Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure

Ivan Jozic, Andrew P. Sawaya, Irena Pastar, Cheyanne R. Head, Lulu L. Wong, George D. Glinos, Tongyu Wikramanayake, Harold Brem, Robert Kirsner, Marjana Tomic-Canic

Research output: Contribution to journalArticle

Abstract

Compartmentalization of signaling events at caveolae is crucial during wound healing. Jozic and colleagues show that human non-healing chronic wounds exhibit elevated levels of Caveolin-1, which inhibits keratinocyte migration by sequestering EGFR while promoting glucocorticoid signaling. They further demonstrate that disruption of caveolae accelerates keratinocyte migration and wound closure.

Original languageEnglish (US)
JournalMolecular Therapy
DOIs
StateAccepted/In press - Jan 1 2019

Fingerprint

Re-Epithelialization
Caveolin 1
Caveolae
Keratinocytes
Pharmacology
Wounds and Injuries
Wound Healing
Glucocorticoids

Keywords

  • Caveolin-1
  • chronic wounds
  • diabetic foot ulcers
  • skin re-epithelialization
  • wound healing

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Pharmacology
  • Drug Discovery

Cite this

Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure. / Jozic, Ivan; Sawaya, Andrew P.; Pastar, Irena; Head, Cheyanne R.; Wong, Lulu L.; Glinos, George D.; Wikramanayake, Tongyu; Brem, Harold; Kirsner, Robert; Tomic-Canic, Marjana.

In: Molecular Therapy, 01.01.2019.

Research output: Contribution to journalArticle

@article{207a136fb4134d0087b734baef70514b,
title = "Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure",
abstract = "Compartmentalization of signaling events at caveolae is crucial during wound healing. Jozic and colleagues show that human non-healing chronic wounds exhibit elevated levels of Caveolin-1, which inhibits keratinocyte migration by sequestering EGFR while promoting glucocorticoid signaling. They further demonstrate that disruption of caveolae accelerates keratinocyte migration and wound closure.",
keywords = "Caveolin-1, chronic wounds, diabetic foot ulcers, skin re-epithelialization, wound healing",
author = "Ivan Jozic and Sawaya, {Andrew P.} and Irena Pastar and Head, {Cheyanne R.} and Wong, {Lulu L.} and Glinos, {George D.} and Tongyu Wikramanayake and Harold Brem and Robert Kirsner and Marjana Tomic-Canic",
year = "2019",
month = "1",
day = "1",
doi = "10.1016/j.ymthe.2019.07.016",
language = "English (US)",
journal = "Molecular Therapy",
issn = "1525-0016",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure

AU - Jozic, Ivan

AU - Sawaya, Andrew P.

AU - Pastar, Irena

AU - Head, Cheyanne R.

AU - Wong, Lulu L.

AU - Glinos, George D.

AU - Wikramanayake, Tongyu

AU - Brem, Harold

AU - Kirsner, Robert

AU - Tomic-Canic, Marjana

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Compartmentalization of signaling events at caveolae is crucial during wound healing. Jozic and colleagues show that human non-healing chronic wounds exhibit elevated levels of Caveolin-1, which inhibits keratinocyte migration by sequestering EGFR while promoting glucocorticoid signaling. They further demonstrate that disruption of caveolae accelerates keratinocyte migration and wound closure.

AB - Compartmentalization of signaling events at caveolae is crucial during wound healing. Jozic and colleagues show that human non-healing chronic wounds exhibit elevated levels of Caveolin-1, which inhibits keratinocyte migration by sequestering EGFR while promoting glucocorticoid signaling. They further demonstrate that disruption of caveolae accelerates keratinocyte migration and wound closure.

KW - Caveolin-1

KW - chronic wounds

KW - diabetic foot ulcers

KW - skin re-epithelialization

KW - wound healing

UR - http://www.scopus.com/inward/record.url?scp=85070284527&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85070284527&partnerID=8YFLogxK

U2 - 10.1016/j.ymthe.2019.07.016

DO - 10.1016/j.ymthe.2019.07.016

M3 - Article

AN - SCOPUS:85070284527

JO - Molecular Therapy

JF - Molecular Therapy

SN - 1525-0016

ER -