Immunohistochemical demonstration of keratins 8 and 14 in benign tumours of the skin appendage

Tsubura, Airo; Okada, Hiyoshi; Sasaki, Masanori; Dairkee, Shanaz H.; Morii, Sotokichi

doi:10.1007/bf01606500

Cited by 35 publications

(23 citation statements)

References 13 publications

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“…This result agrees with Setterfield's report (21). CK-L is known to be immunopositive in secretory cells, such as eccrine gland (22)(23)(24). Degenerated sweat gland was shown the decreased immunoreactivity for CK-L.…”

Section: Discussionsupporting

confidence: 92%

Immunohistochemical investigation of the coma blister and its pathogenesis

et al. 2013

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: The erythematous patches and vesicles that are observed in coma patients, usually from an overdose of medication, are known as coma blisters. However, it is unknown whether the degenerated sweat gland is a necrosis or apoptosis. We immunohistochemically examined such skin lesions to investigate the characteristics and pathogenesis of the coma blister. Skin lesions were obtained from a forensic autopsy case, a woman in her thirties, of caffeine intoxication. Those lesions were observed in the left femoral, the lower left thigh, and the right knee. Histologically, the skin lesions showed that the keratinocytes had necrosed and the epidermis was thin in some areas. Eccrine sweat gland degeneration was observed. Obvious inflammatory cell infiltrations were not detected. Immunohistochemically, we stained each skin lesion against CD3, CD8, CD45RO, cytokeratin, 70 kD heat shock protein, ubiquitin, 150 kD oxygen regulated protein, and caspase-cleaved keratin 18 neo-epitope M30. They were also stained with an in situ apoptosis detection kit. Degenerated sweat glands featured CD45RO and M30 immunoreactivity. Immunohistochemical staining for CD45RO, CK-L, and M30 might be useful to observe sweat gland degeneration in the coma blister. Therefore, the apoptosis might be related to coma blisters and sweat gland degenerations. J. Med. Invest. 60 : 256-261, August, 2013

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Section: Discussionsupporting

confidence: 92%

Immunohistochemical investigation of the coma blister and its pathogenesis

et al. 2013

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“…Real-time PCR confirmed that primary SSG3 expressed a similar level of PPARγ as the immortalized sebocyte line SEB-1 [15] (Figure 2b). However, SEB-1 expresses Keratin 8, a protein associated with skin appendages tumors [28], whereas SSG3 cells do not express Keratin 8 (Figure 2a), akin to sebaceous gland in vivo [29]. Additionally, SSG3 cells express other markers of sebocytes such as Blimp1 and epithelial membrane antigen EMA/Muc1 (Additional file 1: Figure S1c, d and e).…”

Section: Resultsmentioning

confidence: 99%

TGFβ signaling regulates lipogenesis in human sebaceous glands cells

et al. 2013

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BackgroundSebaceous glands are components of the skin essential for its normal lubrication by the production of sebum. This contributes to skin health and more importantly is crucial for the skin barrier function. A mechanistic understanding of sebaceous gland cells growth and differentiation has lagged behind that for keratinocytes, partly because of a lack of an in vitro model that can be used for experimental manipulation.MethodsWe have developed an in vitro culture model to isolate and grow primary human sebocytes without transformation that display functional characteristics of sebocytes. We used this novel method to probe the effect of Transforming Growth Factor β (TGFβ) signaling on sebocyte differentiation, by examining the expression of genes involved in lipogenesis upon treatment with TGFβ1. We also repressed TGFβ signaling through knockdown of the TGFβ Receptor II to address if the effect of TGFβ activation is mediated via canonical Smad signal transduction.ResultsWe find that activation of the TGFβ signaling pathway is necessary and sufficient for maintaining sebocytes in an undifferentiated state. The presence of TGFβ ligand triggered decreased expression in genes required for the production of characteristics sebaceous lipids and for sebocyte differentiation such as FADS2 and PPARγ, thereby decreasing lipid accumulation through the TGFβ RII-Smad2 dependent pathway.ConclusionTGFβ signaling plays an essential role in sebaceous gland regulation by maintaining sebocytes in an undifferentiated state. This data was generated using a novel method for human sebocyte culture, which is likely to prove generally useful in investigations of sebaceous gland growth and differentiation. These findings open a new paradigm in human skin biology with important implications for skin therapies.

