Relevant bibliographies by topics / Keratinocyte

Academic literature on the topic 'Keratinocyte'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Keratinocyte"

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Hildesheim, J., U. Kuhn, C. L. Yee, R. A. Foster, K. B. Yancey, and J. C. Vogel. "The hSkn-1a POU transcription factor enhances epidermal stratification by promoting keratinocyte proliferation." Journal of Cell Science 114, no. 10 (May 15, 2001): 1913–23. http://dx.doi.org/10.1242/jcs.114.10.1913.

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Skn-1a is a POU transcription factor that is primarily expressed in the epidermis and is known to modulate the expression of several genes associated with keratinocyte differentiation. However, the formation of a stratified epidermis requires a carefully controlled balance between keratinocyte proliferation and differentiation, and a role for Skn-1a in this process has not been previously demonstrated. Here, our results show, surprisingly, that human Skn-1a contributes to epidermal stratification by primarily promoting keratinocyte proliferation and secondarily by enhancing the subsequent keratinocyte differentiation. In organotypic raft cultures of both primary human keratinocytes and immortalized HaCaT keratinocytes, human Skn-1a expression is associated with increased keratinocyte proliferation and re-epithelialization of the dermal substrates, resulting in increased numbers of keratinocytes available for the differentiation process. In these same raft cultures, human Skn-1a expression enhances the phenotypic changes of keratinocyte differentiation and the upregulated expression of keratinocyte differentiation genes. Conversely, expression of a dominant negative human Skn-1a transcription factor lacking the C-terminal transactivation domain blocks keratinocytes from proliferating and stratifying. Keratinocyte stratification is dependent on a precise balance between keratinocyte proliferation and differentiation, and our results suggest that human Skn-1a has an important role in maintaining epidermal homeostasis by promoting keratinocyte proliferation.
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Burks, Hope E., Christopher Arnette, Jennifer Koetsier, Joshua Broussard, Quinn Roth-Carter, Pedram Gerami, Jodi Johnson, and Kathleen Green. "Abstract 3186: Keratinocyte desmosomal cadherin Desmoglein 1 as a mediator and target of paracrine signaling in the melanoma niche." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3186. http://dx.doi.org/10.1158/1538-7445.am2022-3186.

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Abstract Melanoma is an aggressive cancer arising from the transformation of melanocytes residing in the basal layer of the epidermis, where they are in direct contact with surrounding keratinocytes. The role of keratinocytes in shaping the melanoma tumor microenvironment, however, remains understudied. We previously showed that the keratinocyte-specific desmosomal cadherin, desmoglein 1 (Dsg1) is reduced in response to acute UV exposure. Here, we show that Dsg1 protein is reduced in keratinocytes surrounding melanoma lesions but is unchanged in keratinocytes adjacent to benign nevi. As Dsg1 reduction by UV exposure is transient, we hypothesized that the persistent loss of Dsg1 observed in the melanoma tumor niche is due to melanoma-keratinocyte paracrine crosstalk. To address this idea, keratinocytes were cultured in conditioned media from melanocytes or melanoma cells. Melanoma conditioned media reduced keratinocyte Dsg1 mRNA and protein levels, suggesting that Dsg1 downregulation in keratinocytes is maintained by melanoma cells post-transformation. Keratinocytes in melanoma conditioned media exhibited reduced Grhl1 (Grainyhead like 1), a transcriptional activator of Dsg1, and increased Snai2, a repressor of Grhl1 expression and epidermal differentiation. These data support the idea that increased Snai2 stimulated by factors secreted by melanoma cells reduces keratinocyte Dsg1 mRNA expression by repressing Grhl1. To determine the impact of keratinocyte Dsg1 loss on melanoma cell behavior, melanoma cells were grown in conditioned media from control or Dsg1-deficient keratinocytes. Melanoma cell migration increased in a trans-well assay when melanoma cells were grown in conditioned media from Dsg1-deficient keratinocytes compared to from control keratinocytes. Supporting the in vivo importance of this finding, we found a significant, negative correlation between keratinocyte Dsg1 expression and melanoma cell movement within the melanoma tumor niche in patient samples. Downregulation of keratinocyte Dsg1 by melanoma cell conditioned media increased Erk1/2 signaling upstream of pro-migratory CXCL1 production, while pharmacological inhibition of keratinocyte Erk1/2 abrogated this effect. Furthermore, inhibition of the CXCL1 receptor, CXCR2 on melanoma cells decreased migration in melanoma cells grown in Dsg1-depleted keratinocyte conditioned media. Together, these data support the idea that paracrine crosstalk between melanoma cells and keratinocytes resulting in chronic keratinocyte Dsg1 reduction is important for melanoma progression and melanoma cell movement in the early stages of metastasis. Citation Format: Hope E. Burks, Christopher Arnette, Jennifer Koetsier, Joshua Broussard, Quinn Roth-Carter, Pedram Gerami, Jodi Johnson, Kathleen Green. Keratinocyte desmosomal cadherin Desmoglein 1 as a mediator and target of paracrine signaling in the melanoma niche [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3186.
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Yan, Feng-Juan, Yong-Jian Wang, Song-En Wang, and Hai-Ting Hong. "PKCα/ERK/C7ORF41 axis regulates epidermal keratinocyte differentiation through the IKKα nuclear translocation." Biochemical Journal 478, no. 4 (February 24, 2021): 839–54. http://dx.doi.org/10.1042/bcj20200879.

