scholarly journals Involvement of a nuclear matrix association region in the regulation of the SPRR2A keratinocyte terminal differentiation marker

1998 ◽  
Vol 26 (23) ◽  
pp. 5288-5294 ◽  
Author(s):  
D. F. Fischer ◽  
G. S. Winkler ◽  
P. van de Putte ◽  
C. Backendorf ◽  
C. M. van Drunen
Keyword(s):  
Nuclear Matrix ◽  
Terminal Differentiation ◽  
Differentiation Marker ◽  
Terminal Differentiation Marker

Opposite Effects of Ras or PKC Activation on the Expression of the SPRR2A Keratinocyte Terminal Differentiation Marker

1999 ◽  
Vol 250 (2) ◽  
pp. 475-484 ◽  
Author(s):  
Muriëlle W.J. Sark ◽  
Anne-Marijke Borgstein ◽  
Jan Paul Medema ◽  
Pieter van de Putte ◽  
Claude Backendorf
Keyword(s):  
Terminal Differentiation ◽  
Differentiation Marker ◽  
Pkc Activation ◽  
Terminal Differentiation Marker

scholarly journals AP-1 and Ets Transcription Factors Regulate the Expression of the HumanSPRR1AKeratinocyte Terminal Differentiation Marker

1998 ◽  
Vol 273 (38) ◽  
pp. 24683-24692 ◽  
Author(s):  
Murielle W. J. Sark ◽  
David F. Fischer ◽  
Emile de Meijer ◽  
Pieter van de Putte ◽  
Claude Backendorf
Keyword(s):  
Transcription Factors ◽  
Terminal Differentiation ◽  
Ets Transcription Factors ◽  
Differentiation Marker ◽  
Terminal Differentiation Marker

scholarly journals The Effect of a Phytosphingosine-like Substance Isolated from Asterina pectinifera on Involucrin Expression in Mite Antigen-Stimulated HaCaT Cells

2010 ◽  
Vol 5 (7) ◽  
pp. 1934578X1000500
Author(s):  
Gui Hyang Choi ◽  
Fazli Wahid ◽  
You Young Kim
Keyword(s):  
High Performance ◽  
Therapeutic Agent ◽  
Hacat Cell ◽  
Terminal Differentiation ◽  
Hacat Cells ◽  
H Nmr ◽  
Immunoblotting Assay ◽  
Differentiation Marker ◽  
Asterina Pectinifera ◽  
Terminal Differentiation Marker

The aim of the present study was to investigate the effect of phytosphingosine (PS) on mite antigen-induced terminal differentiation abnormalities in HaCaT cells. For this purpose, a PS-like substance was isolated from Asterina pectinifera (starfish PS) using high-performance liquid chromatography and was partially characterized through 1H NMR analysis. The level of involucrin expression in HaCaT cell was measured by immunoblotting assay. Our results showed that PS treatments remarkably up-regulated the involucrin expression, which is known as a terminal differentiation marker in the epidermal mite antigen-treated HaCaT cells. This indicates that starfish PS could regulate mite antigen-induced terminal differentiation fluctuation in the epidermis. Taken together, the results suggest that starfish PS might be a useful therapeutic agent for atopic dermatitis.

5-Bromo-2-deoxyuridine regulates invasiveness and expression of integrins and matrix-degrading proteinases in a differentiated hamster melanoma cell

1993 ◽  
Vol 105 (1) ◽  
pp. 191-201 ◽  
Author(s):  
L. Thomas ◽  
P.W. Chan ◽  
S. Chang ◽  
C. Damsky
Keyword(s):  
Extracellular Matrix ◽  
Tumor Progression ◽  
Melanoma Cell ◽  
Critical Role ◽  
Terminal Differentiation ◽  
Cell System ◽  
Melanocyte Stimulating Hormone ◽  
Complex Processes ◽  
Differentiation Marker ◽  
Stimulating Hormone

