Evidence map›Paper›PMID 35551172›Full record

ArticleNature communications2022

Mechanical loading of intraluminal pressure mediates wound angiogenesis by regulating the TOCA family of F-BAR proteins.

Shinya Yuge, Koichi Nishiyama, Yuichiro Arima, Yasuyuki Hanada, Eri Oguri-Nakamura, Sanshiro Hanada, Tomohiro Ishii, Yuki Wakayama, Urara Hasegawa, Kazuya Tsujita and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-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

17 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Dermal Dive: An Overview of Cutaneous Wounding Techniques in Zebrafish.The Journal of investigative dermatology · 2024
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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

16 authors at 9 institutions in 2 countries.

Shinya Yuge *Department of Molecular Pathophysiology, Institute for Advanced Medical Sciences, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.
Koichi Nishiyama *International Research Center for Medical Sciences, Kumamoto University, Kumamoto City, Kumamoto, 860-0811, Japan. koichi_nishiyama@med.miyazaki-u.ac.jp.
Yuichiro ArimaInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto City, Kumamoto, 860-0811, Japan.ORCID 0000-0002-9840-3347
Yasuyuki HanadaInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto City, Kumamoto, 860-0811, Japan.
Eri Oguri-NakamuraDepartment of Molecular Pathophysiology, Institute for Advanced Medical Sciences, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.
Sanshiro HanadaInternational Research Center for Medical Sciences, Kumamoto University, Kumamoto City, Kumamoto, 860-0811, Japan.ORCID 0000-0003-2933-3522
Tomohiro IshiiDepartment of Molecular Pathophysiology, Institute for Advanced Medical Sciences, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.
Yuki WakayamaDepartment of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, 565-8565, Japan.
Urara HasegawaDepartment of Materials Science and Engineering, Pennsylvania State University, University Park, PA, 16802, USA.ORCID 0000-0002-4189-7630
Kazuya TsujitaBiosignal Research Center, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo, 657-8501, Japan.ORCID 0000-0002-1860-6831
Ryuji YokokawaDepartment of Micro Engineering, Graduate School of Engineering, Kyoto University, Kyoto, 615-8540, Japan.ORCID 0000-0002-6306-2693
Takashi MiuraDepartment of Anatomy and Cell Biology, Graduate School of Medical Sciences, Kyushu University, Fukuoka City, Fukuoka, 812-8582, Japan.ORCID 0000-0002-9465-275X
Toshiki ItohBiosignal Research Center, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe, Hyogo, 657-8501, Japan.
Kenichi TsujitaDepartment of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto City, Kumamoto, Japan.
Naoki MochizukiDepartment of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, 565-8565, Japan.ORCID 0000-0002-3938-9602
Shigetomo FukuharaDepartment of Molecular Pathophysiology, Institute for Advanced Medical Sciences, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan. s-fukuhara@nms.ac.jp.ORCID 0000-0003-2777-501X
Nippon Medical School · JPKobe University · JPKumamoto University · JPNational Cerebral and Cardiovascular Center · JPKyoto University · JPKyushu University · JPNagoya City University · JPPennsylvania State University · USUniversity of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is regulated in coordinated fashion by chemical and mechanical cues acting on endothelial cells (ECs). However, the mechanobiological mechanisms of angiogenesis remain unknown. Herein, we demonstrate a crucial role of blood flow-driven intraluminal pressure (IP) in regulating wound angiogenesis. During wound angiogenesis, blood flow-driven IP loading inhibits elongation of injured blood vessels located at sites upstream from blood flow, while downstream injured vessels actively elongate. In downstream injured vessels, F-BAR proteins, TOCA1 and CIP4, localize at leading edge of ECs to promote N-WASP-dependent Arp2/3 complex-mediated actin polymerization and front-rear polarization for vessel elongation. In contrast, IP loading expands upstream injured vessels and stretches ECs, preventing leading edge localization of TOCA1 and CIP4 to inhibit directed EC migration and vessel elongation. These data indicate that the TOCA family of F-BAR proteins are key actin regulatory proteins required for directed EC migration and sense mechanical cell stretching to regulate wound angiogenesis.

Indexed as

ActinsCarrier ProteinsActin-Related Protein 2-3 ComplexEndothelial CellsMorphogenesisActin-Related Protein 2-3 ComplexActinsCarrier Proteins

Identifiers

PMID35551172
PMCPMC9098626
OpenAlexW4280523703

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.