Behaviour of laminin 1 and type IV collagen in uninvolved psoriatic skin. Immunohistochemical study using confocal laser scanning microscopy

Mondello, Maria Rita; Magaudda, Ludovico; Pergolizzi, Simona; Santoro, A; Vaccaro, Mario; Califano, L.; Cannavò, Serafinella Patrizia; Guarneri, Biagio

doi:10.1007/s004030050097

Cited by 17 publications

(32 citation statements)

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“…The enhanced EDA þ fibronectin production that we observed in the psoriatic nonlesional ex vivo culture could reflect an inherent abnormality of psoriatic keratinocytes, or it could be the result of an altered regulatory extracellular milieu. The latter is supported by observations showing alterations in the basement membrane in non-lesional psoriatic skin and MMP-2 overexpression by non-lesional keratinocytes (Mondello et al, 1996;Fleischmajer et al, 2000;Vaccaro et al, 2002).…”

Section: Discussionmentioning

confidence: 58%

Proliferating Keratinocytes Are Putative Sources of the Psoriasis Susceptibility-Related EDA+(Extra Domain A of Fibronectin) Oncofetal Fibronectin

Széll

Bata‐Csörgő

Koreck

et al. 2004

Journal of Investigative Dermatology

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The extra domain A of fibronectin (EDA+ oncofetal isoform of fibronectin was recently reported to be overexpressed in psoriatic uninvolved epidermis. It has been proposed that the abnormal presence of EDA+ oncofetal protein at the dermal-epidermal junction in the uninvolved skin may provide the "psoriatic" environment in which keratinocytes are in a preactivated state with regard to mitogenic signals (e.g., T cell lymphokines). To determine the possible sources of cellular fibronectin in the non-lesional psoriatic skin, we aimed to investigate whether keratinocytes could produce the EDA+ oncofetal form of fibronectin. RT-PCR studies revealed that both cultured normal keratinocytes and HaCaT cells express the EDA+ splice variant of fibronectin mRNA, and in HaCaT cells the EDA+/EDA- transcript ratio was elevated compared with normal keratinocytes. Cultured keratinocytes and HaCaT cells showed intracytoplasmic staining with an EDA+ fibronectin-specific antibody and among the positively stained cells many showed mitosis. Using RT-PCR, western blot analysis, and flow cytometry, we showed that in synchronized HaCaT cells the amount of both total fibronectin and its EDA+ isoform change with the proliferation/differentiation state of HaCaT cells and peak in highly proliferating cells. We show that in short-term ex vivo cultures, a small population of EDA+ fibronectin containing cell population appear among psoriatic uninvolved, but not normal epidermal cells. We also demonstrate that cell attachment has a strong influence on the expression of both total and EDA+ fibronectin. Our results suggest that proliferating keratinocytes could be the sources of the psoriasis susceptibility-related EDA+ oncofetal fibronectin in the epidermis.

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Section: Discussionmentioning

confidence: 58%

Proliferating Keratinocytes Are Putative Sources of the Psoriasis Susceptibility-Related EDA+(Extra Domain A of Fibronectin) Oncofetal Fibronectin

Széll

Bata‐Csörgő

Koreck

et al. 2004

Journal of Investigative Dermatology

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“…Previous studies suggested that cell adhesion of keratinocytes may be altered in psoriasis and these changes may involve cell-cell and cell-matrix interactions. These studies showed decreased adhesiveness between keratinocytes (22) and alterations of the BM at the epidermal-dermal interface (23). Moreover, many of the factors inducing angiogenesis are also known as regulators of MMP gene expression (VEGF, TNFa) (24)(25).…”

mentioning

confidence: 98%

Vegf is Likely a Key Factor in the Link between Inflammation and Angiogenesis in Psoriasis: Results of an Immunohistochemical Study

