A Bayat

A Saraf

AA Salibian

AI Arno

C Rebeyrol

DE Atsma

DE Morris

E Beausang

FB Niessen

GC Gurtner

GG Gauglitz

GP Sreekanth

GY Zhang

H Yasuoka

HP Ehrlich

IE Roseborough

IS Yun

JH Shi

JK Park

JW Lawrence

JY Chen

K Ueno-Shuto

K Wakabayashi

KA Cho

L Formigli

L Li

LA Ortiz

LH Yu

M Aoki

M Hu

M Rolli

M Trojanowska

MA Hardy

MC Canesso

MJ Lee

ML Ramos

MN Shukla

MT Lam

QC Du

RK Nath

S Iyyam Pillai

S Ohgo

S Omori

S Schreml

S Willenborg

S Yi

SH Lee

SR Daher

T Daian

WK Stadelmann

WM Jackson

WS Kim

X Bai

X Hu

X Liu

XZ Bai

Y Li

Y Yeghiazarians

Y Zhao

Y Zhou

English

Abstract
                Background
                Hypertrophic scars (HS) generally occur after injury to the deep layers of the dermis, resulting in functional deficiency for patients. Growing evidence has been identified that the supernatant of adipose tissue-derived stem cells (ADSCs) significantly ameliorates fibrosis of different tissues, but limited attention has been paid to its efficacy on attenuating skin fibrosis. In this study, we explored the effect and possible mechanism of ADSC-conditioned medium (ADSC-CM) on HS.
              
                Method
                Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the expression of collagen I (Col1), collagen III (Col3), and α-smooth muscle actin (α-SMA) after fibroblasts and cultured HS tissues were stimulated with ADSC-CM and p38 inhibitor/activator. Immunofluorescence staining was performed to test the expression of α-SMA. Masson’s trichrome staining, hematoxylin and eosin (H&amp;E) staining, and immunohistochemistry staining were carried out to assess the histological and pathological change of collagen in the BALB/c mouse excisional model. All data were analyzed by using SPSS17.0 software. Statistical analysis was performed by Student’s t tests.
              
                Results
                The in vitro and ex vivo study revealed ADSC-CM decreased the expression of Col1, Col3, and α-SMA. Together, thinner and orderly arranged collagen was manifested in HS tissues cultured with ADSC-CM. Dramatically, the assessed morphology showed an accelerated healing rate, less collagen deposition, and col1- and col3-positive cells in the ADSC-CM treated group. Importantly, the protein level of p-p38 was downregulated in a concentration-dependent manner in HS-derived fibroblasts with ADSC-CM treatment, which further decreased the expression of p-p38 after the application of its inhibitor, SB203580. SB203580 led to an obvious decline in the expression of Col1, Col3, and α-SMA in fibroblasts and cultured HS tissues and presented more ordered arrangement and thinner collagen fibers in BALB/c mice. Lastly, anisomycin, an agonist of p38, upregulated the expression of fibrotic proteins and revealed more disordered structure and denser collagen fibers.
              
                Conclusion
                This study demonstrated that ADSC-CM could decrease collagen deposition and scar formation in in vitro, ex vivo and in vivo experiments. The regulation of the p38/MAPK signaling pathway played an important role in the process. The application of ADSC-CM may provide a novel therapeutic strategy for HS treatment, and the anti-scarring effect can be achieved by inhibition of the p38/MAPK signaling pathway.
              </jats:sec

Yan Li

Wei Zhang

Jianxin Gao

Jiaqi Liu

Hongtao Wang

Jun Li

Xuekang Yang

Ting He

Hao Guan

Zhao Zheng

Shichao Han

Maolong Dong

Juntao Han

Jihong Shi

Dahai Hu

Crossref

Stem Cell Research & Therapy

Adipose tissue-derived stem cells suppress hypertrophic scar fibrosis via the p38/MAPK signaling pathway

https://stemcellres.biomedcentral.com/track/pdf/10.1186/s13287-016-0356-6?site=stemcellres.biomedcentral.com

Adipose tissue-derived stem cells suppress hypertrophic scar fibrosis via the p38/MAPK signaling pathway

Abstract

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