Evidence map›Paper›PMID 25736295›Full record

ArticleJournal of cell science2015

Hsp90α and Hsp90β together operate a hypoxia and nutrient paucity stress-response mechanism during wound healing.

Priyamvada Jayaprakash, Hangming Dong, Mengchen Zou, Ayesha Bhatia, Kathryn O'Brien, Mei Chen, David T Woodley, Wei Li

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 79 citations in OpenAlex.

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  8. LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 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

8 authors at 1 institution in 1 country.

Priyamvada JayaprakashDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
Hangming DongDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
Mengchen ZouDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
Ayesha BhatiaDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
Kathryn O'BrienDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
Mei ChenDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
David T WoodleyDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA.
Wei LiDepartment of Dermatology and the Norris Comprehensive Cancer Center, University of Southern California Keck Medical Center, Los Angeles, CA 90033, USA wli@usc.edu.
University of Southern California · US

Funding

Mechanisms of Human Dermal Fibroblast MigrationR01GM067100 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LI, WEI · 2003 to 2020
$5.2M
PURIFICATION OF EPIDERMOLYSIS BULLOSA ANTIGENR01AR033625 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, MEI, WOODLEY, DAVID T. · 1986 to 2012
$4.8M
MECHANISMS OF KERATINOCYTE MOTILITYR01AR046538 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WOODLEY, DAVID T. · 1999 to 2009
$3.2M
Signal Transduction of Human Keratinocyte MigrationR01GM066193 · NIGMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LI, WEI · 2002 to 2010
$2.3M
Development of Extracellular Heat Shock Protein-90 as a Novel Topical Wound HealingR01AR059853 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LI, WEI · 2011 to 2015
$1.8M
NIAMS NIH HHS AR33625NIAMS NIH HHS AR46538NIAMS NIH HHS R01 AR033625NIAMS NIH HHS R01 AR046538NIAMS NIH HHS R01 AR059853NIGMS NIH HHS GM066193NIGMS NIH HHS GM067100NIGMS NIH HHS R01 GM066193NIGMS NIH HHS R01 GM067100
6 · The paper itself

Abstract

When tissues are injured and blood vessels clot, the local environment becomes ischemic, meaning that there is a lack of adequate supply of oxygen and glucose delivered to the surrounding cells. The heat shock protein-90 (Hsp90) family proteins protect tissues from various environmental insults and participate in the repair of damaged tissue. Here, we report discovery of a new ischemia-responsive mechanism in which the two Hsp90 isoforms Hsp90α and Hsp90β (also known as HSP90AA1 and HSP90AB1, respectively) work together to promote cell motility in wounded skin and accelerate wound closure. We demonstrate that Hsp90α and Hsp90β have distinct and non-exchangeable functions during wound healing. Under hypoxia and when there is a lack of serum factors, Hsp90β binds to the cytoplasmic tail of the LDL receptor-related protein-1 (LRP-1) and stabilizes the receptor at the cell surface. Hsp90α, however, is secreted by the cell into extracellular space where it binds and signals through the LRP-1 receptor to promote cell motility, leading to wound closure. In addition to skin injury, we suggest that this repair mechanism applies broadly to other non-cutaneous injured tissues.

Indexed as

Cell MovementAnimalsCell HypoxiaCells, CulturedFibroblastsHSP90 Heat-Shock ProteinsHumansLow Density Lipoprotein Receptor-Related Protein-1Protein IsoformsSkinSwineWound HealingHSP90 Heat-Shock ProteinsLow Density Lipoprotein Receptor-Related Protein-1Protein IsoformsCell motilityExtracellular Hsp90HypoxiaWound healing

Identifiers

PMID25736295
PMCPMC4518443
OpenAlexW1979746030

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.