TY - JOUR
T1 - Silencing stem cell factor gene in fibroblasts to regulate paracrine factor productions and enhance c-Kit expression in melanocytes on melanogenesis
AU - Li, Pin Hui
AU - Liu, Li Heng
AU - Chang, Cheng Chung
AU - Gao, Rong
AU - Leung, Chung Hang
AU - MA, Edmond Dik Lung
AU - David Wang, Hui Min
N1 - Funding Information:
This work was supported by grants from the Ministry of Science and Technology, Taiwan (MOST104-2221-E-005-096-MY2, MOST 104-2628-E-005-004-MY3 and MOST 106-2622-E-005-002-CC2). We also thank the projects of Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung, Taiwan, KMU-TP104G00, KMU-TP104G01 and KMU-TP104G02-05.
Funding Information:
Acknowledgments: This work was supported by grants from the Ministry of Science and Technology, Taiwan (MOST 104-2221-E-005-096-MY2, MOST 104-2628-E-005-004-MY3and MOST 106-2622-E-005-002-CC2). We also thank the projects of Center for Stem Cell Research, Kaohsiung Medical University, Kaohsiung, Taiwan, KMU-TP104G00, KMU-TP104G01 and KMU-TP104G02-05.
PY - 2018/5/16
Y1 - 2018/5/16
N2 - Melanogenesis is a complex physiological mechanism involving various paracrine factors. Skin cells such as keratinocytes, fibroblasts, and melanocytes communicate with one another through secreted regulators, thereby regulating the melanocytes’ bio-functions. The stem cell factor (SCF) is a paracrine factor produced by fibroblasts, and its receptor, c-kit, is expressed on melanocytes. Binding of SCF to c-kit activates autophosphorylation and tyrosine kinase to switch on its signal transmission. SCF inhibition does not suppress fibroblast proliferation in MTT assay, and SCF silencing induced mRNA expressions of paracrine factor genes, HGF, NRG-1, and CRH in qPCR results. Following UVB stimulation, gene expressions of HGF, NRG, and CRH were higher than homeostasis; in particular, HGF exhibited the highest correlation with SCF variations. We detected fibroblasts regulated SCF in an autocrine-dependent manner, and the conditioned medium obtained from fibroblast culture was applied to treat melanocytes. Melanogenesis-related genes, tyrosinase and pmel17, were upregulated under conditioned mediums with SCF silencing and exposed to UVB treatments. Melanin quantities in the melanocytes had clearly increased in the pigment content assay. In conclusion, SCF silencing causes variations in both fibroblast paracrine factors and melanocyte melanogenesis, and the differences in gene expressions were observed following UVB exposure.
AB - Melanogenesis is a complex physiological mechanism involving various paracrine factors. Skin cells such as keratinocytes, fibroblasts, and melanocytes communicate with one another through secreted regulators, thereby regulating the melanocytes’ bio-functions. The stem cell factor (SCF) is a paracrine factor produced by fibroblasts, and its receptor, c-kit, is expressed on melanocytes. Binding of SCF to c-kit activates autophosphorylation and tyrosine kinase to switch on its signal transmission. SCF inhibition does not suppress fibroblast proliferation in MTT assay, and SCF silencing induced mRNA expressions of paracrine factor genes, HGF, NRG-1, and CRH in qPCR results. Following UVB stimulation, gene expressions of HGF, NRG, and CRH were higher than homeostasis; in particular, HGF exhibited the highest correlation with SCF variations. We detected fibroblasts regulated SCF in an autocrine-dependent manner, and the conditioned medium obtained from fibroblast culture was applied to treat melanocytes. Melanogenesis-related genes, tyrosinase and pmel17, were upregulated under conditioned mediums with SCF silencing and exposed to UVB treatments. Melanin quantities in the melanocytes had clearly increased in the pigment content assay. In conclusion, SCF silencing causes variations in both fibroblast paracrine factors and melanocyte melanogenesis, and the differences in gene expressions were observed following UVB exposure.
KW - Fibroblasts
KW - Melanin
KW - Melanocytes
KW - Paracrine factors
KW - Stem cell factor
UR - http://www.scopus.com/inward/record.url?scp=85047127640&partnerID=8YFLogxK
U2 - 10.3390/ijms19051475
DO - 10.3390/ijms19051475
M3 - Journal article
C2 - 29772675
AN - SCOPUS:85047127640
SN - 1661-6596
VL - 19
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 5
M1 - 1475
ER -
