한빛사 논문
Byung Sun Yoon,1,2,* Jai-Hee Moon,1,* Eun Kyoung Jun,1,3,* Jonggun Kim,4,* Isaac Maeng,1 Jun Sung Kim,1 Jung Han Lee,1,3 Cheong Soon Baik,5 Aeree Kim,6 Kyoung Shik Cho,3 Jang Ho Lee,3 Hwang Heui Lee,3,7 Kwang Youn Whang,4 and Seungkwon You1,#
1 Laboratory of Cell Function Regulation, College of Life Sciences and Biotechnology, 2 Institute of Life Science and Natural Resources, 4 Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, Korea. 3 Division of Stem Cell Research Institute, Stemmedience Corp., Seoul, Korea. 5 SamKwang Medical Laboratories, Seoul, Korea. 6 Department of Pathology, College of Medicine, Korea University Guro Hospital, Seoul, Korea. 7 ChungDam NB Clinic, Seoul, Korea.
*These authors contributed equally to this work.
#Corresponding author
Abstract
Recent evidence shows that amniotic fluid (AF) contains multiple cell types derived from the developing fetus, and may represent a novel source of stem cells for cell therapy. In this study, we examined the paracrine factors released by human amniotic fluid–derived mesenchymal stem cells (AF-MSCs) and their ability to accelerate the wound-healing process by stimulating proliferation and migration of dermal fibroblasts. AF-MSCs expressed the typical MSC marker proteins CD13, CD29, and CD44 and differentiated into adipocytes, osteoblasts, and chondrocytes when exposed to the appropriate differentiation media. In addition, AF-MSC-conditioned media (AF-MSC-CM) significantly enhanced proliferation of dermal fibroblasts. Antibody-based protein array and enzyme-linked immunosorbent assay (ELISA) indicated that AF-MSC-CM contains various cytokines and chemokines that are known to be important in normal wound healing, including IL-8, IL-6, TGF-β, TNFRI, VEGF, and EGF. Application of AF-MSC-CM significantly enhanced wound healing by dermal fibroblasts via the TGF-β/SMAD2 pathway. Levels of p-SMAD2 were increased by AF-MSC-CM, and both the increase in p-SMAD2 and migration of dermal fibroblasts were blocked by inhibiting the TGF-β/SMAD2 pathway. Moreover, in a mouse excisional wound model, AF-MSC-CM accelerated wound healing. These data provide the first evidence of the potential for AF-MSC-CM in the treatment of skin wounds.
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