Leukotriene C4 and TGF-Alpha Are Stimulators of Human Melanocyte Migration In Vitro

Morelli, Joseph G.; Kincannon, Jay; Yohn, Joseph; Zekman, Tamara; Weston, William L.; Norris, David A.

doi:10.1111/1523-1747.ep12497951

Cited by 79 publications

(49 citation statements)

References 15 publications

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“…Due to this there is local oedema, which increases the intercellular spaces of the basal layer for a long time [12]. Active melanocytes with frequently vacuolated cytoplasm are found migrating from the pigmented to the achromic epidermis through these enlarged intercellular spaces [13].…”

Section: Discussionmentioning

confidence: 99%

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Successful Treatment of Vitiligo by Needling with Topical 5 Fluorouracil

Vedamurthy¹,

Moorthy²,

Samuel³

2016

J Pigment Disord

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Section: Discussionmentioning

confidence: 99%

“…Further the inflammatory mediators such as leukotrienes C4 and D4 are locally released, which would stimulate melanocyte proliferation and migration [13,14]. The metalloproteinase 2, synthesized by the keratinocytes during the epidermis remodelling process has been found to help in melanocyte migration [15].…”

Section: Discussionmentioning

confidence: 99%

Successful Treatment of Vitiligo by Needling with Topical 5 Fluorouracil

Vedamurthy¹,

Moorthy²,

Samuel³

2016

J Pigment Disord

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“…This is of major importance as for repigmentation, melanocytes surrounding vitiligo lesions and melanocytes from hair shafts 28 need be stimulated to re-enter vitiligo lesional skin. Observations that LTC-4 and nerve growth factor (NGF) stimulate melanocyte migration 29 are, thus, of great interest for the development of new therapeutic modalities. However, results presented here concerning the abundance of tenascin in vitiligo skin also indicate that vitiligo lesions present a hostile environment for melanocytes.…”

Section: Discussionmentioning

confidence: 99%

Tenascin is overexpressed in vitiligo lesional skin and inhibits melanocyte adhesion

Poole

Wijngaard

Westerhof³

et al. 1997

British Journal of Dermatology

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SummaryThe aetiology of vitiligo remains obscure. In this study, the role of integrins in the observed inability of melanocytes to repopulate lesional skin was investigated. Antibodies directed to a 2 , a 3 , a 5 , a v , a 6 , b 1 and b 3 integrin subunits were used. Immunohistology revealed no marked differences in the overall levels of expression of integrins between control, non-lesional, perilesional or lesional skin. Moreover, no differences were noted in the level of expression of integrins or the adhesive capacity between cultured control cells derived from three separate donors and vitiligo-derived melanocytes from two donors. Rather, it was clearly observed that towards the lesion, vitiligo skin contains increasing amounts of tenascin in the basal membrane and papillary dermis in five patients employing T2H5 antihuman tenascin antibody. The anti-adhesive effect observed in vitro for this extracellular matrix molecule using normal melanocytes may contribute to loss of pigment cells in vitiligo or to ineffective repopulation of the lesions.In vitiligo, melanocytes are gradually lost in depigmenting lesions of the skin. 1 It has been suggested that defective adhesion is involved in loss of melanocytes in this pigmentary disorder. 2 Moreover, the persistence of depigmented lesions is suggestive of defective melanocyte migration which may be reversed by photochemotherapy, 2 and therefore baseline expression of adhesion molecules may differ in vitiligo as compared with control skin. Melanocyte adhesion, spreading and migration is mediated by integrins. 3 Employing antibodies to integrin subunits, the specific integrins involved in each process have been identified in vitro. 3,4 Importantly, all integrins thus far identified on melanocytes can also be found on neighbouring keratinocytes. Although immunohistology has been employed to identify integrins expressed on melanocytes in situ per se, 3 this may not be the method of choice to determine differences in the level of expression by melanocytes. Even by double immunostaining procedures, it is difficult to distinguish between integrin expression by melanocytes vs. neighbouring keratinocytes. Therefore, in vitro cultures derived from control as well as from vitiligo non-lesional skin were employed to investigate further potential differences in adhesive behaviour in vitiligo and control skin. In addition, the use of cultured cells provides the opportunity to perform functional adhesion assays. In this respect it is of great interest to note that cultured melanocytes from nonlesional vitiligo skin appear to retain disease-related characteristics. It has been demonstrated that vitiligo melanocytes have altered growth characteristics under limiting conditions. 5 Moreover, upon electron microscopic observation, dilated rough endoplasmic reticulum (RER) is apparent in diseased cells from human and mouse vitiligo subjects. 6,7 Therefore, the use of cultured cells to investigate differences in adhesive characteristics is justified.The level of expression of relevant i...

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“…The pathogenesis of postinflammatory hypopigmentation is believed to be secondary to melanocyte cell-surface expression of ICAM-1 induced by inflammatory mediators [16]. The theory is that this may lead to leukocyte-melanocyte attachments with the final result being innocent bystander destruction of melanocytes.…”

Section: Disorders Of Hypopigmentation and Depigmentationmentioning

confidence: 99%