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Aberrant differentiation of keratinocytes disrupts the skin barrier and causes a series of skin diseases. However, the molecular basis of keratinocyte differentiation is still poorly understood. In the present study, we examined the expression of C7ORF41 using tissue microarrays by immunohistochemistry and found that C7ORF41 is specifically expressed in the basal layers of skin epithelium and its expression is gradually decreased during keratinocytes differentiation. Importantly, we corroborated the pivotal role of C7ORF41 during keratinocyte differentiation by C7ORF41 knockdown or overexpression in TPA-induced Hacat keratinocytes. Mechanismly, we first demonstrated that C7ORF41 inhibited keratinocyte differentiation mainly through formatting a complex with IKKα in the cytoplasm, which thus blocked the nuclear translocation of IKKα. Furthermore, we also demonstrated that inhibiting the PKCα/ERK signaling pathway reversed the reduction in C7ORF41 in TPA-induced keratinocytes, indicating that C7ORF41 expression could be regulated by upstream PKCα/ERK signaling pathway during keratinocyte differentiation. Collectively, our study uncovers a novel regulatory network PKCα/ERK/C7ORF41/IKKα during keratinocyte differentiation, which provides potential therapeutic targets for skin diseases.
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Toda, K., T. L. Tuan, P. J. Brown, and F. Grinnell. "Fibronectin receptors of human keratinocytes and their expression during cell culture." Journal of Cell Biology 105, no. 6 (December 1, 1987): 3097–104. http://dx.doi.org/10.1083/jcb.105.6.3097.