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“…The starting point of our study was the discovery of a novel type II epithelial keratin, K1b, which proved to exhibit virtually no expression site in the human body other than in luminal cells of the entire eccrine sweat duct. Using the K1b expression in these cells as a reference pattern for co-expression studies with antibodies against the plethora of sweat gland keratins known from previous studies (Kurokawa et al, 1988;Broekaert et al, 1990;Wollina et al, 1990a, Moll and Moll, 1991, 1992Tsubura et al, 1991;Wollina, 1991;Yoneda et al, 1991;Eckert et al, 1992;Watanabe et al, 1993Watanabe et al, , 1994Demirkesen et al, 1995;Biernat et al, 1996;Onishi and Watanabe, 1997;Schö n et al, 1999;Onishi et al, 2002), as well as of further keratins, we were able to provide new insights into the differentiation pathways and the function of both the peripheral and the luminal cell layers of the sweat duct of eccrine sweat glands.…”

Section: Discussionmentioning

confidence: 99%

“…These antibodies were primarily selected on the basis of a large body of previous investigations on the keratin expression in the adult human eccrine sweat gland. Collectively, these studies revealed the expression of an amazingly large number of heterogenous keratins, such as K1, K10, K5, K14, K15, K6, K16, K17 as well as K8, 18, K19, and K7, in this rather small secretory skin appendage (Kurokawa et al, 1988;Broekaert et al, 1990;Wollina et al, 1990a;Moll, 1991, 1992;Tsubura et al, 1991;Wollina, 1991;Yoneda et al, 1991;Eckert et al, 1992;Watanabe et al, 1993Watanabe et al, , 1994Demirkesen et al, 1995;Biernat et al, 1996;Onishi and Watanabe, 1997;Schö n et al, 1999;Onishi et al, 2002). It should be mentioned, however, that in none of the previous studies has the full complement of these keratins been investigated simultaneously and in all segments of the sweat gland.…”

Section: Figurementioning

confidence: 95%

Characterization of a Novel Human Type II Epithelial Keratin K1b, Specifically Expressed in Eccrine Sweat Glands

Langbein

Rogers

Praetzel

et al. 2005

Journal of Investigative Dermatology

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In this study, we show that a novel human type II epithelial keratin, K1b, is exclusively expressed in luminal duct cells of eccrine sweat glands. Taking this luminal K1b expression as a reference, we have used antibodies against a plethora of epithelial keratins to systematically investigate their expression in the secretory globule and the two-layered sweat duct, which was divided into the intraglandular, intradermal, and intraepidermal (acrosyringium) segments, the latter being further subdivided into the sweat duct ridge and upper intraepidermal duct. We show that (i) each of the eccrine sweat gland tissue compartments expresses their own keratin patterns, (ii) the peripheral and luminal duct layers exhibit a sequential keratin expression, with both representing self-renewing cell layers, (iii) the intradermal duct and the sweat duct ridge display hitherto unknown length variations, and (iv) out of all cell layers, the luminal cell layer is the most robust layer and expresses the highest number of keratins, these being concentrated at the apical side of the cells to form the cuticle. We provide evidence that the cellular and intercellular properties of the peripheral and the luminal layers reflect adaptations to different functions.

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Immunohistochemical demonstration of keratins 8 and 14 in benign tumours of the skin appendage

Cited by 35 publications

References 13 publications

Immunohistochemical investigation of the coma blister and its pathogenesis

Immunohistochemical investigation of the coma blister and its pathogenesis

TGFβ signaling regulates lipogenesis in human sebaceous glands cells

Characterization of a Novel Human Type II Epithelial Keratin K1b, Specifically Expressed in Eccrine Sweat Glands

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