Cell interactions with the extracellular matrix play a critical role in regulating complex processes such as terminal differentiation and tumor progression. In these studies we describe a melanoma cell system that should be useful in addressing the regulation of cell-matrix interactions and the roles they play in regulating differentiation and cell invasiveness. CS (suspension)-1 melanoma cells are relatively well differentiated: they are melanotic, responsive to melanocyte-stimulating hormone, and express TA99, a melanosome membrane differentiation marker. Their repertoire of integrin receptors for extracellular matrix ligands is limited; in particular, they lack receptors for vitronectin, accounting for the observation that they are nonadherent when cultured in the presence of serum. CS-1 cells are noninvasive as well, and express low levels of both metalloproteinases and activated plasminogen activators. Treatment of these cells with melanocyte-stimulating hormone causes them to increase melanin production and assume an arborized phenotype, suggesting that it promotes their further differentiation. In contrast, treatment of CS-1 with the thymidine analog 5-bromodeoxyuridine, converts them to a highly invasive cell population (termed BCS-1) that loses its differentiated properties and responsiveness to melanocyte-stimulating hormone, acquires a broad integrin repertoire (including vitronectin receptors), and expresses elevated levels of metalloproteinases and activated urokinase. From these observations and findings of others on BrdU treatment of other developmental lineages, we hypothesize that BrdU both suppresses differentiation and promotes invasiveness of CS-1 cells. The demonstrated manipulability of CS-1 cells should make them extremely useful for studying the regulation of both terminal differentiation and tumor progression in the melanocyte lineage.

Inhibition of cadherin function differentially affects markers of terminal differentiation in cultured human keratinocytes

1999 ◽  
Vol 112 (24) ◽  
pp. 4569-4579
Author(s):  
M.D. Hines ◽  
H.C. Jin ◽  
M.J. Wheelock ◽  
P.J. Jensen
Keyword(s):  
Terminal Differentiation ◽  
Human Keratinocytes ◽  
Keratinocyte Differentiation ◽  
Differentiation Markers ◽  
Protein Levels ◽  
Surface Molecules ◽  
Transglutaminase 1 ◽  
Differentiation Marker ◽  
E Cadherin

Cadherin function is required for normal keratinocyte intercellular adhesion and stratification. In the present study, we have investigated whether cadherin-cadherin interactions may also modulate keratinocyte differentiation, as evidenced by alterations in the levels of several differentiation markers. Confluent keratinocyte cultures, propagated in low Ca(2+) medium in which cadherins are not active, were pre-incubated with antibodies that block the function of E-cadherin and/or P-cadherin; Ca(2+)was then elevated to 1 mM to activate the cadherins and induce differentiation. In control cultures (incubated with no antibody or with antibodies to other cell surface molecules), Ca(2+) elevation induced an increase in type 1 transglutaminase, profilaggrin, and loricrin, as measured by western blotting and in agreement with previous results. However, the concurrent addition of antibodies against both E- and P-cadherin prevented this increase in transglutaminase 1 protein. Incubation with either antibody alone had no consistent effect. Profilaggrin and loricrin, which are later markers of keratinocyte differentiation, responded differently from transglutaminase 1 to addition of antibodies. In the presence of anti-E-cadherin antibody, both loricrin and profilaggrin levels were dramatically enhanced compared to the high Ca(2+) control cells, while addition of antibody to P-cadherin slightly attenuated the Ca(2+)-induced increase. In the presence of both antibodies, loricrin and profilaggrin protein levels were intermediate between those observed in the presence of either antibody alone. The expression of involucrin, however, was unaffected by addition of antibodies. In addition, effects of the anti-cadherin antibodies were not secondary to alterations in proliferation or programmed cell death, as determined by several independent assays of these processes. Thus, the consequences of cadherin inhibition depend upon both the particular cadherin and the differentiation marker under study. Taken together, these data suggest that E-cadherin and P-cadherin contribute to the orderly progression of terminal differentiation in the epidermis in multiple ways.