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Keratinocyte attachment to fibronectin (FN) substrata was inhibited by the peptide Gly-Arg-Gly-Asp-Ser-Pro-Cys, but not by the variant peptide Gly-Arg-Gly-Glu-Ser-Pro. The RGDS-containing peptide did not inhibit keratinocyte adhesion to collagen. Keratinocyte adhesion to FN substrata also was inhibited by polyclonal anti-FN receptor antibodies originally prepared against the 140-kD FN receptors of Chinese hamster ovary (CHO) cells. Anti-CHO FN receptor antibodies did not, however, inhibit keratinocyte adhesion to collagen substrata. A monoclonal antibody designated VM-1 that was prepared against human basal keratinocytes inhibited keratinocyte adhesion to collagen but not to FN. Based on these results, we conclude that keratinocytes have distinct FN and collagen receptors. Experiments were performed to compare the expression of FN receptors on keratinocytes freshly isolated from skin and keratinocytes harvested from cell cultures. Cells harvested from keratinocyte cultures were able to neutralize the inhibitory activity of anti-CHO FN receptor antibodies and were able to attach and spread on anti-CHO FN receptor-coated substrata. Cells freshly harvested from skin, however, did not neutralize the antibodies, nor did they attach and spread on antibody-coated substrata. To learn more about the biochemical nature of the keratinocyte FN receptors, we performed immunoaffinity chromatography and immunoprecipitation experiments using the anti-CHO FN receptor antibodies. Extracts from metabolically radiolabeled, 10-d cultured keratinocytes contained FN receptors that had a 135-kD component under reducing conditions and 115- and 155-kD components under nonreducing conditions. Similar components were observed in extracts from surface-radiolabeled cells indicating that the FN receptors were expressed on keratinocyte cell surfaces. On the other hand, extracts from metabolically radiolabeled, 1-d cultured keratinocytes lacked intact FN receptors but contained a component that migrated at 48 kD under reducing conditions and 50 kD under nonreducing conditions. Because this fragment was not detected in surface-radiolabeled keratinocytes that were freshly isolated from skin, it seems likely that the fragment was located inside the cells rather than on the cell surface. A 50-kD FN receptor fragment also was observed in extracts from 10-d cultured keratinocytes if leupeptin and pepstatin were omitted from the extraction buffer. The results suggested that human keratinocytes cultured for 10 d express the 140-kD class of FN receptors, but that these receptors are not expressed on the surfaces of keratinocytes freshly isolated from skin.(ABSTRACT TRUNCATED AT 400 WORDS)
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Darmstadt, Gary L., Laurel Mentele, Philip Fleckman, and Craig E. Rubens. "Role of Keratinocyte Injury in Adherence ofStreptococcus pyogenes." Infection and Immunity 67, no. 12 (December 1, 1999): 6707–9. http://dx.doi.org/10.1128/iai.67.12.6707-6709.1999.

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ABSTRACT Keratinocytes injured acutely by UVB light or lipopolysaccharide were used to test the hypothesis that keratinocyte injury promotes bacterial adherence and the development of group A streptococcal skin infections. Injury did not affect adherence to undifferentiated and differentiated keratinocytes, but keratinocyte differentiation promoted adherence four- to fivefold.
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HUANG, YI-CHAU, TZU-WEI WANG, JUI-SHENG SUN, and FENG-HUEI LIN. "EFFECT OF CALCIUM ION CONCENTRATION ON KERATINOCYTE BEHAVIORS IN THE DEFINED MEDIA." Biomedical Engineering: Applications, Basis and Communications 18, no. 01 (February 25, 2006): 37–41. http://dx.doi.org/10.4015/s1016237206000087.

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Calcium ion concentration is proposed to be involved in the regulation of the proliferative capacity of keratinocytes, based on its significant actions in the skin. These actions are mediated by Ca2+ influx and inhibition of cell proliferation. To define Ca2+ action in the keratinocyte we investigated its effects on the proliferation and differentiation using the primary keratinocytes model. Primary keratinocytes were incubated in DMEM (containing 1.2mM calcium ion concentration) or DK11 medium (containing 0.4 mM calcium ion concentration) or K medium (containing 0.03mM calcium ion concentration). Cell viability was assessed with the MTT assay. Crystal violet assay was evaluated the proliferation rate and colony formation size of keratinocyte. Real-time PCR used to determine the terminal differentiated keratinocyte which expressed Caspase-14. Proliferation assays and real°Vtime PCR were correlated with either proliferation or differentiation in cultured human skin epidermal keratinocytes. High Ca2+ concentration was inhibited the cell viability and proliferation rate of keratinocyte. Ca2+ also increased caspases-14 expression, and inhibited cell viability, and cell colony forming efficiency. These results are consistent with Ca2+ induction of the keratinocyte differentiation. Thus, the overall Ca2+ actions connote protective functions for the epidermis that appear to include the triggering or acceleration of the differentiation.
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Hatterschide, Joshua, Amelia E. Bohidar, Miranda Grace, Tara J. Nulton, Hee Won Kim, Brad Windle, Iain M. Morgan, Karl Munger, and Elizabeth A. White. "PTPN14 degradation by high-risk human papillomavirus E7 limits keratinocyte differentiation and contributes to HPV-mediated oncogenesis." Proceedings of the National Academy of Sciences 116, no. 14 (March 20, 2019): 7033–42. http://dx.doi.org/10.1073/pnas.1819534116.

