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PubMed1998

Activation of papillomavirus late gene transcription and genome amplification upon differentiation in semisolid medium is coincident with expression of involucrin and transglutaminase but not keratin-10.

The life cycle of the papillomaviruses is closely linked to host cell differentiation, as demonstrated by the fact that amplification of viral DNA and transcription of late genes occur only in the suprabasal cells of a differentiated epithelium. Previous studies examining the pathogenesis of papillomavirus infections have relied on the use of organotypic raft cultures or lesions from patients to examine these differentiation-dependent viral activities. In this study, we used a simple system for epithelial differentiation to study human papillomavirus (HPV) late functions. We demonstrate that the suspension of HPV-infected keratinocytes in semisolid medium containing 1.6% methylcellulose for 24 h was sufficient for the activation of the late promoter, transcription of late genes, and amplification of viral DNA. These activities were shown to be linked to and coincide with cellular differentiation. Expression of the late protein E1(wedge)E4 and amplification of viral DNA were detected in the identical set of cells after suspension in methylcellulose. This technique was also used to analyze the differentiation properties of the cells which expressed the late protein E1(wedge)E4. While induction of the spinous layer markers involucrin and transglutaminase was compatible with late promoter induction, expression of the differentiation-specific keratin-10 was shown not to be required for HPV late functions. Interestingly, while the majority of normal human keratinocytes induced filaggrin expression by 24 h, this marker of the granular layer was induced in a smaller subset of HPV type 31 (HPV-31)-positive cells at this time point. The HPV-31-positive cells which expressed filaggrin did not induce the late protein E1(wedge)E4. Use of the methylcellulose system to induce epithelial differentiation coupled with the ability to perform a genetic analysis of HPV functions by using transfection of cloned viral DNA will facilitate the study of the regulation of the papillomavirus life cycle.

Cells, Cultured↗

PubMed1993

Squamous cell carcinoma of the tonsillar region and the base of the tongue: a morphological and immunohistochemical comparative pilot study.

Sixteen squamous cell carcinomas of the tonsillar region and 13 carcinomas of the base of the tongue were studied in a search for significant differences between the tumours of these two oropharyngeal subsites, which are known to carry a significantly different prognosis. The characteristics of the tumour cells and the tumour-host relationship were scored on H & E-stained slides, as well as on slides stained with a panel of antibodies. The results obtained were cross-tabulated and analysed with respect to the subsite. Ten variables were tested: cytonuclear pleomorphism, mitotic activity, the presence of atypical mitoses, keratinization, tumour grade, presence of eosinophils, severity of inflammatory response, and the expression of keratin-10, blood group antigens and collagen IV. When split up by site, only cytonuclear pleomorphism revealed a significant difference, tonsillar carcinomas more often exhibiting marked pleomorphism (p = 0.04). Despite having some prognostic relevance for squamous cell carcinomas of the head and neck, the variables tested could not provide an explanation for the difference in biological behaviour of the tumours studied.

Adult↗

PubMed1997

Suprabasal expression of a dominant-negative RXR alpha mutant in transgenic mouse epidermis impairs regulation of gene transcription and basal keratinocyte proliferation by RAR-selective retinoids.

To determine whether 9-cis retinoic acid receptors (RXRs) regulate the biological activity of all-trans retinoic acid (tRA) and its receptors (RARs) in skin, we have targeted a dominant-negative RXR alpha (dnRXR alpha) lacking transactivation function AF-2 to differentiated suprabasal keratinocytes in the epidermis of transgenic mice. Driven by the suprabasal-specific keratin-10 gene promoter, expression of dnRXR alpha severely reduced the ability of RAR-selective ligands tRA and CD367 to induce epidermal mRNA levels of the CRABPII, CRBPI, and CRBPII genes, which contain RA-responsive elements (RAREs) DR1 and/or DR2. It also reduced gene-specific, synergistic induction of CRBPI mRNA by a combination of CD367 and RXR-selective SR11237. Like endogenous RXR alpha, dnRXR alpha in epidermal nuclear extracts from the transgenic mice competitively formed heterodimers with endogenous RAR gamma on RAREs, suggesting that dnRXR alpha impairs retinoid signaling by competing with endogenous RAR gamma-RXR alpha heterodimers. Histologically, the epidermis of dnRXR alpha mice showed no detectable developmental abnormalities. Surprisingly, in adult animals, the suprabasal expression of dnRXR alpha significantly reduced the ability of topically applied tRA to stimulate proliferation of undifferentiated keratinocytes in the basal layer of epidermis. RXR-selective ligands alone had no detectable effects on both normal and transgenic mouse epidermis. Accordingly, we suggest that in vivo: (1) in suprabasal keratinocytes, retinoids regulate gene transcription via RAR-RXR heterodimers in which RAR confers a predominant ligand response, whereas RXR AF-2 is required for liganded RAR AF-2 to efficiently trans-activate target genes, and (2) this suprabasal RXR-assisted mechanism indirectly regulates proliferation of basal keratinocytes likely via intercellular signaling.

