1
|
Taïeb A and Picardo M; VETF Members: The
definition and assessment of vitiligo: a consensus report of the
Vitiligo European Task Force. Pigment Cell Res. 20:27–35. 2007.
View Article : Google Scholar : PubMed/NCBI
|
2
|
Le Poole IC, Das PK, van den Wijngaard RM,
Bos JD and Westerhof W: Review of the etiopathomechanism of
vitiligo: a convergence theory. Exp Dermatol. 2:145–153. 1993.
View Article : Google Scholar : PubMed/NCBI
|
3
|
Schallreuter KU: Successful treatment of
oxidative stress in vitiligo. Skin Pharmacol Appl Skin Physiol.
12:132–138. 1999. View Article : Google Scholar : PubMed/NCBI
|
4
|
Maresca V, Roccella M, Roccella F, et al:
Increased sensitivity to peroxidative agents as a possible
pathogenic factor of melanocyte damage in vitiligo. J Invest
Dermatol. 109:310–313. 1997. View Article : Google Scholar : PubMed/NCBI
|
5
|
Dell’Anna ML, Maresca V, Briganti S, et
al: Mitochondrial impairment in peripheral blood mononuclear cells
during the active phase of vitiligo. J Invest Dermatol.
117:908–913. 2001. View Article : Google Scholar
|
6
|
Schallreuter KU, Wood JM and Berger J: Low
catalase levels in the epidermis of patients with vitiligo. J
Invest Dermatol. 97:1081–1085. 1991. View Article : Google Scholar : PubMed/NCBI
|
7
|
Sravani PV, Babu NK, Gopal KV, et al:
Determination of oxidative stress in vitiligo by measuring
superoxide dismutase and catalase levels in vitiliginous and
non-vitiliginous skin. Indian J Dermatol Venereol Leprol.
75:268–271. 2009. View Article : Google Scholar : PubMed/NCBI
|
8
|
Salem MM, Shalbaf M, Gibbons NC, et al:
Enhanced DNA binding capacity on up-regulated epidermal wild-type
p53 in vitiligo by H2O2-mediated oxidation: a
possible repair mechanism for DNA damage. FASEB J. 23:3790–3807.
2009. View Article : Google Scholar : PubMed/NCBI
|
9
|
Giovannelli L, Bellandi S, Pitozzi V, et
al: Increased oxidative DNA damage in mononuclear leukocytes in
vitiligo. Mutat Res. 556:101–106. 2004. View Article : Google Scholar : PubMed/NCBI
|
10
|
Westerhof W and d’Ischia M: Vitiligo
puzzle: the pieces fall in place. Pigment Cell Res. 20:345–359.
2007.PubMed/NCBI
|
11
|
Schallreuter KU, Elwary SM, Gibbons NC,
Rokos H and Wood JM: Activation/deactivation of
acetylcholinesterase by H2O2: more evidence
for oxidative stress in vitiligo. Biochem Biophys Res Commun.
315:502–508. 2004. View Article : Google Scholar : PubMed/NCBI
|
12
|
Jeong YM, Choi YG, Kim DS, et al:
Cytoprotective effect of green tea extract and quercetin against
hydrogen peroxide-induced oxidative stress. Arch Pharm Res.
28:1251–1256. 2005. View Article : Google Scholar : PubMed/NCBI
|
13
|
Nagata H, Takekoshi S, Takeyama R, Homma T
and Yoshiyuki Osamura R: Quercetin enhances melanogenesis by
increasing the activity and synthesis of tyrosinase in human
melanoma cells and in normal human melanocytes. Pigment Cell Res.
17:66–73. 2004. View Article : Google Scholar : PubMed/NCBI
|
14
|
Dell’Anna ML, Mastrofrancesco A, Sala R,
et al: Antioxidants and narrow band-UVB in the treatment of
vitiligo: a double-blind placebo controlled trial. Clin Exp
Dermatol. 32:631–636. 2007. View Article : Google Scholar
|
15
|
Boissy RE, Liu YY, Medrano EE and Nordlund
JJ: Structural aberration of the rough endoplasmic reticulum and
melanosome compartmentalization in long-term cultures of
melanocytes from vitiligo patients. J Invest Dermatol. 97:395–404.
1991. View Article : Google Scholar : PubMed/NCBI
|
16
|
Guan C, Lin F, Zhou M, et al: The role of
VIT1/FBXO11 in the regulation of apoptosis and tyrosinase export
from endoplasmic reticulum in cultured melanocytes. Int J Mol Med.
26:57–65. 2010.PubMed/NCBI
|
17
|
Jinbo L, Zhiyuan L, Zhijian Z and WenGe D:
Olfactory ensheathing cell-conditioned medium protects astrocytes
exposed to hydrogen peroxide stress. Cell Mol Neurobiol.