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High-risk human papillomavirus (HPV) E7 proteins enable oncogenic transformation of HPV-infected cells by inactivating host cellular proteins. High-risk but not low-risk HPV E7 target PTPN14 for proteolytic degradation, suggesting that PTPN14 degradation may be related to their oncogenic activity. HPV infects human keratinocytes but the role of PTPN14 in keratinocytes and the consequences of PTPN14 degradation are unknown. Using an HPV16 E7 variant that can inactivate retinoblastoma tumor suppressor (RB1) but cannot degrade PTPN14, we found that high-risk HPV E7-mediated PTPN14 degradation impairs keratinocyte differentiation. Deletion ofPTPN14from primary human keratinocytes decreased keratinocyte differentiation gene expression. Related to oncogenic transformation, both HPV16 E7-mediated PTPN14 degradation andPTPN14deletion promoted keratinocyte survival following detachment from a substrate. PTPN14 degradation contributed to high-risk HPV E6/E7-mediated immortalization of primary keratinocytes and HPV+but not HPV−cancers exhibit a gene-expression signature consistent with PTPN14 inactivation. We find that PTPN14 degradation impairs keratinocyte differentiation and propose that this contributes to high-risk HPV E7-mediated oncogenic activity independent of RB1 inactivation.
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Ademi, Hyrije, Katarzyna Michalak-Micka, Ueli Moehrlen, Thomas Biedermann, and Agnes S. Klar. "Effects of an Adipose Mesenchymal Stem Cell-Derived Conditioned medium and TGF-β1 on Human Keratinocytes In Vitro." International Journal of Molecular Sciences 24, no. 19 (September 29, 2023): 14726. http://dx.doi.org/10.3390/ijms241914726.

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Human keratinocytes play a crucial role during skin wound healing and in skin replacement therapies. The secretome of adipose-derived stem cells (ASCs) has been shown to secrete pro-healing factors, among which include TGF-β1, which is essential for keratinocyte migration and the re-epithelialization of cutaneous wounds during skin wound healing. The benefits of an ASC conditioned medium (ASC-CM) are primarily orchestrated by trophic factors that mediate autocrine and paracrine effects in keratinocytes. Here, we evaluated the composition and the innate characteristics of the ASC secretome and its biological effects on keratinocyte maturation and wound healing in vitro. In particular, we detected high levels of different growth factors, such as HGF, FGFb, and VEGF, and other factors, such as TIMP1 and 4, IL8, PAI-1, uPA, and IGFBP-3, in the ASC-CM. Further, we investigated, using immunofluorescence and flow cytometry, the distinct effects of a human ASC-CM and/or synthetic TGF-β1 on human keratinocyte proliferation, migration, and cell apoptosis suppression. We demonstrated that the ASC-CM increased keratinocyte proliferation as compared to TGF-β1 treatment. Further, we found that the ASC-CM exerted cell cycle progression in keratinocytes via regulating the phases G1, S, and G2/M. In particular, cells subjected to the ASC-CM demonstrated increased DNA synthesis (S phase) compared to the TGF-β1-treated KCs, which showed a pronounced G0/G1 phase. Furthermore, both the ASC-CM and TGF-β1 conditions resulted in a decreased expression of the late differentiation marker CK10 in human keratinocytes in vitro, whereas both treatments enhanced transglutaminase 3 and loricrin expression. Interestingly, the ASC-CM promoted significantly increased numbers of keratinocytes expressing epidermal basal keratinocyte markers, such DLL1 and Jagged2 Notch ligands, whereas those ligands were significantly decreased in TGF-β1-treated keratinocytes. In conclusion, our findings suggest that the ASC-CM is a potent stimulator of human keratinocyte proliferation in vitro, particularly supporting basal keratinocytes, which are crucial for a successful skin coverage after transplantation. In contrast, TGF-β1 treatment decreased keratinocyte proliferation and specifically increased the expression of differentiation markers in vitro.
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Moon, Jadie Yoonjoo, Sonya Wolf, Christopher Audu, William Melvin, Amrita Joshi, Kevin Mangum, Emily Barrett, et al. "IL-17A-mediated JMJD3 regulation of integrin alpha 3 gene expression alters migration of diabetic keratinocytes and impairs wound repair." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 63.01. http://dx.doi.org/10.4049/jimmunol.210.supp.63.01.