Decreased expression of fibronectin and the alpha 5 beta 1 integrin during terminal differentiation of human keratinocytes

1991 ◽  
Vol 98 (2) ◽  
pp. 225-232 ◽  
Author(s):  
L.J. Nicholson ◽  
F.M. Watt
Keyword(s):  
Messenger Rna ◽  
Basal Layer ◽  
Terminal Differentiation ◽  
Human Keratinocytes ◽  
Epidermal Keratinocytes ◽  
Human Epidermal Keratinocytes ◽  
Fibronectin Receptor ◽  
Beta 1 Integrin ◽  
Differentiation Marker ◽  
Unit Gravity Sedimentation

We have examined the expression of fibronectin and the alpha 5 beta 1 fibronectin receptor during terminal differentiation of human epidermal keratinocytes, using involucrin as a terminal differentiation marker. The levels of mRNAs encoding fibronectin and the alpha 5 and beta 1 integrin subunits were measured in keratinocyte populations that had been enriched for involucrin-negative or -positive cells by unit gravity sedimentation or suspension-induced terminal differentiation. All three mRNAs decreased in abundance during terminal differentiation, and the corresponding proteins were localised by immunofluorescence to the basal layer in stratified colonies. We also examined expression in ndk, a strain of epidermal cells with a complete block in terminal differentiation, which, as a result, do not express involucrin. Messenger RNA levels for fibronectin and the alpha 5 and beta 1 subunits were higher in ndk, than in unfractionated keratinocytes and the corresponding proteins were expressed by all ndk, consistent with a basal keratinocyte phenotype. We conclude that expression of fibronectin and the alpha 5 beta 1 fibronectin receptor decreases during terminal differentiation and that such changes are likely to play a role in the selective migration of terminally differentiating cells from the basal epidermal layer.

Functional down-regulation of alpha 5 beta 1 integrin in keratinocytes is reversible but commitment to terminal differentiation is not

1993 ◽  
Vol 106 (4) ◽  
pp. 1131-1138 ◽  
Author(s):  
N.A. Hotchin ◽  
N.L. Kovach ◽  
F.M. Watt
Keyword(s):  
Extracellular Matrix ◽  
Ligand Binding ◽  
Terminal Differentiation ◽  
Binding Ability ◽  
Cell Extracts ◽  
Beta 1 Integrin ◽  
Loss Of Contact ◽  
Differentiation Marker ◽  
Extracellular Matrix Receptors ◽  
Integrin Family

Extracellular matrix receptors of the integrin family have a dual role in the epidermis, regulating both adhesion and differentiation. Loss of contact with the extracellular matrix causes keratinocytes to become committed to terminal differentiation, and results in a decrease in the ability of the alpha 5 beta 1 integrin to bind fibronectin. We have investigated whether the decrease in ligand-binding ability is reversible and, if so, whether commitment to terminal differentiation can also be reversed. Keratinocytes that had been placed in suspension for 5 hours to induce commitment were compared with the starting population (0 hour cells) in the presence or absence of 8A2, an activating anti-beta 1 antibody. 8A2 IgG or FAb fragments increased the amount of alpha 5 beta 1 in cell extracts that bound to fibronectin-Sepharose and in the presence of 8A2 the amount of bound alpha 5 beta 1 in 0 hour and 5 hour extracts was equal. 8A2 also restored alpha 5 beta 1 function in adhesion assays of intact 5 hour cells. Ca2+, Mg2+ and Mn2+ alone, at concentrations of up to 1 mM, did not increase the adhesiveness of 5 hour cells relative to 0 hour cells; however, the effect of 8A2 on keratinocytes was dependent on Ca2+. Although 8A2 restored alpha 5 beta 1 ligand-binding ability it did not prevent committed cells from withdrawing from the cell cycle and expressing involucrin, a differentiation marker.(ABSTRACT TRUNCATED AT 250 WORDS)

Genesis of an organ: molecular analysis of the pha-1 gene

Development ◽  
1994 ◽  
Vol 120 (10) ◽  
pp. 3005-3017 ◽  
Author(s):  
M. Granato ◽  
H. Schnabel ◽  
R. Schnabel
Keyword(s):  
Terminal Differentiation ◽  
Cell Types ◽  
Transcriptional Level ◽  
Lethal Gene ◽  
C Elegans ◽  
Mosaic Analysis ◽  
Late Step ◽  
Organ Specific ◽  
Differentiation Marker ◽  
Bzip Family

