The effects of platelet-rich clot releasate on the expression of MMP-1 and type I collagen in human adult dermal fibroblasts: PRP is a stronger MMP-1 stimulator

被引:24
作者
Shin, Min Kyung [1 ]
Lee, Jin Woo [2 ]
Kim, Young Il [2 ]
Kim, Young-Ock [3 ]
Seok, Hosik [4 ]
Kim, Nack In [1 ]
机构
[1] Kyung Hee Univ, Sch Med, Dept Dermatol, Seoul 130702, South Korea
[2] Loma Linda Univ, Sch Med, Dept Dermatol, East West Med Res Inst, Loma Linda, CA USA
[3] Rural Dev Adm, Natl Inst Hort & Herbal Sci, Dept Herbal Crop Res, Eumseong 369873, South Korea
[4] Kyung Hee Univ, Kohwang Med Res Inst, Sch Med, Seoul 130701, South Korea
关键词
Collagen; Fibroblast; MMP-1; Platelet-rich clot releasate; Platelet-rich plasma; TENDON STEM-CELLS; GROWTH-FACTOR; EXTRACELLULAR-MATRIX; GENE-EXPRESSION; HEALING-PROCESS; PLASMA; METALLOPROTEINASES; PROLIFERATION; CULTURE; REPAIR;
D O I
10.1007/s11033-013-2718-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Platelet-rich plasma is widely used in acute and chronic ulcers due to its capacity to enhance the wound healing process. Fibroblasts are believed to be the most important cells in the production and remodeling of the extracellular matrix (ECM). Matrix metalloproteinase (MMP)-1 is the proteolytic enzyme of collagen I, and has a key role in collagen remodeling during wound healing. Whether or not platelet-rich clot releasate (PRCR) is able to effectively modulate the ECM, and the effect of PRCR on the expression of type I collagen and MMP-1 in human dermal fibroblasts was evaluated. Specifically, human adult dermal fibroblasts were incubated in PRCR-containing solutions for 24 and 48 h, after which the levels of collagen and MMP-1 were quantified by reverse transcription PCR at the transcriptional level, and ELISA and immunoblot analyses at the post-transcriptional level. PRCR markedly up-regulated the expression of MMP-1 and type I collagen in fibroblasts incubated in 20 % PRCR solutions for 48 h. These findings suggest that increased MMP-1 expression after PRCR treatment enable remodeling the ECM.
引用
收藏
页码:3 / 8
页数:6
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