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Abstract Keratinocytes are key structural cells in cell migration during wound repair. Keratinocyte migration is dysfunctional in diabetes and results in non-healing, however, the reason for this is unclear. Using bulk and single cell sequencing, we identified that Th17 CD4+ T-cells predominate as does an IL-17A signature in human diabetic wound tissue compared to non-diabetic controls. The effects of increased IL-17A in diabetic skin on keratinocyte function is unknown. To examine this, we subjected isolated keratinocytes to scratch injury and a 24hr rIL-17A (20ng) stimulation. We observed a significant decrease in migration rate in IL-17A stimulated keratinocytes compared to their controls. Next, we examined migration related genes in keratinocytes from mice fed with a normal (ND) or a high fat (HFD) diet. Integrin alpha 3 subunit, Itga3, (a protein known to delay keratinocyte migration during wound re-epithelialization) was higher in diabetic (HFD) keratinocytes compared to ND controls at baseline and with rIL-17A. We analyzed epigenetic enzymes known to increase gene expression and identified that JMJD3, a histone demethylase that relaxes chromatin, was increased both in diabetic keratinocytes from our human scRNA-seq and in murine diabetic keratinocytes with rIL17A. Further, treatment with a JMJD3-specific inhibitor (GSK-J4) decreased Itga3 in diabetic keratinocytes, suggesting that JMJD3 may be relevant to IL-17A-mediated regulation of integrin alpha 3 and other keratinocyte migration genes. Continued investigation into upstream IL-17A signaling in normal and diabetic keratinocytes that alters downstream migration is crucial for our understanding of impaired keratinocyte functions associated with diabetic wound repair. NIH T32 AI 007413, Research Training in Experimental Immunology Rackham Pre-Candidate Graduate Student Research Grant, University of Michigan
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Norris, D. A., S. B. Ryan, R. M. Kissinger, K. A. Fritz, and S. T. Boyce. "Systematic comparison of antibody-mediated mechanisms of keratinocyte lysis in vitro." Journal of Immunology 135, no. 2 (August 1, 1985): 1073–79. http://dx.doi.org/10.4049/jimmunol.135.2.1073.

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Abstract We have conducted a systematic comparison of lysis of TNP-coated keratinocyte targets by TNP-specific antibody, by antibody plus complement, by antibody-dependent cellular cytotoxicity (ADCC), and by natural killing with the use of monocyte, lymphocyte, and neutrophil effectors. With chromium-release assays, human keratinocytes, HEp-2 cells (transformed human keratinocytes), PAM 212 cells (transformed mouse keratinocytes), and RSC (transformed rabbit keratinocytes) were all susceptible to monocyte- and lymphocyte-mediated ADCC (p less than 0.01 to p less than 0.02). All trypsinized keratinocyte targets were also susceptible to natural killing by monocyte or lymphocyte effectors (p = 0.05 to p less than 0.001). Antibody and antibody plus complement were poor mediators of keratinocyte lysis. If protein and complex lipid synthesis of keratinocytes were inhibited by 16-hr cycloheximide preincubation, then keratinocytes were susceptible to complement-mediated lysis, implying that the resistance of these cells to complement may be due to repair of transmembrane pores. Comparison of chromium-release assays with fluorescein diacetate dye uptake viability assays showed that human keratinocytes were still susceptible to monocyte and lymphocyte ADCC but not to antibody, antibody plus complement, or natural killing. The reproducible and uniform susceptibility of normal and transformed keratinocyte targets from three different species to monocyte and lymphocyte ADCC supports the hypothesis that this mechanism of cellular lysis may be important in antibody-associated diseases of epidermal cytotoxicity.
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Dissertations / Theses on the topic "Keratinocyte"

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Kalaji, Ruba. "Mechanisms regulating keratinocyte morphology." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501083.

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White, Stephen John. "Ex vivo keratinocyte gene therapy." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268103.

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Allan, G. "Gene expression during keratinocyte differentiation." Thesis, University of Newcastle Upon Tyne, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233424.

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Schilling, David. "Stress and Growth Related Keratinocyte Pathways." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-10451.

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Elliott, Richard John. "Keratinocyte responses to novel proopiomelanocortin agents." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419623.