Animals↗

PubMed1998

Local reduction of organ size in transgenic mice expressing a soluble insulin-like growth factor II/mannose-6-phosphate receptor.

Genetic evidence suggests that the insulin-like growth factor II (IGF-II)/mannose-6-phosphate receptor (IGF2R) slows growth. A soluble form of IGF2R (sIGF2R) is produced by proteolytic cleavage of the intact cellular receptor and is found at high levels in fetal and neonatal plasma. To test the hypothesis that sIGF2R modulates organ size in vivo, we generated transgenic mice expressing a mouse Igf2r complementary DNA in which the transmembrane domain sequence was deleted. The transgene was driven by the keratin-10 promoter and was expressed at the highest levels in the skin and alimentary canal. Transgenics showed disproportionately reduced size of the alimentary canal, where the wet weight was decreased by 9-20% and the dry weight was decreased by 20-30%, whereas the water content per unit dry weight was not significantly changed. In addition, the circulating levels of IGF-II and the latent form of transforming growth factor-beta1 were increased by 58-77% and 56-140%, respectively, whereas plasma epidermal growth factor levels showed a 24-35% reduction. The serum and tissue activities of four lysosomal enzymes were not affected, with the exception of the colon in the line expressing the transgene at highest levels, where enzyme activities were decreased compared with control values. These results support a significant role for the sIGF2R in local modulation of organ size in vivo.

Animals↗

PubMed1997

From newborn to adult: phenotypic and functional properties of skin equivalent and human skin as a function of donor age.

The skin's most important function is to act as a barrier against fluid loss, microorganism infections, and percutaneous absorption. To fulfill this role, keratinocytes proliferate and differentiate to produce a protective layer: the stratum corneum. Because stem cells are responsible for the production of differentiated progeny and stem cells (K19-expressing cells) are less abundant in skin from older donors, the purpose of this study was to establish whether histological and functional properties of differentiating skin is influenced by donor age. The in vitro model developed for the evaluation of skin properties (Michel et al., 1995) was used to produce skin equivalents from newborn, child, and adult keratinocytes. Throughout maturation, skin equivalents were compared with corresponding skin biopsies for keratin, filaggrin, and transglutaminase expression. Percutaneous absorptions of hydrocortisone also were measured and correlated with lipid content. After 1 wk of immersed culture, the epidermal layer of newborn skin equivalents was thicker than child and adult epidermis. As expected, a greater proportion of cutaneous stem cells was present in newborn compared with children and adult skin equivalents. No age-related difference was observed for differentiation markers. When skin equivalents were cultured at the air-liquid interface, cell differentiation and stratum corneum formation were induced, and the age-related variation in the thickness of the epidermal layer disappeared. Percutaneous absorption through these matured skin equivalents did not vary with age. Their lipid density and profile were similar. Accordingly, skin biopsies exhibited comparable percutaneous absorption profiles independently of donor age. In conclusion, although newborn skin equivalents, or skin biopsies, contained more stem cells than child and adult counterparts, no age-related histological difference was observed in the differentiated tissues. Moreover, the functional barrier property of skins and matured skin equivalents did not vary with age. Therefore, both newborn and adult keratinocytes produce useful in vitro models to study epidermal differentiation processes involved in both normal and pathological states.

Absorption↗

PubMed1998

Staurosporine-induced versus spontaneous squamous metaplasia in pre- and postmenopausal breast tissue.

