Monoclonal Antibody Labeling for Cytokeratins and Filaggrin in the Human Pilosebaceous Unit of Normal, Seborrhoeic and Acne Skin

Kurokawa, Ichiro; Mayer-da-Silva, Augusto; Gollnick, Harald; Orfanos, Constantin E.

doi:10.1111/1523-1747.ep12477026

Cited by 80 publications

(67 citation statements)

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“…In the normal pilosebaceous unit, CK and filaggrin expression has been reported previously (10)(11)(12). CK1 and 10 are detected in suprabasal layers in the epidermis and follicular infundibulum.…”

Section: ------------------------------------------------------------mentioning

confidence: 62%

Cutaneous dermoid cyst: Cytokeratin and filaggrin expression suggesting differentiation towards follicular infundibulum and mature sebaceous gland

Kurokawa

Nishimura²,

Hakamada³

et al. 2006

Oncol Rep

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Abstract. We experienced two cases of cutaneous dermoid cysts (DC). To elucidate the histogenesis of DC, we have studied cytokeratin (CK) expression in DC using ten different anti-keratin antibodies against CK1,7,8,10,14, 15, 16, 17, 18 and 19, antibody. In the cyst wall of DC, CK1 and 10 were expressed in suprabasal layer, and CK14 was limited to the basal layer. In sebaceous gland-like structures, CK14 was detected in sebaceous acinus, and CK17 was detected in sebaceous duct. The other CKs were not detected. Filaggrin was intensely detected in the granular layer in the cyst wall of DC. CK expression profile of DC was similar to follicular infundibulum and sebaceous gland. These results suggested that DC differentiates towards follicular infundibulum and mature sebaceous gland. IntroductionCutaneous dermoid cysts result from the sequestration of cutaneous tissue along lines of embryonic fusion (1). DC in the periorbital area, midline of the neck, nasal root, forehead, mastoid area and the scalp have been reported (2). DCs of the auricle are very rare (3). The histogenesis of DC still remains unclear.CK is an essential marker to evaluate the origin of epithelial tumors (4). Besides CK, filament aggregating protein (filaggrin), a histidine-rich phosphorylated basic protein of major constituents of keratohyaline granules, is a marker of terminal differentiation of epidermis (5). No immunohistochemical study of CK and filaggrin in DC has been reported.To elucidate the histogenesis of DC, we studied CK and filaggrin expression in DC using ten different anti-keratin antibodies against CK1,7,8,10,14, 15, 16, 17, 18 and 19, and anti-filaggrin antibody. Materials and methodsThe patient, a 48-year-old male had DC located on the left postauriclar area from at birth. The other patient, a 31-yearold female developed DC on the right postauriclar area ten years ago. The lesions were surgically excised. Each specimen was formalin-fixed, paraffin-embedded, stained with hematoxylin and eosin, and serially-cut sections were used for the immunohistochemical study. The anti-keratin antibodies used were as follows: 34ßB4 (CK1) (6), LHP1 (CK10) (7), LL002 (CK14) (7), LHK15 (CK15) (8), LL025 (CK16) (7), E3 (CK17) (7), 5D3 (CK18) (7) and b170 (CK19) (9) (all from Novocastra Laboratories Ltd., Newcastle-upon-Tyne, UK).The immunohistochemical study was carried out with the labeled streptoavidin-biotin method (LSAB, Dako, Carpenteria, CA, USA) was performed as previous study (10). Normal skin from the auricle served as controls. ResultsHematoxylin and eosin staining. Histopathological findings of the cases were similar. The cyst wall of DC was located in the deep dermis. Cyst wall was partly ruptured, resulting in the fibrosis with vellus hairs. The cyst wall was formed with keratinizing epithelium in granular layers. The keratinizing epithelium partly projected into the lumen-like crenulation. Thick laminated corneocytes were observed. In the vicinity of the cyst wall, sebaceous gland-like structure was observed (Fig. 1).Immunohistochem...

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Section: ------------------------------------------------------------mentioning

confidence: 62%

Cutaneous dermoid cyst: Cytokeratin and filaggrin expression suggesting differentiation towards follicular infundibulum and mature sebaceous gland

Kurokawa

Nishimura²,

Hakamada³

et al. 2006

Oncol Rep

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“…167 In sebaceous cells of seborrheic skin immunostaining with an antibody specific for keratins K7, K16, K17 and K19 increased from undifferentiated to mature cells. 154 Increased expression of K17 could be detected in sebaceous glands and sebaceous ducts of uninvolved skin of acne patients, although sebaceous glands showed heterogeneity in keratin expression, with some lobules expressing keratins K1, K5, K7, K10, K14 and K17. 155 Inhibiton of the ectopeptidases dipeptidyl peptidase IV and aminopeptidase N on human sebocytes induced IL-1ra and slightly decreased total neutral lipid production, suppressed proliferation of sebocytes and enhanced terminal differentiation.…”

