The Development of a Wound Healing Model Using Nerve Growth Factor(NGF) Expression in Raft Culture

2000 ◽  
Vol 12 (2) ◽  
pp. 106
Author(s):  
Kyu Han Kim ◽  
Dong Youn Lee ◽  
Kyoung Chan Park
1998 ◽  
Vol 187 (3) ◽  
pp. 297-306 ◽  
Author(s):  
Hiroshi Matsuda ◽  
Hiromi Koyama ◽  
Hiroaki Sato ◽  
Junko Sawada ◽  
Atsuko Itakura ◽  
...  

Four full-thickness skin wounds made in normal mice led to the significant increase in levels of nerve growth factor (NGF) in sera and in wounded skin tissues. Since sialoadenectomy before the wounds inhibited the rise in serum levels of NGF, the NGF may be released from the salivary gland into the blood stream after the wounds. In contrast, the fact that messenger RNA and protein of NGF were detected in newly formed epithelial cells at the edge of the wound and fibroblasts consistent with the granulation tissue produced in the wound space, suggests that NGF was also produced at the wounded skin site. Topical application of NGF into the wounds accelerated the rate of wound healing in normal mice and in healing-impaired diabetic KK/Ta mice. This clinical effect of NGF was evaluated by histological examination; the increases in the degree of reepithelialization, the thickness of the granulation tissue, and the density of extracellular matrix were observed. NGF also increased the breaking strength of healing linear wounds in normal and diabetic mice. These findings suggested that NGF immediately and constitutively released in response to cutaneous injury may contribute to wound healing through broader biological activities, and NGF improved the diabetic impaired response of wound healing.


1985 ◽  
Vol 43 (2) ◽  
pp. 274-281 ◽  
Author(s):  
Michael J.P. Lawman ◽  
Michael D.P. Boyle ◽  
Adrian P. Gee ◽  
Michael Young

2004 ◽  
Vol 12 (1) ◽  
pp. 44-52 ◽  
Author(s):  
Pornprom Muangman ◽  
Lara A. Muffley ◽  
Joanne P. Anthony ◽  
Michelle L. Spenny ◽  
Robert A. Underwood ◽  
...  

2013 ◽  
Vol 121 (02) ◽  
pp. 84-89 ◽  
Author(s):  
O. Nakagaki ◽  
H. Miyoshi ◽  
T. Sawada ◽  
T. Atsumi ◽  
T. Kondo ◽  
...  

2005 ◽  
Vol 80 (5) ◽  
pp. 633-642 ◽  
Author(s):  
Heung-Myong Woo ◽  
Ellison Bentley ◽  
Sean F. Campbell ◽  
Carl F. Marfurt ◽  
Christopher J. Murphy

2012 ◽  
Vol 16 (3+4) ◽  
pp. 51-65 ◽  
Author(s):  
Masahiko Mori ◽  
Toshiro Yamamoto ◽  
Takeshi Amemiya ◽  
Narisato Kanamura ◽  
Tetsunari Nishikawa ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Auspreeya Rujirachotiwat ◽  
Supaporn Suttamanatwong

Abstract Background Curcumin accelerates healing of oral wounds; however, the responsible mechanisms remain underexplored. Our hypothesis is curcumin regulates the expression of wound healing-related genes in human gingival fibroblasts (hGFs). This study investigated whether curcumin regulates transforming growth factor (TGF)-β1, type I TGF-β receptor (TGF-βRI), type II TGF-β receptor (TGF-βRII), and vascular endothelial growth factor (VEGF) expression in unwounded hGFs and an in vitro hGF wound healing model. Methods The cytotoxicity of curcumin was evaluated using the MTT assay. Unwounded hGFs were treated with non-cytotoxic concentrations of curcumin for 24 h. Gene expression was determined by quantitative polymerase chain reaction. Then, hGFs were treated with 1 µM curcumin in an in vitro wound healing model. PD98059 pretreatment was performed to determine whether extracellular signal-regulated kinase (ERK) signaling was required for regulation of gene expression by curcumin. Results Curcumin at 0.1–20 µM caused no significant change in cell viability. In unwounded hGFs, curcumin had no significant effect on TGF-β1, TGF-βRI, TGF-βRII, or VEGF expression. Conversely, curcumin significantly upregulated the expression of these genes in the in vitro wound healing model. PD98059 significantly attenuated the curcumin-stimulated TGF-βRI, TGF-βRII, and VEGF expression, whereas it had no effect on TGF-β1 expression. Conclusions Curcumin upregulated TGF-β1, TGF-βRI, TGF-βRII, and VEGF expression in an in vitro hGF wound healing model. The ERK pathway is required for TGF-βRI, TGF-βRII, and VEGF induction by curcumin. Our findings support the development of curcumin as a therapeutic agent for gingival ulcers.


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