標題: Bone marrow concentrate-induced mesenchymal stem cell conditioned medium facilitates wound healing and prevents hypertrophic scar formation in a rabbit ear model
作者: Hu, Ching-Hsuan
Tseng, Yi-Wen
Chiou, Chih-Yung
Lan, Kuan-Chun
Chou, Chih-Hung
Tai, Chun-San
Huang, Hsien-Da
Hu, Chiung-Wen
Liao, Ko-Hsun
Chuang, Shiow-Shuh
Yang, Jui-Yung
Lee, Oscar K.
交大名義發表
生物科技學系
分子醫學與生物工程研究所
National Chiao Tung University
Department of Biological Science and Technology
Institute of Molecular Medicine and Bioengineering
關鍵字: Hypertrophic scar;Bone marrow concentrate;Mesenchymal stem cell-conditioned medium
公開日期: 28-Aug-2019
摘要: Background Hypertrophic scars (HSs) are formed via an aberrant response to the wound healing process. HSs can be cosmetic or can result in functional problems. Prolonged proliferation and remodeling phases disrupt wound healing, leading to excessive collagen production and HS formation. However, there are currently no satisfactory drugs to prevent HS formation. Mesenchymal stem cell (MSC) conditioned medium (CM) has therapeutic effects on wound healing and preventing HS formation. Bone marrow concentrate (BMC) contains various growth factors and cytokines that are crucial for regeneration and has been applied in the clinical setting. In this study, we evaluated the effects of BMC-induced MSC CM on HS formation in a rabbit ear model. Methods We established a rabbit ear wound model by generating full-thickness wounds in the ears of rabbits (n = 12) and treated wounds with MSC CM, BMC CM, or BMC-induced MSC CM. Dermal fibroblasts from human hypertrophic scar were stimulated with transforming growth factor beta 1 (TGF-beta 1) for 24 h and cultured in each culture medium for 72 h. We measured the hypertrophic scar (HS) formation during the skin regeneration by measuring the expression of several remodeling molecules and the effect of these conditioned media on active human HS fibroblasts. Results Our results showed that BMC-induced MSC CM had greater antifibrotic effects than MSC CM and BMC CM significantly attenuated HS formation in rabbits. BMC-induced MSC CM accelerated wound re-epithelization by increasing cell proliferation. Additionally, BMC-induced MSC CM also inhibited fibrosis by decreasing profibrotic gene and protein expression, promoting extracellular matrix turnover, inhibiting fibroblast contraction, and reversing myofibroblast activation. Conclusions BMC-induced MSC CM modulated the proliferation and remodeling phases of wound healing, representing a potential wound healing agent and approach for preventing HS formation.
URI: http://dx.doi.org/10.1186/s13287-019-1383-x
http://hdl.handle.net/11536/152835
DOI: 10.1186/s13287-019-1383-x
期刊: STEM CELL RESEARCH & THERAPY
Volume: 10
Issue: 1
起始頁: 0
結束頁: 0
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