The organisation of organ formation is still an unsolved problem. Mutations in the zygotic lethal gene pha-1 affect a late step during organ development in the nematode C. elegans. In mutant embryos all tissues in the pharynx fail to undergo terminal differentiation and morphogenesis. The expression of an early differentiation marker in pharyngeal muscle precursors is not impaired in mutant embryos, which suggests that pharynx cells still acquire their identity. Therefore the gene defines an organ-specific terminal differentiation function. We cloned and sequenced the pha-1 gene and found that the deduced protein sequence contains features characteristic of the bZIP family of transcription factors. During embryogenesis a transgenic pha-1 reporter construct is expressed transiently in all pharynx precursor cells at the time when these cells become restricted to form the pharynx organ. A mosaic analysis of the requirement of pha-1 activity during pharynx formation is consistent with the notion that pha-1 acts cell-autonomously in all cells of the pharynx primordium. The data suggest that pha-1 initiates and coordinates programs required for cytodifferentiation and morphogenesis in all cell types of the entire organ on the transcriptional level. We propose that organs are independent developmental units whose identity is reflected on the gene regulatory level.

scholarly journals Changes in the abundance and distribution of actin and associated proteins during terminal differentiation of human epidermal keratinocytes

1991 ◽  
Vol 100 (1) ◽  
pp. 153-165 ◽  
Author(s):  
M.D. Kubler ◽  
P.W. Jordan ◽  
C.H. O'Neill ◽  
F.M. Watt
Keyword(s):  
Terminal Differentiation ◽  
Immunoblot Analysis ◽  
Epidermal Keratinocytes ◽  
Basal Cells ◽  
Filamentous Actin ◽  
Human Epidermal Keratinocytes ◽  
Before And After ◽  
Associated Proteins ◽  
Differentiation Marker ◽  
Abundance And Distribution

We have examined the abundance and distribution of actin and several actin-associated proteins in human epidermal keratinocytes before and after initiation of terminal differentiation. Keratinocytes were placed in suspension in methylcellulose for 1 h or 24 h and then extracted for immunoblotting. At 24 h, when the proportion of cells expressing the terminal differentiation marker, involucrin, had increased approximately 3-fold, there were marked decreases in the levels of vinculin, talin, filamin and gelsolin. The level of actin was unchanged and the level of alpha-actinin decreased only slightly. To complement the immunoblot analysis, we also examined the distribution of each protein in basal (involucrin-negative) and suprabasal (involucrin-positive) cells in stratified colonies, using confocal microscopy. Gelsolin, filamin, vinculin, talin, alpha-actinin and filamentous actin were all less abundant in suprabasal cells than in basal cells. There were also differences in the distribution of all the proteins in the basal compared to the suprabasal layers. In addition to the changes associated with terminal differentiation, there was variation in the distribution of focal contacts and stress fibres and in gelsolin levels between basal cells at the periphery of colonies and those in the centre. These results are discussed in the context of the known association of the actin cytoskeleton with receptors of the integrin family, the loss of integrins that occurs during keratinocyte terminal differentiation, and the possible role of the cytoskeleton in signalling between integrins and the nucleus.

Altered Fine Structure of B Lymphocytes Correlated with Defective Terminal Differentiation

1973 ◽  
Vol 31 ◽  
pp. 386-387
Author(s):  
Dale E. Bockman ◽  
L. Y. Frank Wu ◽  
Alexander R. Lawton ◽  
Max D. Cooper
Keyword(s):  
Immune Deficiency ◽  
B Lymphocytes ◽  
Plasma Cells ◽  
Present Report ◽  
Specific Antigen ◽  
Terminal Differentiation ◽  
Second Stage ◽  
Two Stages ◽  
Deficiency Diseases ◽  
Cell Line Generation

B-lymphocytes normally synthesize small amounts of immunoglobulin, some of which is incorporated into the cell membrane where it serves as receptor of antigen. These cells, on contact with specific antigen, proliferate and differentiate to plasma cells which synthesize and secrete large quantities of immunoglobulin. The two stages of differentiation of this cell line (generation of B-lymphocytes and antigen-driven maturation to plasma cells) are clearly separable during ontogeny and in some immune deficiency diseases. The present report describes morphologic aberrations of B-lymphocytes in two diseases in which second stage differentiation is defective.

Sign in / Sign up

Export Citation Format

Share Document