Genes Encoding Structural Proteins of Epidermal Cornification and S100 Calcium-Binding Proteins Form a Gene Complex (“Epidermal Differentiation Complex”) on Human Chromosome 1q21

Mischke, Dietmar; Korge, Bernhard; Marenholz, Ingo; Volz, Armin; Ziegler, Andreas

doi:10.1111/1523-1747.ep12338501

Cited by 466 publications

(365 citation statements)

References 26 publications

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“…We investigated the role of airway epithelial integrin α v β 6 -mediated autocrine TGF-β in promoting the expression of a panel of 6 genes that were differentially expressed during serial passage and that include members of gene clusters on chromosome 1q21 known as the epidermal differentiation complex (EDC) ( Table 1 and http://www.ncbi.nlm.nih.gov/geo/, series accession GSE7557; IVL, DSC2, SPRR1A, SPRR1B, SPRR3, S100A7) (42,43). Neutralizing anti-β 6 decreased the transcript expression of all 6 tested members of the EDC ( Figure 7D).…”

Section: Il-1β-dependent Increase In α V β 8 -Mediated Activation Of mentioning

confidence: 99%

“…Densitometry values were normalized to β-actin, and the results were expressed as fold decrease (± SE) relative to control antibody-treated cells where a value of 1 represents no change from control antibody-treated cells. *P < 0.05 (D) P2 human bronchial epithelial cells in 2D culture were treated with control antibody or neutralizing anti-β6, and total RNA was harvested and assessed for the EDC genes (42,43), involucrin (IVL), desmocollin-2 (DSC2), small proline rich protein-1A (SPRR1A), -1B (SPRR1B) (n = 3), -3 (SPRR3), or S100A7 (n = 2) using realtime PCR. Shown is the fold reduction (log 10) in expression of EDC genes after treatment with anti-β6 compared with control antibody-treated samples.…”

Section: Figurementioning

confidence: 99%

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Squamous metaplasia amplifies pathologic epithelial-mesenchymal interactions in COPD patients

Araya¹,

Cambier²,

Markovics³

et al. 2007

J. Clin. Invest.

232

228

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Squamous metaplasia (SM) is common in smokers and is associated with airway obstruction in chronic obstructive pulmonary disease (COPD). A major mechanism of airway obstruction in COPD is thickening of the small airway walls. We asked whether SM actively contributes to airway wall thickening through alteration of epithelial-mesenchymal interactions in COPD. Using immunohistochemical staining, airway morphometry, and fibroblast culture of lung samples from COPD patients; genome-wide analysis of an in vitro model of SM; and in vitro modeling of human airway epithelial-mesenchymal interactions, we provide evidence that SM, through the increased secretion of IL-1β, induces a fibrotic response in adjacent airway fibroblasts. We identify a pivotal role for integrin-mediated TGF-β activation in amplifying SM and driving IL-1β-dependent profibrotic mesenchymal responses. Finally, we show that SM correlates with increased severity of COPD and that fibroblast expression of the integrin α v β 8 , which is the major mediator of airway fibroblast TGF-β activation, correlated with disease severity and small airway wall thickening in COPD. Our findings have identified TGF-β as a potential therapeutic target for COPD.

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Section: Il-1β-dependent Increase In α V β 8 -Mediated Activation Of mentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Squamous metaplasia amplifies pathologic epithelial-mesenchymal interactions in COPD patients

Araya¹,

Cambier²,

Markovics³

et al. 2007

J. Clin. Invest.

232

228

View full text Add to dashboard Cite

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“…6). S100 proteins are therefore involved in the process of terminal differentiation of human epidermis and have been implicated in cancer as altered expression levels of several S100 proteins have been reported to correlate with tumor differentiation including ESCCs (7)(8)(9)(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer