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St, George-Smith Stephen. "Psoriasis : the role of the keratinocyte." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339965.

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Roshan, Amit. "Stochasticity and order : studies of keratinocyte proliferation." Thesis, University of Cambridge, 2014. https://www.repository.cam.ac.uk/handle/1810/252966.

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A central tenet of stem cell biology has been that proliferating tissues are maintained through a cellular hierarchy comprising of self-renewing stem cells at the apex, multiple lineage-restricted short-lived progenitor cells, and post-mitotic differentiated cells. The wide range of colony sizes in cultured human keratinocytes has been taken to support this hypothesis. Contrary to this model, researchers using genetic lineage tracing in mouse epidermis have inferred a single progenitor population for homeostasis, and a quiescent stem cell population activated upon wounding or genetic mutation. To study the proliferative behaviour of human keratinocytes, I used live imaging in vitro at single cell resolution. This shows two modes of proliferation: Type 1 cell division is stochastic with equal odds of generating dividing or non-dividing progeny, while Type 2 cell division predominantly produces two dividing daughters. These two modes are sufficient to explain the entire range of colony sizes seen after 7-12 days of culture and does not require a spectrum of proliferative ability. This insight provides a simple way to study the effects of external factors on cell fate. To exemplify this, I observed the effects of epidermal growth factor (EGF) and the Wnt agonist R-spondin on proliferation. Here I find proliferation in type 2 colonies changes by changing the proportion of cells dividing. This has implications for the limited success of EGF therapies in clinical trials following burns. To examine clonal contributions to wound repair, I used the mouse oesophageal epithelium which is exclusively composed of, and maintained by, a single progenitor population. I developed a micro-endoscopic wounding technique that produced localised superficial wounds. Here, I found that these wounds healed by uniform contribution from surrounding keratinocytes, demonstrating that reserve stem cells are not obligatory for wound repair. In summary, my work shows that human keratinocytes in vitro have two, and only two, modes of proliferation: a stochastic mode that is insensitive to external EGF signalling, and a EGF-sensitive exponential mode. Additionally, proliferation during wound repair can occur with stochastically dividing progenitors, and does not obligate stem cell recruitment in vivo.
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Norgett, Elizabeth Emma. "Intercellular junctions in keratinocyte differentiation and disease." Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417795.

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Liebig, Timo Christian. "Rho GTPases in Keratinocyte adhesion and differentiation." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499127.

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McMullan, Rachel Jane. "Regulation of keratinocyte function by Rho kinase." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275126.

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Books on the topic "Keratinocyte"

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Irene, Leigh, and Watt Fiona M, eds. Keratinocyte methods. Cambridge: Cambridge University Press, 1994.

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Irene, Leigh, Lane E. Birgitte, and Watt Fiona M, eds. The keratinocyte handbook. Cambridge [England]: Cambridge University Press, 1994.

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Jemec, Gregor B. E., Lajos Kemeny, and Donald Miech, eds. Non-Surgical Treatment of Keratinocyte Skin Cancer. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-79341-0.

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Michel, Darmon, and Blumenberg Miroslav Lj, eds. Molecular biology of the skin: The keratinocyte. San Diego: Academic Press, 1993.

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McMullan, Rachel Jane. Regulation of keratinocyte function by Rho Kinase. Birmingham: University of Birmingham, 2002.

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Dittlein, Daniela. Influence of keratinocyte derived mediators on CD4+ T cell plasticity. München: Universitätsbibliothek der TU München, 2016.

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M, Milstone Leonard, Edelson Richard L, and New York Academy of Sciences., eds. Endocrine, metabolic, and immunologic functions of keratinocytes. New York, N.Y: New York Academy of Sciences, 1988.

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Merendino, John Jerome. Keratinocytes produce a PTH-sensitive adenylate cyclase-stimulating factor. [New Haven: s.n.], 1985.

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Stacey, Michael William. Studies on cultured skin keratinocytes from normal and basal cell naevus syndrome patients. Birmingham: University of Birmingham, 1989.

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1935-, Ōkawara Akira, and McGuire Joseph, eds. The biology of the epidermis: Molecular and functional aspects : proceedings of the Fifth Japan-United States Symposium on the Biology of the Epidermis, Niseko, Hokkaido, 21-25 July 1991. Amsterdam: Elsevier, 1992.

