Biomedical subjects

M B Abdel-Naser

Publications and source records attributed to M B Abdel-Naser.

7 recordsLinked to original sources

PubMed1999

Differential effects on melanocyte growth and melanization of low vs. high calcium keratinocyte-conditioned medium.

Epidermal keratinocytes secrete several growth factors that stimulate melanocyte proliferation and melanin pigment synthesis in vitro. As the epidermis is formed of two distinct layers, i.e. basal cell layer and suprabasal cell layers, and both are functionally and biologically different compartments, it was interesting to investigate which type of epidermal keratinocytes modulate melanocyte proliferation and function most. Normal human epidermal melanocytes (HMel) were incubated with melanocyte-conditioned medium (M-CM) and low Ca2+ and high Ca2+ keratinocyte-conditioned medium (K-CM) obtained from the same skin source of melanocytes. The morphology, proliferation rate and melanin synthesis were evaluated at days 3, 6 and 12 of incubation. The results showed no evidence of major morphological changes in the epidermal melanocytes with any of the conditioned media, although marked dendrite formation was observed in coculture of melanocytes and differentiated keratinocytes. On the other hand, low Ca2+ K-CM induced a mild but statistically significant stimulation of melanocyte growth in a time-dependent manner. The significant percentage increase was evident on day 6 (124.6%, P < 0.05) and on day 12 (138.1%, P < 0.01) of incubation. In contrast, high Ca2+ K-CM showed no significant effect on melanocyte proliferation (P > 0.05). Both low Ca2+ and high Ca2+ K-CM stimulated melanin synthesis, although synthesis induced by low Ca2+ K-CM was higher than that of high Ca2+ K-CM. The significant percentage increase induced by low Ca2+ K-CM was evident on day 6 (117.9%, P < 0.05) and on day 12 (127.8%, P < 0.05) of incubation, whereas it was evident with high Ca2+ K-CM only on day 12 (119.7%, P < 0.05) of incubation. It is concluded from the above data that keratinocytes grown at a low Ca2+ level release factors that stimulate melanocyte proliferation as well as melanin synthesis, whereas keratinocytes grown at a high Ca2+ level release factors that only stimulate melanin synthesis. This may provide an explanation of the anatomical position of melanocytes and may play a part in the pigmentary changes following injury to epidermal cells.

Calcium↗

PubMed1997

Oral psoralen with UV-A therapy releases circulating growth factor(s) that stimulates cell proliferation.

BACKGROUND: The mechanism by which oral psoralen with UV-A (PUVA) stimulates melanocyte proliferation in vitiligo is unknown. This study was conducted to examine the hypothesis that it does so by stimulating the release of growth factors that stimulate melanocyte proliferation. DESIGN: We examined the effect of serum samples obtained from patients with vitiligo before and following 2 and 4 months of PUVA therapy, and from non-PUVA-treated patients with vitiligo and normal individuals on the growth of melanocytes in vitro. SETTING: Outpatient clinic in referral center. PATIENTS: The study was conducted on serum samples obtained from 18 patients with vitiligo, 8 of whom were treated with PUVA, and from 10 normal individuals. INTERVENTION: Treatment with PUVA. MAIN OUTCOME MEASURE: Ability of serum samples to stimulate the growth of melanocytes in culture. RESULTS: Proliferation of melanocytes in serum collected after 4 months of PUVA therapy was on the average 3-fold greater than that in serum samples collected from the same patients prior to therapy with PUVA. This circulating growth factor was absent in serum samples of non-PUVA-treated patients with vitiligo and normal individuals. The effect was nonspecific, as it also stimulated the proliferation of fibroblasts. CONCLUSIONS: These findings suggest that PUVA treatment results in the release into the circulation of growth factor(s) that can stimulate a proliferation of melanocytes and of other cells. This could account for the repigmentation of vitiligo by PUVA treatment. As the growth factor(s) also stimulated the growth of other cells, it could also explain the thickening of the epidermis that occurs following exposure to UV light.

Administration, Oral↗

PubMed1995

[Pre-myopathic versus amyopathic dermatomyositis. 2 personal cases and review of the literature].

The so-called amyopathic dermatomyositis is a rare variant of dermatomyositis which has attracted increasing interest during the last years. One finds the classical signs of dermatomyositis such as periorbital edema and erythema, erythematous macular and papular lesions localized at bony prominences (so-called Gottron's papules), generalized pruritus, photosensitivity, and a cutaneous histopathologic picture compatible with skin lesions of dermatomyositis. Crucial for the diagnosis is the exclusion of myositis by clinical examination, EMG and histology. Furthermore, longterm supervision of patients is advisable in order not to miss the appearance of early signs of myositis. The longest reported follow-up of amyopathic dermatomyositis patient is 4 years; however, it cannot be excluded that these cases will eventually culminate in classical dermatomyositis. In this paper we describe two cases and discuss the differential diagnosis and therapy; also, the term "Premyopathic dermatomyositis" is proposed, to indicate that the full picture is to be expected in most cases.

