Preliminary findings on levels of collagenase and its tissue inhibitor in some vulval dystrophies

Barnes, Colin; Douglas, Charles P

doi:10.3109/01443618509079141

Cited by 6 publications

(3 citation statements)

References 6 publications

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“…This discrepancy in TIMP activity may contribute to local invasion of this tumor and it could also occur in LS. Vulvar LS cultured cells also showed increased collagenase inhibitor levels [14], confirming our results. MMPs and TIMPs are activated in the extracellular environment and are found predominantly in the active form in ECM [25,26].…”

Section: Commentsupporting

confidence: 90%

“…system [9], and the diminution of CD44 expression [13] confirms that changes in cell-cell and cell-ECM interactions followed by catabolism of these ECM components, occur in LS tissue. Nevertheless, little is known about the ECM remodeling system in LS [7,14,15]. Here, we analyzed the expression of collagenases, MMP-1 and MMP-13, the gelatinases, MMP-2 and MMP-9, the tissue inhibitors, TIMP-1 and TIMP-2, and also the immunohistochemistry distribution of MMP-2, MMP-9, TIMP-1 and TIMP-2 in vulvar biopsies from patients with LS.…”

Section: Introductionmentioning

confidence: 99%

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Metalloproteinases 2 and 9 and their tissue inhibitors 1 and 2 are increased in vulvar lichen sclerosus

Oliveira

Almeida

Soares

et al. 2012

European Journal of Obstetrics & Gynecology and Reproductiv

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Section: Commentsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Metalloproteinases 2 and 9 and their tissue inhibitors 1 and 2 are increased in vulvar lichen sclerosus

Oliveira

Almeida

Soares

et al. 2012

European Journal of Obstetrics & Gynecology and Reproductiv

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“…While there is still debate about whether lichen sclerosus is a primary connective tissue or immunologic disorder, there is a welter of evidence implicating the immune system in its pathogenesis (41)(42)(43) . Thus, a predominantly T-lymphocyte predominant infiltrate, vacuolar degeneration of the basal layer, which is shared by other immunologically mediated disorders such as lichen planus, erythema multiforme, lupus erythematosis, and graft vs. host disease, increased number of epidermal Langerhan's cells, increased cytokine expression, and good response to corticosteroids have been observed (44)(45)(46) .…”

Section: Immunogenetic Mechanismsmentioning

confidence: 99%

Does lichen sclerosus play a central role in the pathogenesis of human papillomavirus negative vulvar squamous cell carcinoma? The itch-scratch-lichen sclerosus hypothesis

Scurry¹

1999

Int J Gynecol Cancer

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In the past decade, two types of vulvar squamous cell carcinoma (SCC) have been delineated, Human papillomavirus (HPV) positive and negative. Clinicopathologic, virologic, cytomorphometric, and genetic differences support the view that these two types of carcinoma are fundamentally different and that HPV‐negative carcinoma is not simply carcinoma where viral DNA has not been able to be identified. The traditional view of HPV‐negative carcinoma is that it is caused by chronic tissue damage from itching and scratching. However, itching and scratching alone do not explain the close association of carcinoma with lichen sclerosus, nor the absence of such an association with other itchy conditions such as eczema or psoriasis. These observations point to a role for lichen sclerosus in the pathogenesis of vulvar carcinoma. Most observations about the etiology of lichen sclerosus can be grouped into its immunogenetic or genital predisposition, or the Köbner phenomenon. In the itch‐scratch‐lichen sclerosus hypothesis, lichen sclerosus is postulated to occur as a Köbner phenomenon in women with the susceptible immunophenotype who scratch because of genital irritants such as urine, vaginal secretions and smegma, and psychological factors. Lichen sclerosus, itself a very itchy condition, contributes to a vicious cycle of itching and scratching which leads to superimposed lichen simplex chronicus, squamous cell hyperplasia, and ultimately carcinoma. The itch‐scratch‐lichen sclerosus hypothesis reconciles the traditional itch‐scratch hypothesis with the strong clinicopathologic association of lichen sclerosus with carcinoma.

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Direct measurement of collagenase in colonic anastomosis

Chowcat

Savage

Lewin

et al. 1990

Journal of British Surgery

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Collagenase has been implicated in colonic anastomotic dehiscence but the enzyme has not previously been specifically measured in colonic healing. A 72 h tissue culture method for colonic tissue and a radiochemical assay for collagenase were adapted to measure the enzyme in healing rabbit colon, with specificity of the assay confirmed by sodium dodecylsulphate polyacrylamide gel electrophoresis. Normal and postoperative colon secreted collagenase, predominantly in a latent form, in the first 24 h of culture. Total activity reached a plateau after 48 and 72 h in culture, when 50-70 per cent of the enzyme was in an active form. At these times in culture, activity was significantly higher than after 24 h (P less than 0.001). One day after anastomosis the total amount of collagenase secreted in culture was higher than normal but the increase did not achieve significance. Three days after anastomosis the colon secreted more collagenase than explants from 1 day postoperative tissue (P less than 0.002). The proportion of active enzyme in the first 24 h in culture was also increased. Since active collagenase can be measured in culture medium from both normal and postoperative colon, the tissue may be secreting plasminogen activator which allows plasmin to activate the enzyme. The increase in collagenase after operation coincided with a decrease in collagen concentration in the colon wall, measured by hydroxyproline. This supports previous suggestions that collagenase contributes to anastomotic dehiscence. However, the findings must be interpreted with caution as the variance of the results was shown to be predominantly due to time in culture, suggesting this could be a bigger influence than the operation itself. In addition, our previously reported immunohistochemical study of this system indicated that collagenase only occurred in a localized region, restricted to the everted portion of the anastomosis, with the activity being tightly controlled by its inhibitor, tissue inhibitor of metalloproteinases.

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Preliminary findings on levels of collagenase and its tissue inhibitor in some vulval dystrophies

Cited by 6 publications

References 6 publications

Metalloproteinases 2 and 9 and their tissue inhibitors 1 and 2 are increased in vulvar lichen sclerosus

Metalloproteinases 2 and 9 and their tissue inhibitors 1 and 2 are increased in vulvar lichen sclerosus

Does lichen sclerosus play a central role in the pathogenesis of human papillomavirus negative vulvar squamous cell carcinoma? The itch-scratch-lichen sclerosus hypothesis

Direct measurement of collagenase in colonic anastomosis

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