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Archives of Dermatological Research

, Volume 307, Issue 3, pp 281–289 | Cite as

A comparative study of mitochondrial ultrastructure in melanocytes from perilesional vitiligo skin and perilesional halo nevi skin

  • Gao-Zhong Ding
  • Wen-E Zhao
  • Xue Li
  • Qing-Li Gong
  • Yan LuEmail author
Concise Communication

Abstract

Vitiligo and halo nevi are both pigmentary disorders of the skin characterized by the acquired loss of functional epidermal melanocytes manifesting as white macules and patches. The cellular mechanism(s) and biochemical changes that result in the appearance of these two types of achromic lesions are still uncertain; and the relationship between vitiligo and halo nevi has been in dispute. In this study, we investigated the ultrastructure of mitochondria in melanocytes and in keratinocytes from perilesional vitiligo skin and from perilesional halo nevi skin using Transmission Electron Microscopy. Furthermore, we performed a quantitative analysis of mitochondrial morphology through a stereological study. As previously reported, we found that melanocytes from perilesional active vitiligo skin were loosely connected with their surroundings by their retracted dendrites. The surface density and the volume density of mitochondria in melanocytes and in keratinocytes from perilesional vitiligo skin are increased significantly compared with the controls, especially in active vitiligo. In contrast, there are no significant differences in mitochondria in melanocytes and in keratinocytes from perilesional halo nevi skin compared with the controls. In summary, the tendency of different morphologic alterations in mitochondria from perilesional vitiligo skin and from perilesional halo nevi skin reflect heterogeneous backgrounds between the two diseases, revealing that vitiligo and halo nevi may have separate pathogenic mechanisms. These findings may help elucidate the relationship of these two diseases and their underlying mechanisms.

Keywords

Melanocyte Keratinocyte Mitochondria Ultrastructure Vitiligo Halo nevi 

Notes

Acknowledgments

This study was funded by the National Natural Science Foundation of China (Grant NO.81171517).

Conflict of interest

The authors declare that they have no conflict of interest.

Ethical standards

Informed consent was obtained from all patients. Procedures were carried out in accordance with the ethical standards of the First Affiliated Hospital, Nanjing Medical University and with the 1964 Helsinki declaration and its later amendments.