Simonetti

Lucarini²,

Goteri

et al. 2006

Int J Immunopathol Pharmacol

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Psoriasis is a chronic skin disease, characterized by epidermal hyperplasia, inflammation, angiogenesis and vascular remodelling. An immunohistochemical study on fifteen cryosections of psoriatic skin was performed using antibodies against VEGF, HIFl-a, CD34, Factor VIII, MMP-2, MMP-9, TIMP-l and TIMP-2. Psoriatic skin showed a diffuse VEGF positive staining (13.15± 6.6), while no expression was observed in normal epidermis. No or faint HIF-la immunostaining was detected in healthy skin, while in psoriatic skin HIF-la was diffusely expressed. A positive correlation between HIF-la and VEGF was reported in psoriatic skin (r= 0.644; p=0.010). In psoriatic sections CD34 expression was significantly higher in respect to control skin (19.15 ± 12.61 vs 3.0 ± 0.23; p= 0.04), factor VIII immunostaining also demonstrated a significant increased development of the microvasculature in comparison with healthy skin (18.39 ± 8.16 vs 7.4 ± 0.20; p= 0.033). Total MMP-2 expression of healthy skin (30± 2.26) was significantly lower in respect to the MMP-2 psoriatic skin (71.5±4.13; p= 0.0001) an4-a-positive correlation was observed between VEGF and MMP-2 in psoriatic patients (r= 0.688; p= 0.046). In psoriatic skin MMP-9 expression was significantly increased in comparison to control skin (31±3.3 vs 8±6.1; p=0.007). All cases of psoriatic skin tissue showed that TIMP-2 and TIMP-l expression statistically decreased in psoriatic skin (respectively 11±1.2 and 12±1.5) in comparison with healthy skin (respectively 15±3.2 and 53±3.8; p=O.OOOI). In conclusion, we observed that VEGF overexpression correlated with HIF-la and MMP-2 expression, underlining the role of VEGF in psoriasis as a key factor in the link between inflammation and angiogenesis.Psoriasis is a chronic skin disease, characterized by epidermal hyperplasia, inflammation, angiogenesis and vascular remodelling (1-2). Microvascular changes within lesional skin include pronounced dilatation, tortuosity, increased permeability and endothelial cell proliferation within the venous limb of capillaries in the dermal papillae (3). Morphometric analysis of the vascular changes in psoriasis has shown that there is an increase in the capillary mass, compared with normal skin (4). Other studies have demonstrated that increased blood flow and tortuosity of the dermal capillary loops occur early in the progression of a lesion, before epidermal hyperplasia can be

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“…[3][4][5] LAD-1, the 120-kDa ectodomain of BP180, was originally found as an autoantigen of linear IgA bullous dermatosis (LABD), but also interacts with IgG and/or IgA antibodies in some patients with mucous membrane pemphigoid or bullous pemphigoid. 6 In this study, we present a unique case with herpetiform bullous skin lesions, which showed IgG antibodies reactive to Dsc1/Dsc3 and LAD-1, but not to Dsgs.…”

mentioning

confidence: 79%

“…5,6 This is associated with integrin expression, in keeping with 'unstable' basal keratinocytes more prone to proliferate if stimulated.…”

mentioning

confidence: 99%

Psoriasis and basement-membrane laminin

et al. 2013

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References1 Kim YH, Jensen RA, Watanabe GL et al. Clinical stage IA (limited patch and plaque) mycosis fungoides. A long-term outcome analysis. Arch Dermatol 1996; 132:1309-13. 2 Kim YH, Hoppe RT. Mycosis fungoides and the S ezary syndrome. Semin Oncol 1999; 26:276-89. 3 Agar NS, Wedgeworth E, Crichton S et al. Survival outcomes and prognostic factors in mycosis fungoides/S ezary syndrome: validation of the revised International Society for Cutaneous Lymphomas/European Organisation for Research and Treatment of Cancer staging proposal. J Clin Oncol 2010; 28:4730-9. 4 Quir os PA, Jones GW, Kacinski BM et al. Total skin electron beam therapy followed by adjuvant psoralen/ultraviolet-A light in the management of patients with T1 and T2 cutaneous T-cell lymphoma (mycosis fungoides). Int J Radiat Oncol Biol Phys 1997; 38:1027-35. 5 Kaye FJ, Bunn PA Jr, Steinberg SM et al. A randomized trial comparing combination electron-beam radiation and chemotherapy with topical therapy in the initial treatment of mycosis fungoides. N Engl J Med 1989; 321:1784-90. 6 Page V, Gardner A, Karzmark CJ. Patient dosimetry in the electron treatment of large superficial lesions. Radiology 1970; 94:635-41. 7 Rampino M, Ragona R, Monetti U et al. Total skin electron beam therapy in mycosis fungoides. Our experience from 1985 to 1999. Radiol Med 2002; 103:108-14. 8 Duvic M, Apisarnthanarax N, Cohen DS et al. Analysis of long-term outcomes of combined modality therapy for cutaneous T-cell lymphoma. J Am Acad Dermatol 2003; 49:35-49. 9 Reddy S, Parker CM, Shidnia H et al. Total skin electron beam radiation therapy for mycosis fungoides. Am J Clin Oncol 1992; 15:119-24. 10 Roberge D, Muanza T, Blake G et al. Does adjuvant alpha-interferon improve outcome when combined with total skin irradiation for mycosis fungoides? Br J Dermatol 2007; 156:57-61.Funding sources: none.Conflicts of interest: none declared.

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Behaviour of laminin 1 and type IV collagen in uninvolved psoriatic skin. Immunohistochemical study using confocal laser scanning microscopy

Cited by 17 publications

References 0 publications

Proliferating Keratinocytes Are Putative Sources of the Psoriasis Susceptibility-Related EDA+(Extra Domain A of Fibronectin) Oncofetal Fibronectin

Proliferating Keratinocytes Are Putative Sources of the Psoriasis Susceptibility-Related EDA+(Extra Domain A of Fibronectin) Oncofetal Fibronectin

Vegf is Likely a Key Factor in the Link between Inflammation and Angiogenesis in Psoriasis: Results of an Immunohistochemical Study

Psoriasis and basement-membrane laminin

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