Breast cancers from pre- vs. postmenopausal women display unique characteristics that may be related to differences in epithelial differentiation between these two populations. In addition to lobular development, lactational changes, and involution, breast epithelium can undergo metaplastic alterations, often in association with carcinoma. Because protein kinase C (PKC) regulates differentiation and proliferation in many cell types, we asked whether modulation of PKC activity could define biochemical differences in breast epithelium from pre- vs. postmenopausal women. Organ cultures of normal human breast were treated with PKC agonists and antagonists. Epithelial differentiation was evaluated based on morphologic criteria and the expression of cell-type specific proteins. Staurosporine, a nonspecific but extremely potent inhibitor of PKC, induced squamous metaplasia in eight of eight cases within 2 weeks of treatment. Other inhibitors of PKC, such as calphostin C and tamoxifen, had no effect on epithelial differentiation. Long-term treatment with phorbol esters also did not induce squamous metaplasia. However, stimulation of cAMP levels by forskolin and isobutyl-methyl-xanthene (IMX) rapidly induced squamous metaplasia, as has been previously reported. Surprisingly, squamous metaplasia occurred in 10 of 12 cultures derived from postmenopausal women in the absence of exogenous agents. Untreated cultures derived from premenopausal women never developed this type of epithelium (0 of 11). Therefore, breast epithelium from pre- and postmenopausal women responded differently to in vitro culture. Forskolin/IMX or staurosporine can reproduce these conditions, acting independent of menopausal status. Because staurosporine's action was unique among PKC inhibitors, staurosporine may induce squamous metaplasia of breast epithelium by a PKC-independent mechanism.

Adult↗

PubMed1997

Delays in malignant tumor development in transgenic mice by forced epidermal keratin 10 expression in mouse skin carcinomas.

The keratin cytoskeleton is formed in different epidermal compartments by distinct polypeptides. Basal, proliferative keratinocytes express keratin (K) 5 and K14, whereas, suprabasal, post-mitotic keratinocytes express K1 and K10. Changes in this keratin pattern have been found to occur in hyperproliferative skin disorders and, in particular, throughout mouse epidermal carcinogenesis. Whereas some keratins not found in normal epidermis (K6, K16, K13, and K8) are induced at different stages of tumor development, K1 and K10 expression is lost. To determine whether K1 and K10 loss is just a consequence of the altered differentiation program or an event required for tumor progression, we generated transgenic mice carrying the human keratin 10 gene (hK10) under the control of a bovine keratin 6 gene regulatory region, which is silent in normal skin but is induced and drives transgene expression in hyperproliferative skin keratinocytes and, therefore, in skin tumors. Transgenic animals subjected to a complete carcinogenesis protocol developed tumors that contained various amounts of transgenic hK10. Although no significant difference was found in tumor number or malignancy, tumor onset was significantly delayed in transgenic mice, indicating that the presence of K10 actually impairs tumor development.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1997

Mouse vaginal opening is an apoptosis-dependent process which can be prevented by the overexpression of Bcl2.

In the mouse, opening of the vaginal cavity to the skin is a late event, occurring around the fifth week of life; it can be induced in sexually immature mice by beta-estradiol injections. We have generated two lines of transgenic mice expressing the human Bcl2 protein in a variety of tissues. The vaginal cavity of the transgenic females remained permanently closed, a condition completely resistant to beta-estradiol injections; this was accompanied by a considerable distension of the genital tract. Histologic studies of vaginal sections at the time of opening to the skin in normal mice showed, by the TUNEL method which detects nuclei with fragmented DNA characteristic of apoptosis, that this event coincides with extensive apoptosis in the lower part of the vaginal mucosa, a process prevented in the bcl2 transgenic mice, which express Bcl2 in suprabasal epithelial cells and in subepithelial cells of the vaginal mucosa. In contrast, two lines of mice bearing a Bcl2 transgene placed under the control of a K10 keratin promoter, whose expression is restricted to the suprabasal layers of the epidermis, had a normal phenotype. Eyelids' formation and opening of the external ear canals, which also occur after birth in the mouse, were not altered in any of these transgenic lines; histological study of eye and ear sections at the time of these events failed to detect apoptosis. In conclusion, the tissue remodeling required to complete maturation of the mouse female genital tract at the time of puberty is an hormonally triggered apoptosis-dependent process.

