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J J Rijzewijk

Publications and source records attributed to J J Rijzewijk.

8 recordsLinked to original sources
PubMed1992

Cell kinetics in skin disorders with disturbed keratinization.

A relatively simple immunohistochemical method was developed and used on cryostat sections. The monoclonal antibody Ki67 was used as marker for actively cycling cells and Pab601 for germinative cells. Counts were expressed as Ki67- or Pab601-positive cells/mm. In order to improve our understanding of the pathogenetic mechanisms in skin disorders with disturbed keratinization we have measured cell kinetic values in dyskeratosis follicularis, pemphigus benigna familiaris chronica, autosomal dominant ichthyosis vulgaris, X-linked recessive ichthyosis, atopic dermatitis and psoriasis and compared them with previous values derived with autoradiography using tritiated thymidine. The results showed that microscopical acanthosis is related to an increase of the germinative population, while the increased epidermal turnover is associated with increased numbers of cycling cells. The cell kinetic changes seem to be all secondary except in psoriasis where a dysregulation in the epidermal growth may cause the epidermal changes. This simple method allows quick evaluation of drug efficacy which might be useful in atopic dermatitis and psoriasis.

Cell Count↗
PubMed1989

A sequential double immunoenzymic staining procedure to obtain cell kinetic information in normal and hyperproliferative epidermis.

A sequential double immunoenzymic staining procedure was developed using the monoclonal antibody anti-BrdUrd and Ki67 in order to determine whether hyperproliferative skin disorders, such as psoriasis, are characterized by an increased growth fraction rather than a much shorter cell cycle time of all germinative cells. Ki67 binds to a proliferation-associated nuclear antigen in a variety of human cell types, and anti-BrdUrd can be used to identify DNA-synthesizing cells. Although in hyperproliferative epidermis the absolute numbers of BrdUrd-positive cells as well as Ki67-positive cells were grossly increased, the ratio of these values was not changed compared to the ratio found in the epidermis of the clinically uninvolved skin of psoriatic patients and in normal epidermis. This suggests an increased growth fraction in hyperproliferative epidermis. Our data show that immunohistochemical double-staining techniques can be a valuable tool in the study of cell cycle kinetics in epithelial tissues.

Antibodies, Monoclonal↗
PubMed1989

Topical corticosteroids delay the proliferative response to sellotape stripping.

Tape stripping of normal human skin results in a hyperproliferative response brought about by a recruitment of resting (G0) cells. The effect of diprosone and hydrocortisone on this response was studied by flow cytometric techniques. Both corticosteroids were found to delay the appearance of the cohort of recruited cells in the S-phase, the more potent antipsoriatic (diprosone) giving the greatest delay. These data indicate that corticosteroids cause a temporary block in late G1 or an inhibition of the recruitment process itself. The model may serve for the evaluation of (future) antipsoriatic drugs.

Administration, Topical↗
PubMed1989

Flow cytometric analysis of epidermal subpopulations from normal and psoriatic skin using monoclonal antibodies against intermediate filaments.

Keratin-type intermediate filament proteins show characteristic expression in normal and pathologic epidermis. Some keratins are restricted to the basal cell layers, and others occur exclusively in the suprabasal compartment. SDS-gel-electrophoresis and immunohistochemistry are generally used for the assessment of keratin profiles and their localizations. In the present investigation, flow cytometric analysis of four different monoclonal antibodies (MAb) against intermediate filament-type proteins, in addition to measurement of relative DNA content, was performed on cell suspensions derived from lesional and clinically uninvolved skin of psoriatic patients and from skin of healthy controls. MAb Ks8.12, reacting with keratins 13 and 16, was used as a marker for hyperproliferation. Pab601 recognizes the basal cell layer(s) of human epidermis. Keratin 10 expression as a marker of keratinization was quantified with RKSE60 and the anti-vimentin MAb MVI was used as a marker for non-keratinocytes. Psoriatic skin showed significantly reduced numbers of RKSE60-positive cells and MVI-positive cells compared with normal skin. In contrast to normal skin and uninvolved skin of psoriatic patients in which only a minority of the cells were Ks8.12 positive, up to 60% of the cell population in psoriatic lesions bound with MAb. Simultaneous measurement of relative DNA content and MAb binding showed that Pab601 binding was associated with cells in S-phase and G2M-phase of the cell cycle, whereas RKSE60 and Ks8.12 binding were associated with diploid cells. Multiparameter flow cytometry allows quantitative population analysis that could lead to a better understanding of the complex mechanisms of epidermal growth control under normal and pathologic conditions.

Adult↗
PubMed1989

Two binding sites for Ki67 related to quiescent and cycling cells in human epidermis.

The monoclonal antibody Ki67 (Ki67) binds to a nuclear antigen expressed by cycling cells of several human tissues and to the cytoplasm of the basal layer cells of squamous epithelia. We have used an immunohistochemical method to visualize the binding sites of Ki67 in normal and hyperproliferative epidermis. Cytoplasmic staining was present in the basal layer cells of normal epidermis, but was decreased in psoriatic and post-tapestripping epidermis. In sections of normal epidermis only a small minority of nuclei were positive, but sections of psoriatic epidermis and epidermis 40 and 48 h after tapestripping showed large numbers of positive nuclei in the basal and suprabasal layers. Since recent reports strongly suggest that the cell production rate is regulated by changes in the number of cycling cells, the hypothesis that Ki67 binds also in human epidermis to the nuclei of cycling cells is supported by the present findings.

Antibodies, Monoclonal↗
PubMed1988

Recruitment of quiescent (G0) cells following epidermal injury is initiated by activation of the phosphoinositol cycle.

Under normal circumstances, the rate of production of new cells by the epidermis is rather low, but injury results in a burst of mitotic activity that continues until repair is complete. It is now recognized that most cells of the germinative population are in a resting (G0) state, and "postinjury cell renewal" is the consequence of G0 cells entering the mitotic cycle. The biochemical events triggering this process, however, are unknown. Here we show that phorbol myristate acetate (PMA) is able to induce G0 mobilization in the epidermis of the nude mouse. Further, we demonstrate that amiloride (an inhibitor of the membrane Na+-H+ pump), applied topically to human skin, abolishes almost completely the regenerative response after experimental injury. We suggest that activation of the phosphoinositol cycle may initiate recruitment of G0 cells in the epidermis.

Adult↗
PubMed1988

Synchronized growth in human epidermis following tape-stripping: its implication for cell kinetic studies.

A recent investigation of the hyperproliferative activity of human epidermis following sellotape stripping showed a wave of cell divisions with a maximal percentage of cells in mid-S phase at about 39 h after stripping. Here we present a study over the period of 52-76 h following stripping, showing a second wave of cell divisions with a maximal percentage of cells in mid-S at about 63 h. This indicates an average cell cycle time of about 23 h. Human epidermis after tape-stripping provides us with a useful model of synchronized growth, allowing us to study drug influences on cell kinetics accurately.

Cell Cycle↗