FK506 promotes melanocyte and melanoblast growth and creates a favourable milieu for cell migration via keratinocytes: possible mechanisms of how tacrolimus ointment induces repigmentation in patients with vitiligo

Lan, C.‐C. E.; Chen, G.-S.; Chiou, Min-Hsi; Wu, Ching‐Shuang; Chang, Chia-Wen; Yu, Hsin‐Su

doi:10.1111/j.1365-2133.2005.06739.x

Cited by 115 publications

(104 citation statements)

References 52 publications

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“…Normal human keratinocytes were obtained from adult foreskin through routine circumcision as previously described (22). Briefly, the skin specimens were washed with phosphate-buffered saline (PBS), cut into small pieces and incubated in medium containing 0.25% trypsin (Gibco BRL, Gaithersburg, MD, USA) overnight at 4°C.…”

Section: Cell Proliferation and Cell Morphologymentioning

confidence: 99%

High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-3 Expression in Keratinocytes

Lan

Huang

et al. 2011

Mol Med

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Diabetes mellitus is characterized by elevated plasma glucose and increased rates of skin infections. Altered immune responses have been suggested to contribute to this prevalent complication, which involves microbial invasion. In this study we explored the effects of a high-glucose environment on the innate immunity of keratinocytes by focusing on β defensin-3 (BD3) using in vivo and in vitro models. Our results demonstrated that the perilesional skins of diabetic rats failed to show enhanced BD3 expression after wounding. In addition, high-glucose treatment reduced human BD3 (hBD3) expression of cultured human keratinocytes. This pathogenic process involved inhibition of p38MAPK signaling, an event that resulted from increased formation of advanced glycation end products. On the other hand, toll-like receptor-2 expression and function of cultured keratinocytes were not significantly affected by high-glucose treatment. In summary, high-glucose conditions inhibited the BD3 expression of epidermal keratinocytes, which in turn contributed to the frequent occurrences of infection associated with diabetic wounding.

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Section: Cell Proliferation and Cell Morphologymentioning

confidence: 99%

High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-3 Expression in Keratinocytes

Lan

Huang

et al. 2011

Mol Med

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“…Uyguland klar alanda TNF-düzeyini bask lad klar ndan karsinojenik hücrelerin inhibisyonunu azaltabilirler. Bu nedenle olas kanser riski uzun süreli kullan mlarda göz ard edilmemelidir (25). endur ve ark.…”

Section: B Yeni Tedavi Yöntemleri 1 Topikal Immunmodülatörlerunclassified

Treatment of Vitiligo and New Treatment Approaches

Demirel¹,

Borlu²

2010

Turk J Dermatol

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ÖzetVitiligo, melanositlerin sayı ve işlev kaybı ile karakterize bir pigment hastalığıdır. Etyolojisi bilinmemektedir ancak otoimmun, genetik, biyokimyasal faktörler ve nöral mekanizmalar etyolojide suçlanmaktadır. Melanosit antijenlerini hedef alan sitotoksik T hücrelerinin varlığı ve sitokin seviyelerindeki dengesizliğin melanosit hasarına ve ölümüne neden olduğu düşünülmektedir. Vitiligo tedavisi lezyonların yaygınlığına, lokalizasyonuna, yaşa ve önceki tedavilere verilen yanıta göre değişmektedir. Bu derlemede vitiligo tedavisi geleneksel tedaviler, yeni tedavi seçenekleri, cerrahi tedaviler, deneysel ve diğer tedavi seçenekleri başlıkları altında ele alınmış ve güncel literatür bilgileri ışığında değerlendirilmiştir. (Turk J Dermatol 2010; 4: 33-9 AbstractVitiligo is an pigmentary disorder characterized by loss of functional melanocytes. Altough the aetiology is unknown, autoimmunity, genetic factors, biochemical factors and neural mechanisms were suspected. Cytotoxic T cells targeting melanocyte antigens are present and also an imbalance of the cytokine levels leading to melanocyte damage and death. It is believed that the treatment of vitiligo differs according to the severity of disease, localisation, age and response to previous medications. In this article we reviewed the current literature about vitiligo and classified the treatment options of vitiligo as traditional and current treatment options, surgical treatments, experimental therapies and other treatment options. (Turk J Dermatol 2010; 4: 33-9)

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“…It is empirically used in vitiligo due to its ability to increase melanocyte proliferation as well as stem cell factors, and down-regulate a number of interleukins, interferon-gamma, tumor necrosis factor-alpha, and granulocyte monocytecolony stimulating factor (Grimes, Soriano et al, 2002;Lan, Chen et al, 2005). Tacrolimus ointment (0.1%) and NB-UVB combination treatment is more effective than NB-UVB monotherapy and the effect of tacrolimus is dose-dependent (Nordal, Guleng et al, 2011).…”

Section: Tacrolimusmentioning

confidence: 99%