Transcriptional control of skin reepithelialization

被引：30

作者：

Bellavia, Gabriella ^{[1
]}

Fasanaro, Pasquale ^{[1
]}

Melchionna, Roberta ^{[1
]}

Capogrossi, Maurizio C. ^{[1
]}

Napolitano, Monica ^{[1
]}

机构：

[1] Ist Dermopat Immacolata IRCCS, Lab Patol Vasc, I-00167 Rome, Italy

来源：

JOURNAL OF DERMATOLOGICAL SCIENCE | 2014年 / 73卷 / 01期

关键词：

Wound healing; Transcription factor; Skin; PROLIFERATOR-ACTIVATED RECEPTOR; WOUND REPAIR; BETA-CATENIN; GRAINY-HEAD; C-JUN; INFLAMMATORY RESPONSE; TGF-BETA; MICE; DROSOPHILA; SMAD3;

D O I：

10.1016/j.jdermsci.2013.08.007

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

The wound healing process is characterized by a series of overlapping phases, such as coagulation, inflammation, reepithelialization/granulation tissue generation and remodeling. It is important to obtain a deeper insight into the cutaneous wound repair mechanisms, in order to develop novel pharmacological tools for the treatment of chronic non-healing ulcers which are a frequent and high morbidity complication of diabetes, ischaemia, venous insufficiency, and other local or systemic factors. Several transcription factors, many of which belong to gene families, are known to play a role in cutaneous wound repair through the orchestration of cellular responses which promote the reconstitution of skin integrity. The aim of this review is to provide an updated analysis of the transcription factor role in the reepithelialization process, in the context of skin wound repair. (C) 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.

引用

页码：3 / 9

页数：7

共 68 条

[1] HDAC activity is required for p65/RelA-dependent repression of PPARδ-mediated transactivation in human keratinocytes [J].

Aarenstrup, Lene ;

Flindt, Esben Noerregaard ;

Otkjaer, Kristian ;

Kirkegaard, Morten ;

Andersen, Jens Skorstensgaard ;

Kristiansen, Karsten .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2008, 128 (05) :1095-1106

[2] Peripheral blood fibrocytes: Differentiation pathway and migration to wound sites [J].

Abe, R ;

Donnelly, SC ;

Peng, T ;

Bucala, R ;

Metz, CN .

JOURNAL OF IMMUNOLOGY, 2001, 166 (12) :7556-7562

[3] Function and regulation of AP-1 subunits in skin physiology and pathology [J].

Angel, P ;

Szabowski, A ;

Schorpp-Kistner, M .

ONCOGENE, 2001, 20 (19) :2413-2423

[4] Role of Smad3 in the hormonal modulation of in vivo wound healing responses [J].

Ashcroft, GS ;

Mills, SJ ;

Flanders, KC ;

Lyakh, LA ;

Anzano, MA ;

Gilliver, SC ;

Roberts, AB .

WOUND REPAIR AND REGENERATION, 2003, 11 (06) :468-473

[5] Androgen receptor-mediated inhibition of cutaneous wound healing [J].

Ashcroft, GS ;

Mills, SJ .

JOURNAL OF CLINICAL INVESTIGATION, 2002, 110 (05) :615-624

[6] Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response [J].

Ashcroft, GS ;

Greenwell-Wild, T ;

Horan, MA ;

Wahl, SM ;

Ferguson, MWJ .

AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (04) :1137-1146

[7] Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response [J].

Ashcroft, GS ;

Yang, X ;

Glick, AB ;

Weinstein, M ;

Letterio, JJ ;

Mizel, DE ;

Anzano, M ;

Greenwell-Wild, T ;

Wahl, SM ;

Deng, CX ;

Roberts, AB .

NATURE CELL BIOLOGY, 1999, 1 (05) :260-266

[8] Estrogen accelerates cutaneous wound healing associated with an increase in TGF-beta 1 levels [J].

Ashcroft, GS ;

Dodsworth, J ;

vanBoxtel, E ;

Tarnuzzer, RW ;

Horan, MA ;

Schultz, GS ;

Ferguson, MWJ .

NATURE MEDICINE, 1997, 3 (11) :1209-1215

[9] Platelet transcriptome: The application of microarray analysis to platelets [J].

Bahou, WF ;

Gnatenko, DV .

SEMINARS IN THROMBOSIS AND HEMOSTASIS, 2004, 30 (04) :473-484

[10]

Baum CL, 2005, DERMATOL SURG, V31, P674

← 1 2 3 4 5 6 7 →