Effects of Pemphigus Antibody on the Regeneration of Cell-Cell Contact in Keratinocyte Cultures grown in Low to Normal Ca+ + Concentration

Kitajima, Yasuo; Inoue, S; Yaoita, Hideo

doi:10.1111/1523-1747.ep12470554

Cited by 82 publications

(54 citation statements)

References 24 publications

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“…Western immunoblotting previously revealed that human keratinocyte DJM-1 cells (Kitajima et al, 1987) expressed 90-kDa T-cadherin protein (Zhou et al, 2002). We used a commercially available antibody in the previous Western immunoblotting.…”

Section: Resultsmentioning

confidence: 99%

Loss of T-Cadherin (CDH13, H-Cadherin) Expression in Cutaneous Squamous Cell Carcinoma

Takeuchi

Liang

Matsuyoshi

et al. 2002

Laboratory Investigation

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SUMMARY:We previously reported that T-cadherin (CDH13, H-cadherin), a unique cadherin molecule, was expressed on the basal cell layer in normal murine and human epidermis. In the present study, T-cadherin expression in archival human skin specimens comprising a spectrum of human squamous cell neoplasia was investigated. T-cadherin expression was observed in both normal epidermal basal cells and adnexal epithelial cells of formalin-fixed and paraffin-embedded tissue sections. Western immunoblotting also revealed that mature T-cadherin protein was expressed in cultured human skin tissue equivalent. Atypical keratinocytes in 27 of 53 specimens of actinic keratosis and 23 of 30 specimens of Bowen's disease expressed T-cadherin. In contrast, T-cadherin was focally expressed in 6 of 56 invasive cutaneous squamous cell carcinomas. To explore the molecular mechanism of down-regulation of T-cadherin expression in invasive squamous cell carcinoma, loss of heterozygosity, genetic alternations, and methylation status in the 5Ј region of the T-cadherin gene were investigated. Loss of heterozygosity at intron 1 of the T-cadherin gene was observed in 8 of 28 informative cases of invasive squamous cell carcinoma. Although no structural genomic alternations were found by sequence analysis, aberrant promoter methylation of the T-cadherin gene was found in 12 of 28 invasive squamous cell carcinomas. T-cadherin expression was restored in cultured A431 cells, in which aberrant methylation was found by treatment with the demethylating agent 5Ј-aza-2-deoxycytidine. These findings suggest that a combination of deletion and aberrant methylation of the T-cadherin gene may play a role in loss of gene expression in a considerable number of invasive cutaneous squamous cell carcinomas. (Lab Invest 2002, 82:1023-1029.

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Section: Resultsmentioning

confidence: 99%

Loss of T-Cadherin (CDH13, H-Cadherin) Expression in Cutaneous Squamous Cell Carcinoma

Takeuchi

Liang

Matsuyoshi

et al. 2002

Laboratory Investigation

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“…In addition to interfering with the function of desmosomes, Pab exhibit a more general effect on KC manifested by rearrangement of the cytoskeleton and adhesive units [10]. Electron-microscopic studies of patients’ skin showed that retraction of tonofilaments precedes disappearance of desmosomes [11], indicating that disruption of desmosomal bridges is secondary to shrinkage of KC.…”

Section: Acantholytic Activity Of Pab Harbors Pharmacologic Effects Omentioning

confidence: 99%

Autoimmunity to Keratinocyte Acetylcholine Receptors in Pemphigus

Grando¹

2000

Dermatology

120

106

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Pemphigus autoimmunity is not limited to antides- moglein antibodies. Nondesmoglein antibodies induce pemphigus-like lesions in neonatal mice. Acantholytic activity of pemphigus IgG harbors pharmacologic effects on keratinocyte shape and adhesion. Acantholytic antireceptor autoantibodies target: (1) a novel human α9 acetylcholine receptor regulating keratinocyte adhesion, and (2) pemphaxin, a novel keratinocyte annexin-like molecule binding acetylcholine. A ‘multiple-hit’ hypothesis reconciles recent findings of anti-acetylcholine-receptor autoimmunity in pemphigus and the fact that pemphigus patients also develop autoantibodies to adhesion molecules. The antiacantholytic activity of cholinergic agonists suggests a novel avenue for the development of a nonhormonal treatment of pemphigus.