Animals↗

PubMed1996

Regulation of differentiation and keratin 10 expression by all-trans retinoic acid during the estrous cycle in the rat vaginal epithelium.

In rodents, the vaginal epithelium shows cyclic changes with an alternating pattern of keratinization under estrogen control and mucification under progesterone control. Retinoids are powerful regulators of cell differentiation, an excess of retinoids suppressing the keratinizing differentiation of keratinocytes. Here, we have examined the vaginal epithelium during the estrous cycle and compare the effects of retinoids on both types of hormonally induced differentiation, i.e. keratinization and mucification. All-trans retinoic acid was administered either by daily injections during the estrous cycle or by a single injection before the estrogen rise; these two protocols gave similar results. Retinoic acid suppressed estrogen-induced vaginal keratinization and cytokeratin K10 expression (a biochemical marker of terminal differentiation). Progesterone-induced mucification was not impaired; however, retinoic acid impeded mucous cell desquamation, suggesting an effect of retinoic acid on cell adhesiveness. Retinoic acid induced the appearance of apoptotic-like cells, as revealed by immunocytochemical staining of DNA fragmentation.

Animals↗

PubMed1993

Keratin expression reveals mosaic differentiation in vaginal epithelium.

OBJECTIVE: Analyzing the expression of keratins has proved to be valuable for identifying of pathways of epithelial differentiation. In stratified epithelia K10 and K13 are representative for either the keratinizing (epidermal-type) or the nonkeratinizing pathway. STUDY DESIGN: We have investigated keratin expression in "normal" vaginal epithelium from 30 women, applying two-color immunofluorescence with monoclonal antibodies to K10 and K13 on cryostat sections and cell smears. RESULTS: A differential expression pattern of vaginal cells dependent on their localization within the epithelium was found. In cells of the first suprabasal layers differentiation began and became identifiable by a weak expression of K13. The adjacent layers displayed cells that concurrently expressed K10 and K13. In contrast, cells within the superficial strata expressed exclusively either one of the two keratins. CONCLUSION: Thus vaginal epithelium appears to be mosaic in differentiation, showing simultaneous expression of keratins K10 and K13, thought to be representative for distinct routes of differentiation.

Adult↗

PubMed1992

Exons I and VII of the gene (Ker10) encoding human keratin 10 undergo structural rearrangements within repeats.

A genomic fragment containing the K51 gene previously isolated from a rat genomic library by hybridization with the v-mos probe in nonstringent conditions [Chumakov et al., Dokl. Akad. Nauk SSSR 290 (1986) 1252-1254], resembles a human keratin type-I-encoding gene [Shvets et al., Mol. Biol. 24 (1990) 663-677]. This genomic clone, K51, has been used as a probe to search for related human genes. A recombinant clone, HK51, with a 1.5-kb insert, was isolated from a human embryonic skin cDNA library, and its nucleotide (nt) sequence was determined. Analysis has shown that the cloned cDNA encodes human keratin 10 (Ker10). All presently known nt sequences of the human Ker10-encoding gene (Ker10) are not identical. Differences are concentrated in the 5'-end of the first exon and in the middle of the seventh exon within repeats. In spite of structural rearrangements in two of eight exons, the reading frame and position of the stop codon are preserved. The genetic rearrangements cause changes in hydrophobicity profiles of the N and C termini of Ker10. It was also noticed that insertion of one nt leads to the formation of an unusual 3'-end of the transcript.

Amino Acid Sequence↗

PubMed1996

Gene targeting at the mouse cytokeratin 10 locus: severe skin fragility and changes of cytokeratin expression in the epidermis.

Bullous congenital ichthyosiform erythroderma (BCIE) is a dominantly inherited blistering skin disorder caused by point mutations in the suprabasal cytokeratins 1 or 10. Targeting the murine cytokeratin 10 gene in ES cells resulted in mice with different phenotypes in the homozygotes and heterozygotes; both of which exhibit similarities to specific clinical characteristics of BCIE. Homozygotes suffered from severe skin fragility and died shortly after birth. Heterozygotes were apparently unaffected at birth, but developed hyperkeratosis with age. In both genotypes, aggregation of cytokeratin intermediate filaments, changes in cytokeratin expression, and alterations in the program of epidermal differentiation were observed. In addition we demonstrate, for the first time, the existence of the murine equivalent of human cytokeratin 16.