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Book chapters on the topic "Keratinocyte"

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Moll, I. "Keratinocyte Carcinogenesis: Introduction." In Skin Carcinogenesis in Man and in Experimental Models, 151–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84881-0_11.

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Hunziker, T., and A. Limat. "Cultured Keratinocyte Grafts." In Management of Leg Ulcers, 57–64. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000060609.

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Jimenez, Pablo A., Dale Greenwalt, Donna L. Mendrick, Mark A. Rampy, Jeffrey Su, Kam H. Leung, and Kevin M. Connolly. "Keratinocyte growth factor-2." In New Cytokines as Potential Drugs, 101–19. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8456-3_7.

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Breitkreutz, Dirk, Petra Boukamp, Andrea Hülsen, Cathy Ryle, Hans-Jürgen Stark, Hans Smola, Gabi Thiekötter, and Norbert E. Fusenig. "Human Keratinocyte Cell Lines." In Pharmaceutical Applications of Cell and Tissue Culture to Drug Transport, 283–96. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4757-0286-6_23.

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Li, Luowei. "Mouse Epidermal Keratinocyte Culture." In Methods in Molecular Biology, 177–91. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-125-7_12.

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Lucero, Olivia M., Fiona O’Reilly Zwald, and David Lambert. "Chemoprevention of Keratinocyte Carcinomas." In Skin Cancer Management, 335–51. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-50593-6_21.

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Nozzoli, Filippo, and Daniela Massi. "Dermatopathology of Keratinocyte Tumors." In Non-melanoma Skin Cancer, 59–72. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003226017-5.

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Brakebusch, Cord. "Keratinocyte Migration in Wound Healing." In Cell Migration in Development and Disease, 275–98. Weinheim, FRG: Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527604669.ch15.

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Rice, R. H., R. Chakravarty, J. Chen, W. O’Callahan, and A. L. Rubin. "Keratinocyte Transglutaminase: Regulation and Release." In Advances in Post-Translational Modifications of Proteins and Aging, 51–61. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-9042-8_4.

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Blumenberg, M., and M. Tomić-Canić. "Human epidermal keratinocyte: Keratinization processes." In Formation and Structure of Human Hair, 1–29. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-9223-0_1.

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Conference papers on the topic "Keratinocyte"

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Ishida, Yoshihiro, Nobuyuki Kakiuchi, Yoichi Fujii, Tomonori Hirano, Yoshikage Inoue, Tomomi Nishimura, Tatsuki Ogasawara, et al. "Abstract 2675: Clonal expansion of skin keratinocyte." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2675.

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Serener, Ali, and Sertan Serte. "Keratinocyte Carcinoma Detection via Convolutional Neural Networks." In 2019 3rd International Symposium on Multidisciplinary Studies and Innovative Technologies (ISMSIT). IEEE, 2019. http://dx.doi.org/10.1109/ismsit.2019.8932828.

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Arnette, Christopher, Jodi L. Johnson, Hope E. Burks, Jennifer L. Koetsier, and Kathleen J. Green. "Abstract LB-355: Loss of keratinocyte desmoglein 1 occurs during melanoma development and alters crosstalk between keratinocytes and melanocytes." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-355.

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Kottmann, J., T. Rosskopf, J. M. Rey, J. Luginbuhl, E. Reichmann, and M. W. Sigrist. "Mid-infrared photoacoustic sensing of glucose in keratinocyte solutions." In 12th European Quantum Electronics Conference CLEO EUROPE/EQEC. IEEE, 2011. http://dx.doi.org/10.1109/cleoe.2011.5943084.

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Katsantonis, John C., Savas K. Georgiou, Mary G. Providaki, John G. Vlahonikolis, and Andronicki D. Tosca. "Collagen-gel-induced resistance of overlying keratinocyte cultures to photosensitization." In BiOS Europe '97, edited by Kristian Berg, Benjamin Ehrenberg, Zvi Malik, Johan Moan, and Abraham Katzir. SPIE, 1997. http://dx.doi.org/10.1117/12.297792.