33:699–705. 2013. View Article : Google Scholar : PubMed/NCBI
|
18
|
Hong WS, Hu DN, Qian GP, McCormick SA and
Xu AE: Ratio of size of recipient and donor areas in treatment of
vitiligo by autologous cultured melanocyte transplantation. Br J
Dermatol. 165:520–525. 2011.PubMed/NCBI
|
19
|
Malhotra JD and Kaufman RJ: The
endoplasmic reticulum and the unfolded protein response. Semin Cell
Dev Biol. 18:716–731. 2007. View Article : Google Scholar : PubMed/NCBI
|
20
|
Ron D and Walter P: Signal integration in
the endoplasmic reticulum unfolded protein response. Nat Rev Mol
Cell Biol. 8:519–529. 2007. View Article : Google Scholar : PubMed/NCBI
|
21
|
Hartley T, Siva M, Lai E, et al:
Endoplasmic reticulum stress response in an INS-1 pancreatic
beta-cell line with inducible expression of a folding-deficient
proinsulin. BMC Cell Biol. 11:592010. View Article : Google Scholar : PubMed/NCBI
|
22
|
Zuber C, Fan JY, Guhl B and Roth J:
Misfolded proinsulin accumulates in expanded pre-Golgi
intermediates and endoplasmic reticulum subdomains in pancreatic
beta cells of Akita mice. FASEB J. 18:917–919. 2004.PubMed/NCBI
|
23
|
Toyofuku K, Wada I, Valencia JC, Kushimoto
T, Ferrans VJ and Hearing VJ: Oculocutaneous albinism types 1 and 3
are ER retention diseases: Mutation of tyrosinase or Tyrp1 can
affect the processing of both mutant and wild-type proteins. Faseb
J. 15:2149–2161. 2001. View Article : Google Scholar : PubMed/NCBI
|
24
|
Halaban R, Cheng E, Zhang Y, et al:
Aberrant retention of tyrosinase in the endoplasmic reticulum
mediates accelerated degradation of the enzyme and contributes to
the dedifferentiated phenotype of amelanotic melanoma cells. Proc
Natl Acad Sci USA. 94:6210–6215. 1997. View Article : Google Scholar : PubMed/NCBI
|
25
|
Berson JF, Frank DW, Calvo PA, et al: A
common temperature-sensitive allelic form of human tyrosinase is
retained in the endoplasmic reticulum at the nonpermissive
temperature. J Biol Chem. 275:12281–12289. 2000. View Article : Google Scholar : PubMed/NCBI
|
26
|
Chiang PW, Oiso N, Gautam R, et al: The
Hermansky-Pudlak syndrome 1 (HPS1) and HPS4 proteins are components
of two complexes, BLOC-3 and BLOC-4, involved in the biogenesis of
lysosome-related organelles. J Biol Chem. 278:20332–20337. 2003.
View Article : Google Scholar : PubMed/NCBI
|
27
|
Kushimoto T, Valencia JC, Costin GE, et
al: The Seiji memorial lecture: the melanosome: an ideal model to
study cellular differentiation. Pigment Cell Res. 16:237–244. 2003.
View Article : Google Scholar : PubMed/NCBI
|
28
|
Saffari Y and Sadrzadeh SM: Green tea
metabolite EGCG protects membranes against oxidative damage in
vitro. Life Sci. 74:1513–1518. 2004. View Article : Google Scholar : PubMed/NCBI
|
29
|
Quevedo WC Jr, Holstein TJ, Dyckman J and
McDonald CJ: The responses of the human epidermal melanocyte system
to chronic erythemal doses of UVR in skin protected by topical
applications of a combination of vitamins C and E. Pigment Cell
Res. 13:190–192. 2000. View Article : Google Scholar : PubMed/NCBI
|
30
|
Smit N, Vicanova J, Cramers P, Vrolijk H
and Pavel S: The combined effects of extracts containing
carotenoids and vitamins E and C on growth and pigmentation of
cultured human melanocytes. Skin Pharmacol Physiol. 17:238–245.
2004. View Article : Google Scholar : PubMed/NCBI
|
31
|
Bischoff SC: Quercetin: potentials in the
prevention and therapy of disease. Curr Opin Clin Nutr Metab Care.
11:733–740. 2008. View Article : Google Scholar : PubMed/NCBI
|
32
|
Murakami A, Ashida H and Terao J:
Multitargeted cancer prevention by quercetin. Cancer Lett.
269:315–325. 2008. View Article : Google Scholar : PubMed/NCBI
|