Animals↗

PubMed1996

Overexpression of bone morphogenetic protein-6 (BMP-6) in the epidermis of transgenic mice: inhibition or stimulation of proliferation depending on the pattern of transgene expression and formation of psoriatic lesions.

Bone morphogenetic protein-6 (BMP-6) belongs to the family of TGF-beta-related growth factors. In the developing epidermis, expression of BMP-6 coincides with the onset of stratification. Expression persists perinatally but declines after day 6 postpartum, although it can still be detected in adult skin by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. We constitutively overexpressed BMP-6 in suprabasal layers of interfollicular epidermis in transgenic mice using a keratin 10 promoter. All mice expressing the transgene developed abnormalities in the skin, indicating an active transgene-derived factor. Depending on the pattern of transgene expression, the effects on proliferation and differentiation were completely opposite. Strong and uniform expression of the BMP-6 transgene resulted in severe repression of cell proliferation in embryonic and perinatal epidermis but had marginal effects on differentiation. Weaker and patchy expression of the transgene evoked strong hyperproliferation and parakeratosis in adult epidermis and severe perturbations of the usual pattern of differentiation. These perturbations included changes in the expression of keratins and integrins. Together with an inflammatory infiltrate both in the dermis and in the epidermis, these aspects present all typical histological and biochemical hallmarks of a human skin disease: psoriasis.

Acanthosis Nigricans↗

PubMed1997

Expression of keratins (K10 and K17) in steatocystoma multiplex, eruptive vellus hair cysts, and epidermoid and trichilemmal cysts.

We compared the patterns of keratin 10 (K10) and keratin 17 (K17) expression in epidermoid cysts, trichilemmal cysts, eruptive vellus hair cysts, and steatocystoma multiplex. Epidermoid cysts expressed K10 and eruptive vellus hair cysts expressed K17, whereas trichilemmal cysts and steatocystoma multiplex showed expression of both K10 and K17. Our findings support the opinion that eruptive vellus hair cysts, which stained negative for K10, and steatocystoma multiplex are distinct entities and not variants of one disorder.

Cysts↗

PubMed1996

Characterization of an immortalized cell line from a patient with epidermolytic hyperkeratosis.

The most frequent mutation that causes the autosomal dominant skin disease epidermolytic hyperkeratosis (EHK) is an arginine to histidine substitution at position 10 in the 1A segment of the rod domain of keratin 10. As an initial step toward developing a strategy for treating EHK, a cell line, EH18-1, was established after keratinocytes derived from an EHK patient with this mutation were immortalized by a recombinant retrovirus encoding the E6 and E7 genes of human papillomavirus type 18. EH18-1 cells synthesize considerable amounts of keratin 10 mRNA and protein when maintained in either submerged cultures or in organotypic cultures. When grown in organotypic culture, EH18-1 cells form multiple layers and express keratin 10 and filaggrin predominantly in the upper layers. Thus, the EH18-1 cell line exhibits several morphological and biochemical markers of terminal epidermal differentiation. A semiquantitative reverse transcriptase polymerase chain reaction assay for keratin 10 mRNA was developed to distinguish between expression of the normal and the mutant alleles. The EH18-1 keratinocyte cell line will be useful in developing protocols for gene therapy of EHK that may be monitored by reverse transcriptase polymerase chain reaction of either allele.

Alleles↗

PubMed1994

Abnormal keratin 1 and 10 cytoskeleton in cultured keratinocytes from epidermolytic hyperkeratosis caused by keratin 10 mutations.

Epidermolytic hyperkeratosis is caused by mutations of the differentiation-specific keratins K1 and K10. These mutations produce a weakened cytoskeleton that is prone to collapse resulting in cell fragility and lysis. In this study we have analyzed cultured keratinocytes from EHK patients bearing 10R-to-H and 15L-to-S mutations within the 1A segment of the K10 rod domain. Keratinocytes were grown submerged in serum-free medium and induced to differentiate by growing to confluence and increasing the Ca++ concentration in the medium. Cultures were either harvested for mRNA sequence analysis or subjected to immunofluorescence microscopy. Differentiating keratinocytes from these patients were found to express these K10 mutations in their mRNA. Moreover, these cells could be distinguished from normal keratinocytes by their aberrant morphology. EHK keratinocytes frequently exhibited a collapsed perinuclear network of K1/K10 filaments and sometimes peripheral granules of K1 and K10 aggregates, reminiscent of the cells of the suprabasal layers in these patients. This report documents the expression of mutant keratin 10 in cultured EHK keratinocytes.