Section: Interleukin-1α and Sebocyte Activationmentioning

confidence: 93%

“…Expression of K6, K16 and K17 has been detected with cytokeratin-specific antibodies in infundibular epithelial cells, sebaceous duct cells and differentiated sebaceous cells of normal controls and acne patients. 154 In comparison to controls, acne patients exhibited an increased filaggrin expression. 155 In the comedone wall an increased suprabasal expression of K6 and K16, and panepithelial expression of K17 could be demonstrated.…”

Section: Ser252trp-fgfr2-mutation and Comedogenesismentioning

confidence: 99%

Role of FGFR2-signaling in the pathogenesis of acne

Melnik

2009

Dermato-Endocrinology

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It is the purpose of this review to extend our understanding of the fibroblast growth factor (FGF) receptor-2b-signaling network in the pathogenesis of acne. A new concept of the role of FGFR2b-signaling in dermal-epithelial interaction for skin appendage formation, pilosebaceous follicle homeostasis, comedogenesis, sebaceous gland proliferation and lipogenesis is presented. The FGFR2-gain-of-function mutations in Apert syndrome and unilateral acneiform nevus are most helpful model diseases pointing the way to androgen-dependent dermalepithelial FGFR2-signaling in acne. Androgen-mediated upregulation of FGFR2b-signaling in acne-prone skin appears to be involved in the pathogenesis of acne vulgaris. In organotypic skin cultures, keratinocyte-derived interleukin-1α stimulated fibroblasts to secrete FGF7 which stimulated FGFR2b-mediated keratinocyte proliferation. Postnatal deletion of FGFR2b in mice resulted in severe sebaceous gland atrophy. The importance of FGFR2b in sebaceous gland physiology is further supported by the mode of action of anti-acne agents which have been proposed to attenuate FGFR2b-signaling. Downregulation of FGFR2b-signaling by isotretinoin explains its therapeutic effect in acne. Downregulation of FGFR2b-signaling during the first trimester of pregnancy disturbs branched morphogenesis and explains retinoid embryotoxicity. Insulin-like growth factor-1 (IGF-1), the mediator of growth hormone during puberty, intracts with androgen-dependent FGFR2b-signaling and links androgen-and FGF-mediated signal transduction important in sebaceous gland homeostasis. The search for a follicular defect in the dermalepithelial regulation of growth factor-signaling in acne-prone skin appears to be a most promising approach to clarify the pathogenesis of acne.

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“…The SD is a transitional zone between infundibulum (interfollicular epidermis) and sebocytes, suggesting that a bimodality of these cells to differentiate into both directions exists [56]. In wounds, undifferentiated ductal cells migrate to the surface and differentiate into epidermal keratinocytes, and some undergo conversion into sebocytes [57].…”

Section: Sebaceous Duct (Sd) Cells Are Bimodal Epithelial Cellsmentioning

confidence: 99%

Beyond acne: Current aspects of sebaceous gland biology and function

Zouboulis¹,

Picardo

Qiang

et al. 2016

Rev Endocr Metab Disord

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116

112

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The sebaceous gland is mostly found in association with a hair follicle. Its traditional function is the holocrine production of sebum, a complex mixture of lipids, cell debris, and other rather poorly characterized substances. Due to the gland central role in acne pathogenesis, early research had focused on its lipogenic activity. Less-studied aspects of the sebaceous gland, such as stem cell biology, the regulation of cellular differentiation by transcription factors, the significance of specific lipid fractions, the endocrine and specially the neuroendocrine role of the sebaceous gland, and its contribution to the innate immunity, the detoxification of the skin and skin aging have recently attracted the attention of researchers from different disciplines. Here, we summarize recent, multidisciplinary progress in sebaceous gland research and discuss how sebaceous gland research may stimulate the development of novel therapeutic strategies targeting specific molecular pathways of the pathogenesis of skin diseases.

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Monoclonal Antibody Labeling for Cytokeratins and Filaggrin in the Human Pilosebaceous Unit of Normal, Seborrhoeic and Acne Skin

Cited by 80 publications

References 24 publications

Cutaneous dermoid cyst: Cytokeratin and filaggrin expression suggesting differentiation towards follicular infundibulum and mature sebaceous gland

Cutaneous dermoid cyst: Cytokeratin and filaggrin expression suggesting differentiation towards follicular infundibulum and mature sebaceous gland

Role of FGFR2-signaling in the pathogenesis of acne

Beyond acne: Current aspects of sebaceous gland biology and function

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