1.The effects of chitosan on different-derived fibroblasts.
Jing-De ZHANG ; Xin XING ; Mei-qing SUN ; Jian-xing SONG ; Tian-xiang OUYANG
Chinese Journal of Plastic Surgery 2004;20(1):53-56
OBJECTIVETo investigate the effects of chitosan on the biological activities of the fibroblasts derived from different tissues.
METHODSThe biological activities of the fibroblasts derived from different tissues were evaluated with a MTT method for fibroblast proliferation, photic and electronic microscope for morphologic and subcellular structure, 3H-proline uptake method for collagen secretion and ELISA box for the secretion of TGF-beta 1, FGF-AB, and IL-8.
RESULTSThis study showed that the chitosan inhabited the proliferation of the fibroblasts and the secretion of the TGF-beta 1, FGF-AB and collagen of the fibroblasts with a dose-depended manner in the normal skin, hypertrophic scar and keloid groups, but it stimulated the IL-8. However, there were no significant differences among the three groups (P > 0.05).
CONCLUSIONThe chitosan could inhibit the growth, proliferation, biosynthesis and secretion of the fibroblasts, and it may be used to treat different scars.
Adolescent ; Adult ; Cell Division ; drug effects ; Chitin ; analogs & derivatives ; pharmacology ; Chitosan ; Dose-Response Relationship, Drug ; Female ; Fibroblast Growth Factors ; secretion ; Fibroblasts ; drug effects ; metabolism ; ultrastructure ; Hemostatics ; pharmacology ; Humans ; Interleukin-8 ; secretion ; Male ; Microscopy, Electron ; Peptide Fragments ; secretion ; Transforming Growth Factor beta ; secretion
2.Induction of tissue inhibitor of matrix metalloproteinase-2 by cholesterol depletion leads to the conversion of proMMP-2 into active MMP-2 in human dermal fibroblasts.
Sangmin KIM ; Jang Hee OH ; Youngae LEE ; Jeongyoon LEE ; Kwang Hyun CHO ; Jin Ho CHUNG
Experimental & Molecular Medicine 2010;42(1):38-46
Cholesterol is one of major components of cell membrane and plays a role in vesicular trafficking and cellular signaling. We investigated the effects of cholesterol on matrix metalloproteinase-2 (MMP-2) activation in human dermal fibroblasts. We found that tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) expression and active form MMP-2 (64 kD) were dose-dependently increased by methyl-beta-cyclodextrin (MbetaCD), a cholesterol depletion agent. In contrast, cholesterol depletion-induced TIMP-2 expression and MMP-2 activation were suppressed by cholesterol repletion. Then we investigated the regulatory mechanism of TIMP-2 expression by cholesterol depletion. We found that the phosphorylation of JNK as well as ERK was significantly increased by cholesterol depletion. Moreover, cholesterol depletion-induced TIMP-2 expression and MMP-2 activation was significantly decreased by MEK inhibitor U0126, and JNK inhibitor SP600125, respectively. While a low dose of recombinant TIMP-2 (100 ng/ml) increased the level of active MMP-2 (64 kD), the high dose of TIMP-2 (> or = 200 ng/ml) decreased the level of active MMP-2 (64 kD). Taken together, we suggest that the induction of TIMP-2 by cholesterol depletion leads to the conversion of proMMP-2 (72 kD) into active MMP-2 (64 kD) in human dermal fibroblasts.
Anthracenes/pharmacology
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Butadienes/pharmacology
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Cells, Cultured
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Child
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Child, Preschool
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Cholesterol/metabolism/*physiology
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Cyclodextrins/pharmacology
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Enzyme Inhibitors/pharmacology
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Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/physiology
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Fibroblasts/*drug effects/*metabolism/ultrastructure
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Humans
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Immunoblotting
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Immunoprecipitation
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JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors/physiology
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Matrix Metalloproteinase 2/*metabolism
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Microscopy, Electron, Transmission
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Nitriles/pharmacology
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Tissue Inhibitor of Metalloproteinase-2/*metabolism