Evidence map›Paper›PMID 32665806›Full record

ArticleBiomicrofluidics2020

Intracellular calcium response of primary cilia of tubular cells to modulated shear stress under oxidative stress.

Masatomo Chikamori, Hiroshi Kimura, Reiko Inagi, Jing Zhou, Masaomi Nangaku, Teruo Fujii

Open access · hybridAbstract read
In one paragraph

Article in Biomicrofluidics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
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

6 authors at 3 institutions in 2 countries.

Masatomo ChikamoriInstitute of Industrial Science, The University of Tokyo, Tokyo 153-8505, Japan.ORCID 0000-0002-5949-8291
Reiko InagiDepartment of Nephrology and Endocrinology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.ORCID 0000-0001-7032-7736
Jing ZhouCenter for Polycystic Kidney Disease Research and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.ORCID 0000-0003-0914-4994
Masaomi NangakuDepartment of Nephrology and Endocrinology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan.ORCID 0000-0001-7401-2934
Teruo FujiiInstitute of Industrial Science, The University of Tokyo, Tokyo 153-8505, Japan.ORCID 0000-0001-7529-6238
The University of Tokyo · JPBrigham and Women's Hospital · USTokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary cilia of tubular cells are sensory organelles. Bending of the primary cilia with shear stress from urinary flow results in the elevation of intracellular calcium levels and activation of signaling pathways that maintain kidney function. Elongation of primary cilia is reported to occur due to oxidative stress, which is a major cause of ischemia-reperfusion injury and is accompanied by decreased kidney function. However, in the context of diminished kidney function, this elongation is yet to be investigated. In this study, we developed a new microfluidic device to monitor changes in the intracellular calcium levels while modulating shear stress on the cilia under different degrees of oxidative stress. The microfluidic device was designed to expose even shear stress in the observed area while supplying drugs in four different stepwise concentrations. The results showed that primary cilia were elongated by hydrogen peroxide, which induces oxidative stress. It was also observed that the elongated primary cilia were more sensitive to shear stress than those with normal morphology. This microfluidic device could, thus, be useful in the analysis of the morphology of the primary cilia, under low perfusion conditions.

Identifiers

PMID32665806
PMCPMC7334031
OpenAlexW3039925851

What OpenQuestion holds

Textmetadata
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.