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Kadikoylu, Gulce, Gunnur Onak, Ozan Karaman, and Nermin Topaloglu. "How Does Antibacterial Photodynamic Therapy Affect Healthy Human Keratinocyte Cells?" In 2018 Medical Technologies National Congress (TIPTEKNO). IEEE, 2018. http://dx.doi.org/10.1109/tiptekno.2018.8597047.

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Clement, Amanda L., and George D. Pins. "Every cell has its niche: Harnessing microtopography to control keratinocyte fate." In 2014 40th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2014. http://dx.doi.org/10.1109/nebec.2014.6972759.

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Kosol, Wilai, Renea Faulknor, and Francois Berthiaume. "The effect of a simulated diabetic wound environment on keratinocyte migration." In 2015 41st Annual Northeast Biomedical Engineering Conference (NEBEC). IEEE, 2015. http://dx.doi.org/10.1109/nebec.2015.7117041.

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Bi, Jing, Lin Tong, lin Y. Song, and Chun-xue Bai. "Keratinocyte Growth Factor-2 Protects Ventilator-Induced Lung Injury In Rats." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1157.

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Haider, Zain, Yves Le Drean, Ronan Sauleau, Laura Caramazza, Micaela Liberti, and Maxim Zhadobov. "Microdosimetry in a realistic keratinocyte cell model at mmWave and HF frequencies." In 2022 3rd URSI Atlantic and Asia Pacific Radio Science Meeting (AT-AP-RASC). IEEE, 2022. http://dx.doi.org/10.23919/at-ap-rasc54737.2022.9814391.

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Reports on the topic "Keratinocyte"

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Meyer, Anthony A. Efficacy of Allogenic Cultured Keratinocyte Grafts for Burn Wounds. Fort Belvoir, VA: Defense Technical Information Center, June 1993. http://dx.doi.org/10.21236/ada267262.

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Simon, Marcia, Steve A. McClain, and Thomas Zimmerman. Keratinocyte Spray Technology for the Improved Healing of Cutaneous Sulfur Mustard Injuries. Fort Belvoir, VA: Defense Technical Information Center, July 2008. http://dx.doi.org/10.21236/ada485524.

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Simon, Marcia, Steve A. McClain, and Thomas Zimmerman. Keratinocyte Spray Technology for the Improved Healing of Cutaneous Sulfur Mustard Injuries. Fort Belvoir, VA: Defense Technical Information Center, July 2009. http://dx.doi.org/10.21236/ada508243.

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Boissy, Raymond E. On the Pathophysiology of Cutaneous Cafe-au-lait Lesions in Neurofibromatosis and the Role of Keratinocyte and/or Fibroblast-Synthesized Cytokines. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada586812.

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Varghese, Shyni. Proteomic Analyses of NF1-Interacting Proteins in Keratinocytes. Fort Belvoir, VA: Defense Technical Information Center, April 2015. http://dx.doi.org/10.21236/ada620279.

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Morhenn, Vera B., Gregory J. Wastek, Anastasia B. Cua, and Jonathan N. Mansbridge. The Effects of Recombinant Interleukin-1 and Interleukin-2 on Human Keratinocytes Running Head: Interleukins-1 and 2 Effect on Keratinocytes. Fort Belvoir, VA: Defense Technical Information Center, January 1987. http://dx.doi.org/10.21236/ada206079.

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Guzman, Juantia J., Clark L. Gross, William J. Smith, and Susan A. Kelly. In Vitro Cytotoxicity Assays of Human Epidermal Keratinocytes in Culture Exposed to Sulfur Mustard. Fort Belvoir, VA: Defense Technical Information Center, January 2000. http://dx.doi.org/10.21236/ada390628.

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Guess, Jennifer C., and Dennis J. McCance. Decreased Migration of Langerhans Precursor-Like Cells in Response to Human Keratinocytes Expressing HPV-16 E6/E7 is Related to Reduced Macrophage Inflammatory Protein-3Alpha Production. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada435872.

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Exposure to the antimicrobial chemical triclosan disrupts keratinocyte function and skin integrity in a model of reconstructed human epidermis (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, January 2023. http://dx.doi.org/10.26616/nioshrd-1054-2023-0.

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