepartment of Dermatology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Kazuyoshi HirotaDepartment of Anesthesiology, Hirosaki University Graduate School of Medicine, Hirosaki, Aomori, Japan.
Shirou ItagakiCollaboration Center for Community and Industry, Sapporo Medical University, Sapporo, Hokkaido, Japan.
Yujiro AsadaDivision of Pathophysiology, Department of Pathology, Faculty of Medicine, University of Miyazaki, Miyazaki, Miyazaki, Japan.
Ichiro MiyoshiDepartment of Laboratory Animal Medicine, Tohoku University School of Medicine, Sendai, Miyagi, Japan.
Hirosaki University · JPUniversity of Miyazaki · JPAkita University · JPSapporo Medical University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystic kidney disease (PKD) is the most common genetic cause of kidney failure in humans. Among the various PKD-related molecules, PKD2L1 forms cation channels, but its physiological importance is obscure. In the present study, we established a transgenic mouse line by overexpressing the dominant-negative form of the mouse PKD2L1 gene (i.e., lacking the pore-forming domain). The resulting PKD2L1del-Tg mice exhibited supraventricular premature contraction, as well as enhanced sensitivity to β-adrenergic stimulation and unstable R-R intervals in electrocardiography. During spontaneous atrial contraction, PKD2L1del-Tg atria showed enhanced sensitivity to isoproterenol, norepinephrine, and epinephrine. Action potential recording revealed a shortened action potential duration in PKD2L1del-Tg atria in response to isoproterenol. These findings indicated increased adrenergic sensitivity in PKD2L1del-Tg mice, suggesting that PKD2L1 is involved in sympathetic regulation.

Indexed as

Adrenergic beta-AgonistsIsoproterenolMice, TransgenicAction PotentialsAnimalsCalcium ChannelsElectrocardiographyEpinephrineHeart AtriaMaleMiceNorepinephrineReceptors, Adrenergic, betaReceptors, Cell SurfaceAdrenergic beta-AgonistsCalcium ChannelsEpinephrineIsoproterenolNorepinephrinePkd2l1 protein, mouseReceptors, Adrenergic, betaReceptors, Cell Surface

Identifiers

PMID35051185
PMCPMC8775249
OpenAlexW4205250130

What OpenQuestion holds

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LicenceCC BY
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.