HIF-1α promotes the keloid development through the activation of TGF-β/Smad and TLR4/MyD88/NF-κB pathways

A keloid is defined as an overgrowth of the dense fibrous tissues that form around a wound. Since they destroy the vascular network, keloid tissues often exhibit anoxic conditions. Hypoxia-inducible factor-1α (HIF-1α) is a core factor that mediates hypoxia stress responses and regulates the hypoxic...

Full description

Saved in:
Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Vol. 18; no. 23; pp. 3239 - 3250
Main Authors: Lei, Rui, Li, Jian, Liu, Feng, Li, Weihan, Zhang, Shizhen, Wang, Yang, Chu, Xi, Xu, Jinghong
Format: Journal Article
Language:English
Published: United States Taylor & Francis 02.12.2019
Subjects:
fibroblasts
HIF-1α
keloid
NF-κB
Research Paper
TGF-β/Smad
TLR4
TGF-β/Smad
keloid
NF-κB
fibroblasts
HIF-1α
TLR4
ISSN:1538-4101, 1551-4005, 1551-4005
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:A keloid is defined as an overgrowth of the dense fibrous tissues that form around a wound. Since they destroy the vascular network, keloid tissues often exhibit anoxic conditions. Hypoxia-inducible factor-1α (HIF-1α) is a core factor that mediates hypoxia stress responses and regulates the hypoxic cellular and biological behaviors. In this study, we found that the expression level of HIF-1α in keloid tissue was significantly higher than that in the normal skin tissue. Hypoxia-induced HIF-1α expression significantly inhibited cellular apoptosis and promoted cellular proliferation in keloid fibroblasts but not in normal fibroblasts. Specifically, HIF-1α activated the TGF-β/Smad and TLR4/MyD88/NF-κB pathways, and the interaction of these two pathways may promote the development of keloids. Moreover, in vivo experiments showed that the inhibition of HIF-1α significantly reduced the growth of keloids.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1538-4101
1551-4005
1551-4005
DOI:10.1080/15384101.2019.1670508