Adult↗

PubMed1994

Further evidence for involvement of both cell mediated and humoral immunity in generalized vitiligo.

Immunohistochemical and immunoserological evidence supports the involvement of both cell-mediated and humoral mechanisms in the pathogenesis of melanocyte destruction in vitiligo. Punch biopsies from depigmented vitiliginous skin (VS), normal-looking pigmented skin (PS), and marginal skin (MS) from patients with generalized vitiligo (n = 15) were labeled with K 1.2.58, OKM1 (CD11b), Leu 11b (CD16), Leu 19 (CD56), IFN-gamma receptor, IL-2 receptor (CD25), IgG, IgM, C3c, and C3d MoAbs. In addition, in vitro effects of vitiligo sera (n = 13) on human newborn melanocytes (HMel) under different culture conditions were studied. The immunohistochemical findings showed absence of K 1.2.58+ epidermal melanocytes in VS and abnormal morphology in MS. In these areas, a few CD11b+ cells in the dermis and epidermis could be detected but no significant numbers of CD16+ or CD56+ cells were seen among the mononuclear cellular infiltrate. IL-2 and IFN-gamma receptors were clearly expressed by the cellular infiltrate. No significant deposition of complement or immunoglobulin was seen. The addition of vitiligo sera to HMel cultures induced a significant cellular proliferation. The stimulation of cell proliferation occurred regardless whether the sera were added alone or when preheated (56 degrees C for 1 hr) and then supplemented with a complement source (P < 0.01 at 2%, P < 0.001 at 10%, and P < 0.01 at 20% for sera alone) (P > 0.05 at 2%, P < 0.05 at 10%, and P < 0.01 at 20% for decomplemented sera plus complement).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1994

Evidence for a complement-mediated inhibition and an antibody-dependent cellular cytotoxicity of dermal fibroblasts in alopecia areata.

Immunological mechanisms have long been suggested to mediate hair loss in alopecia areata. In this process hair bulb melanocytes and dermal papilla fibroblasts are believed to be primarily involved. In the present study we further investigated the role of humoral factors in alopecia areata. Three different experiments were performed on normal human epidermal melanocytes as well as normal human dermal fibroblasts: (i) incubation with medium containing 2, 10, or 20% alopecia areata serum (n = 12 patients) for 16 h, (ii) incubation with medium supplemented with preheated alopecia areata serum (1 h at 56 degrees C) and healthy human fresh serum as a complement source (1:1) and (iii) incubation with 2, 10 or 20% alopecia areata serum but, in addition, containing peripheral blood mononuclear cells from healthy subjects (effector/target ratio, 50:1). As controls, normal human fibroblasts and normal human epidermal melanocyte cultures were also incubated with serum from healthy individuals (n = 5) under the same culture conditions. The results showed that alopecia areata serum exerted a significant stimulation of proliferation of both normal human fibroblasts (p > 0.05 at 2%, p > 0.05 at 10%, p < 0.05 at 20%), and normal human epidermal melanocytes (p > 0.05 at 2%, p < 0.05 at 10%, p > 0.05 at 20%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1993

Aquagenic pruritus as a presenting symptom of polycythemia vera.

A female patient was presented because of a prickling sensation that appeared shortly after warm water contact. Examination revealed no abnormality, but water exposure was followed by pruritus without any visible skin changes. Blood and bone marrow examinations revealed abnormalities typical of polycythemia vera. Skin biopsy before and after warm water challenge showed increased numbers of mononuclear cells in the papillary dermis and epidermis particularly after water exposure. Phlebotomy was associated with prompt cessation of pruritus.

Biopsy↗

PubMed1992

Nonsegmental vitiligo: decrease of the CD45RA+ T-cell subset and evidence for peripheral T-cell activation.

Peripheral T-lymphocytes from 16 randomly selected patients with nonsegmental vitiligo were labeled with monoclonal antibodies recognizing T-cell receptor (TCR) alpha/beta, TCR gamma/delta, CD3, CD4, CD8, CD45RA, CD45RO, CD11b, CD11c, CD16, CD56, CD25, CD54, and HLA-DR antigens. In comparison with matched controls, a significant decrease of the CD45RA+ subset (P less than 0.03) together with significant increase of the circulating HLA-DR+ cells (P less than 0.02) was found. No other alterations were detected. These findings may point to some autoimmune phenomena involved in the pathogenesis of the disease. The increased HLA-DR expression indicates the presence of activated peripheral T-cells. Thus, our data provide new and further evidence for T-cell dysregulation in nonsegmental vitiligo.

Adolescent↗