Chen

Sunkel

et al. 2013

Molecular Cancer Research

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Aberrant keratinocyte differentiation is a key mechanism in the initiation of cancer. Because activities regulating differentiation exhibit altered or reduced capacity in esophageal cancer cells, it is vital to pinpoint those genes that control epidermal proliferation and terminal differentiation to better understand esophageal carcinogenesis. S100A14 is a member of the S100 calcium-binding protein family and has been suggested to be involved in cell proliferation, apoptosis, and invasion. The present study used immunohistochemistry analysis of S100A14 in clinical specimens of esophageal squamous cell carcinoma (ESCC) to show that decreased S100A14 is strongly correlated with poor differentiation. Furthermore, both mRNA and protein expression of S100A14 was drastically increased upon 12-O-tetra-decanoylphorbol-13-acetate (TPA) and calcium-induced esophageal cancer cell differentiation. Overexpression of S100A14 resulted in a G 1 -phase cell cycle arrest and promoted calcium-inhibited cell growth. Conversely, decreasing S100A14 expression significantly promoted G 1 -S transition and prevented the morphologic changes associated with calcium-induced cell differentiation. Molecular investigation demonstrated that S100A14 altered the calcium-induced expression of late markers of differentiation, with the most prominent effect on involucrin (IVL) and filaggrin (FLG). Finally, it was determined that S100A14 is transcriptionally regulated by JunB and that S100A14 and JunB status significantly correlated in ESCC tissue. In summary, these data demonstrate that S100A14 is transcriptionally regulated by JunB and involved in ESCC cell differentiation.

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“…S100 proteins S100 proteins constitute an extensive family of AMPs/HDPs characterized by the presence of two calcium-binding EF-hand motifs. Twenty-one types of S100 proteins have been identified, and the majority of these proteins (13 members) are located in the epidermal differentiation complex region, which also encodes various members of epidermal differentiation markers 51) . These proteins expressed in the epidermis have been involved in the pathology of various skin diseases 52) .…”

Section: Human Cathelicidin Ll-37mentioning

confidence: 99%

Novel Insight Into the Role of Antimicrobial (Host Defense) Peptides/Proteins in Human Skin Diseases

Niyonsaba

2016

Juntendo Medical Journal

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In addition to functioning as a physical barrier, the skin has evolved several innate defense mechanisms for the rapid recognition of and protection against harmful microorganisms. As a part of this process, the skin releases a vast and powerful arsenal of antimicrobial peptides/proteins (AMPs), also called host defense peptides/proteins (HDPs), which are key players in the cutaneous immune system. Although originally named antimicrobial peptides, recent evidence has demonstrated that AMPs/HDPs play additional roles in orchestrating the adaptive immune response, such as the regulation of inflammation, induction of cell proliferation and differentiation, regulation of cytokine/chemokine production, facilitation of cell migration, promotion of wound healing and regulation of tight junction barriers. Additionally, numerous skin diseases show altered expression of AMPs/HDPs in the lesional skin, suggesting the crucial roles of these molecules in the pathophysiology of skin diseases. The purpose of this review is to describe the current knowledge regarding some of the most common and well-known AMPs/HDPs derived from the skin, to discuss the regulation of their expression and their antimicrobial and immunomodulatory functions, and to outline their roles in various skin diseases. We believe that understanding the basic knowledge of skin-derived AMPs/HDPs would provide new insight into the pathophysiology of skin disorders and offer novel therapeutic opportunities for skin infectious diseases.

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Genes Encoding Structural Proteins of Epidermal Cornification and S100 Calcium-Binding Proteins Form a Gene Complex (“Epidermal Differentiation Complex”) on Human Chromosome 1q21

Cited by 466 publications

References 26 publications

Squamous metaplasia amplifies pathologic epithelial-mesenchymal interactions in COPD patients

Squamous metaplasia amplifies pathologic epithelial-mesenchymal interactions in COPD patients

S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer

Novel Insight Into the Role of Antimicrobial (Host Defense) Peptides/Proteins in Human Skin Diseases

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