References

  1. 1.
    Akasu R, From L, Kahn HJ (1994) Characterization of the mononuclear infiltrate involved in regression of halo nevi. J Cutan Pathol 21:302–311CrossRefPubMedGoogle Scholar
  2. 2.
    Amaral A, Lourenco B, Marques M, Ramalho-Santos J (2013) Mitochondria functionality and sperm quality. Reproduction 146:R163–R174CrossRefPubMedGoogle Scholar
  3. 3.
    Benzekri L, Hmamouchi I, Gauthier Y (2014) Possible patterns of epidermal melanocyte disappearance in nonsegmental vitiligo: a clinicopathological study. Br J Dermatol. doi: 10.1111/bjd.13160 PubMedGoogle Scholar
  4. 4.
    Cario-Andre M, Pain C, Gauthier Y, Taieb A (2007) The melanocytorrhagic hypothesis of vitiligo tested on pigmented, stressed, reconstructed epidermis. Pigment Cell Res 20(5):385–393PubMedGoogle Scholar
  5. 5.
    Coto-Montes A, Boga JA, Rosales-Corral S, Fuentes-Broto L, Tan DX, Reiter RJ (2012) Role of melatonin in the regulation of autophagy and mitophagy: a review. Mol Cell Endocrinol 361:12–23CrossRefPubMedGoogle Scholar
  6. 6.
    Dell’Anna ML, Urbanelli S, Mastrofrancesco A, Camera E, Iacovelli P, Leone G, Manini P, D’Ischia M, Picardo M (2003) Alterations of mitochondria in peripheral blood mononuclear cells of vitiligo patients. Pigment Cell Res 16:553–559CrossRefPubMedGoogle Scholar
  7. 7.
    de Vijlder HC, Westerhof W, Schreuder GM, de Lange P, Claas FH (2004) Difference in pathogenesis between vitiligo vulgaris and halo nevi associated with vitiligo is supported by an HLA association study. Pigment Cell Res 17:270–274CrossRefPubMedGoogle Scholar
  8. 8.
    Ezzedine K, Diallo A, Leaute-Labreze C, Seneschal J, Mossalayi D, AlGhamdi K, Prey S, Bouchtnei S, Cario-Andre M, Boralevi F, Jouary T, Taieb A (2012) Halo nevi association in nonsegmental vitiligo affects age at onset and depigmentation pattern. Arch Dermatol 148(4):497–502CrossRefPubMedGoogle Scholar
  9. 9.
    Ezzedine K, Diallo A, Leaute-Labreze C, Seneschal J, Prey S, Ballanger F, Alghamdi K, Cario-Andre M, Jouary T, Gauthier Y, Taieb A (2012) Halo naevi and leukotrichia are strong predictors of the passage to mixed vitiligo in a subgroup of segmental vitiligo. Br J Dermatol 166(3):539–544CrossRefPubMedGoogle Scholar
  10. 10.
    Gauthier Y (2010) Electron microscopy of vitiligo. Taieb A, Picardo M(eds) Vitiligo. Springer-Verlag, Berlin Heidelberg, pp 197–203Google Scholar
  11. 11.
    Gauthier Y, Cario-Andre M, Lepreux S, Pain C, Taieb A (2003) Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo. Br J Dermatol 148(1):95–101CrossRefPubMedGoogle Scholar
  12. 12.
    Gauthier Y, Cario Andre M, Taieb A (2003) A critical appraisal of vitiligo etiologic theories. Is melanocyte loss a melanocytorrhagy? Pigment Cell Res 16(4):322–332Google Scholar
  13. 13.
    Gauthier Y, Surleve-Bazeille JE, Gauthier O, Texier L (1975) Ultrastructure of halo nevi. J Cutan Pathol 2(2):71–81CrossRefPubMedGoogle Scholar
  14. 14.
    Gauthier Y, Surleve-Bazeille JE, Texier L (1978) Halo nevi without dermal infiltrate. Arch Dermatol 114(11):1718CrossRefPubMedGoogle Scholar
  15. 15.
    Glassman SJ (2011) Vitiligo, reactive oxygen species and T-cells. Clin Sci (Lond) 120(3):99–120CrossRefGoogle Scholar
  16. 16.
    Laddha NC, Dwivedi M, Mansuri MS, Gani AR, Ansarullah M, Ramachandran AV, Dalai S, Begum R (2013) Vitiligo: interplay between oxidative stress and immune system. Exp Dermatol 22(4):245–250CrossRefPubMedGoogle Scholar
  17. 17.
    Lerner AB (1959) Vitiligo. J Invest Dermatol 32:285–310CrossRefPubMedGoogle Scholar
  18. 18.
    Moellmann G, Klein-Angerer S, Scollay DA, Nordlund JJ, Lerner AB (1982) Extracellular granular material and degeneration of keratinocytes in the normally pigmented epidermis of patients with vitiligo. J Invest Dermatol 79(5):321–330CrossRefPubMedGoogle Scholar
  19. 19.
    Musette P, Bachelez H, Flageul B, Delarbre C, Kourilsky P, Dubertret L, Gachelin G (1999) Immune-mediated destruction of melanocytes in halo nevi is associated with the local expansion of a limited number of T cell clones. J Immunol 162:1789–1794PubMedGoogle Scholar
  20. 20.
    Passeron T, Ortonne JP (2012) Activation of the unfolded protein response in vitiligo: the missing link? J Invest Dermatol 132(11):2502–2504CrossRefPubMedGoogle Scholar
  21. 21.
    Prignano F, Pescitelli L, Becatti M, Di Gennaro P, Fiorillo C, Taddei N, Lotti T (2009) Ultrastructural and functional alterations of mitochondria in perilesional vitiligo skin. J Dermatol Sci 54(3):157–167CrossRefPubMedGoogle Scholar
  22. 22.
    Schallreuter KU (1999) Successful treatment of oxidative stress in vitiligo. Skin Pharmacol Appl Skin Physiol 12(3):132–138CrossRefPubMedGoogle Scholar
  23. 23.
    Schallreuter KU, Buttner G, Pittelkow MR, Wood JM, Swanson NN, Korner C (1994) Cytotoxicity of 6-biopterin to human melanocytes. Biochem Biophys Res Commun 204(1):43–48CrossRefPubMedGoogle Scholar
  24. 24.
    Schallreuter KU, Kothari S, Elwary S, Rokos H, Hasse S, Panske A (2003) Molecular evidence that halo in Sutton’s naevus is not vitiligo. Arch Dermatol Res 295(6):223–228CrossRefPubMedGoogle Scholar
  25. 25.
    Schallreuter KU, Moore J, Wood JM, Beazley WD, Gaze DC, Tobin DJ, Marshall HS, Panske A, Panzig E, Hibberts NA (1999) In vivo and in vitro evidence for hydrogen peroxide (H2O2) accumulation in the epidermis of patients with vitiligo and its successful removal by a UVB-activated pseudocatalase. J Invest Dermatol Symp Proc 4(1):91–96CrossRefGoogle Scholar
  26. 26.
    Schallreuter KU, Salem MA, Holtz S, Panske A (2013) Basic evidence for epidermal H2O2/ONOO(−)-mediated oxidation/nitration in segmental vitiligo is supported by repigmentation of skin and eyelashes after reduction of epidermal H2O2 with topical NB-UVB-activated pseudocatalase PC-KUS. FASEB J. 27(8):3113–3122CrossRefPubMedGoogle Scholar
  27. 27.
    Scherz-Shouval R, Elazar Z (2007) ROS, mitochondria and the regulation of autophagy. Trends Cell Biol 17(9):422–427CrossRefPubMedGoogle Scholar
  28. 28.
    Tobin DJ, Swanson NN, Pittelkow MR, Peters EM, Schallreuter KU (2000) Melanocytes are not absent in lesional skin of long duration vitiligo. J Pathol 191(4):407–416CrossRefPubMedGoogle Scholar
  29. 29.
    Yaghoobi R, Omidian M, Bagherani N (2011) Vitiligo: a review of the published work. J Dermatol 38(5):419–431CrossRefPubMedGoogle Scholar
  30. 30.
    Zeff RA, Freitag A, Grin CM, Grant-Kels JM (1997) The immune response in halo nevi. J Am Acad Dermatol 37:620–624CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  • Gao-Zhong Ding
    • 1
  • Wen-E Zhao
    • 2
  • Xue Li
    • 1
  • Qing-Li Gong
    • 1
  • Yan Lu
    • 1
    Email author
  1. 1.Dermatology Department, The First Affiliated HospitalNanjing Medical UniversityNanjingPeople’s Republic of China
  2. 2.Department of Analysis and Testing CenterNanjing Medical UniversityNanjingPeople’s Republic of China

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