Base Sequence↗

PubMed1997

Out of balance: consequences of a partial keratin 10 knockout.

Recently we generated keratin 10 knockout mice which provided a valuable model for the dominantly inherited skin disorder epidermolytic hyperkeratosis. Here we investigated the molecular basis for their phenotype. Hetero- and homozygotes expressed a truncated keratin 10 peptide which has been identified directly by microsequencing. Epitope mapping of monoclonal antibodies to keratin 10T enabled us to study its distribution relative to keratin 6, which is highly expressed in keratin 10 knockout mice, by double-immunogold electron microscopy. This revealed that keratin 10T was restricted to complexes with keratin 1 but did not mix with keratin 6. The latter did not form extended filaments with keratins 16/17 but aggregates. Keratins 6/16 were unable to compensate for the lack of normal keratin 1/10 filaments. Remarkably keratin 6 aggregates strictly colocalized with keratohyalin granules. Residual keratin 1/10T clumps were located in the cell periphery and at desmosomes which maintained a normal architecture. Surprisingly keratin 2e, a keratin tailored to sustain mechanical stress, was completely lost in paw sole epidermis of homozygous keratin 10 knockout mice, pointing to keratin 10 as its partner. The selective pairing of keratin 10T and the loss of keratin 2e indicate that in vivo keratins are less promiscuous than in vitro. Skin fragility in keratin 10 knockout mice and in epidermolytic hyperkeratosis is probably the consequence of two complementing mechanisms namely a decrease of normal keratin 1/10 filaments and an increase in keratins 6/16 with a poor filament-forming capacity.

Amino Acid Sequence↗

PubMed1997

Keratin intermediate filament dynamics in cell heterokaryons reveals diverse behaviour of different keratins.

To study the dynamics of keratin intermediate filaments, we fused two different types of epithelial cells (PtK2 and BMGE+H) and studied how the keratins from the parental cells recombine and copolymerize to form the heterokaryon cytoskeleton. The behaviour of the keratins during this process was followed by immunofluorescence using specific antibodies. After fusion, the parental cytoskeletons undergo a depolymerization process most apparent in the region adjacent to the fusion area. The depolymerized subunits spread throughout the heterokaryon and copolymerize into a new hybrid cytoskeleton. The complete process is very rapid, occurring in 3-4 hours, thus demonstrating the highly dynamic nature of the keratin cytoskeleton. Although newly synthesised subunits contribute to the formation of the hybrid cytoskeleton, the process takes place with similar kinetics in the absence of protein synthesis, showing the dynamic nature of the keratins from pre-existing cytoskeletons. During this process, specific keratins behave differently. Keratins K8, K18, K5 and K10 are mobilised from the parental cytoskeletons and reassemble rapidly into the hybrid cytoskeleton (3-6 hours), whereas K14 requires a substantially longer period (9-24 hours). Thus, different keratins, even when they form part of the same heterodimeric/tetrameric complexes, as is the case for K5 and K14, exhibit different dynamics. This suggests that individual polypeptides or homopolymeric complexes rather than exclusively heterodimeric/ tetrameric subunits, as is currently thought, can also take part in keratin intermediate filament assembly and dynamics. Biochemical analysis performed in the absence of protein synthesis revealed greater amounts of K5 than of K14 in the soluble pool of BMGE+H cells. Crosslinking and immunoprecipitation experiments indicated an excess of monomeric K5, as well as of K5/K14 heterodimers and K5 homodimers in the soluble pool. These results are in agreement with the different dynamic behaviour of these keratins observed in immunofluorescence. On the contrary, the phosphorylation levels of K5 and K14 are similar in both the soluble pool and the polymerized fraction, suggesting that phosphorylation does not play an important role in the different dynamics displayed by these two proteins. In summary, our results demonstrate that, following fusion, the keratin intermediate filament network reshapes rather rapidly and that keratins are highly dynamic proteins, although this mobility depends on each particular polypeptide.

Animals↗