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“…DJM-1 cells, a human squamous cell carcinoma cell line (Kitajima et al, 1986(Kitajima et al, , 1987, were cultured in s-MEM (Life Technologies, Inc.) supplemented with 10% (v/v) Ca 2+ -chelated fetal bovine serum (IS-Japan, Tokyo, Japan), 84 ng/ml choleratoxin (Life Technologies, Inc.) and 0.4 mg/ ml hydrocortisone (Sigma) and CaCl2 (the final Ca 2+ concentration of the medium was adjusted to 0.09 mM). Cells were cultured on 24´24 mm glass coverslips (Matsunami Glass Co. Tokyo, Japan) for immunofluorescent microscopy in 35 mm cell culture dishes (Becton-Dickinson and Co., Franklin Lakes, NJ, USA) and 100 mm cell culture dishes (Corning Costar Corp., Cambridge, MA, USA) for biochemical study in 37°C CO2-incubator.…”

Section: Cellsmentioning

confidence: 99%

Scraped-Wounding Causes Activation and Association of C-Src Tyrosine Kinase with Microtubules in Cultured Keratinocytes.

Yamada¹,

Aoyama²,

Owada³

et al. 2000

Cell Struct. Funct.

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ABSTRACT. In order to elucidate the function of c-Src in keratinocytes, we studied the intracellular distribution of its active and inactive form in cultured normal human keratinocyte, using anti-c-Src monoclonal antibody clone 28, which recognizes the active form of c-Src (dephosphorylated at COOH-terminal residue Tyr 530), and monoclonal antibody clone 327 which recognizes both active and inactive forms. Since c-Src has been suggested to be involved in the control of cell adhesion in other cells, we produced a dynamic condition of cell migration by cutting culture cell colonies into squares to form a mesh pattern with a blade (culture wound model). Before cutting, the active form was expressed in cells located only at the periphery of colonies or isolated migrating cells, and was associated with microtubules. Wounding the colony generated a dramatic and rapid activation of c-Src in a few rows of cells along the cut edges, which were made even at the middle of colony, resulting in the association of the active form with microtubules. This increase of the active form was also detected by immunoblotting of cell extracts. These reactions were inhibited by 1 mM sodium orthovanadate, a protein-tyrosine phosphatase inhibitor. ST 638, a potent Src family tyrosine kinase inhibitor, inhibited the migration of keratinocytes in the culture wound healing model. These results suggest that wounding the culture causes activation of c-Src in keratinocytes, and thus activated c-Src may play a role in the function of microtubules during cell migration, especially at an early stage of wound healing.Key words: c-Src/keratinocyte/wound healing/microtubules During wound healing, keratinocytes (KCs) must dynamically regulate cell-cell contacts and cytoskeletons in order to migrate to and cover the surface of the wound. Major cell-cell contacts between KCs are adherens junctions and desmosomes, the former of which are specifically associated with actin microfilaments and the latter with keratin-intermediate filaments. The intercellular contacts of adherens junctions are mediated in a homotypic manner with Ecadherin (Takeichi, 1991), and linked to actin filaments via vinculin, =-actinin, =-catenin, >-catenin, plakoglobin and P120-Cas (Kam et al., 1995;Tsukita et al., 1992;Reynolds et al., 1992Reynolds et al., , 1994Reynolds et al., , 1996. Increase in tyrosine phosphorylation of >-catenin, plakoglobin and P120-Cas, which are known as substrate of c-Src, has been shown to be correlated with decrease of cell adhesion, which is one of the typical characteristics of neoplastic transformation (Matsuyoshi et al., 1992; Behrens et al., 1993;Hamaguchi et al., 1993;Papkoff, 1997). The regulation of cell-cell contacts is thought to be one of the most important events for KCs to cover the wound surface (Grinnell, 1990), and the following differentiation. Therefore, it is of potential importance to clarify the intracellular signaling mechanisms involved in wound healing in skin.Src is a non receptor type tyrosine kinase, which is widely expressed ...

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Effects of Pemphigus Antibody on the Regeneration of Cell-Cell Contact in Keratinocyte Cultures grown in Low to Normal Ca+ + Concentration

Cited by 82 publications

References 24 publications

Loss of T-Cadherin (CDH13, H-Cadherin) Expression in Cutaneous Squamous Cell Carcinoma

Loss of T-Cadherin (CDH13, H-Cadherin) Expression in Cutaneous Squamous Cell Carcinoma

Autoimmunity to Keratinocyte Acetylcholine Receptors in Pemphigus

Scraped-Wounding Causes Activation and Association of C-Src Tyrosine Kinase with Microtubules in Cultured Keratinocytes.

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