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Partial epithelial-mesenchymal transition in keloid scars: regulation of keloid keratinocyte gene expression by transforming growth factor-β1

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Burns & Trauma 2016年第3期4卷 199-215页

作者： Jennifer M.Hahn Kevin L.McFarland Kelly A.Combs Dorothy M.Supp Research Department Shriners Hospitals for Children-CincinnatiCincinnatiOHUSA Research Department Shriners Hospitals for Children-CincinnatiCincinnatiOHUSA Department of Surgery University of Cincinnati College of MedicineCincinnatiOHUSA

Background:Keloids are an extreme form of abnormal scarring that result from a pathological fibroproliferative wound healing *** molecular mechanisms driving keloid pathology remain incompletely understood,hindering development of targeted,effective *** studies in our laboratory demonstrated that keloid keratinocytes exhibit adhesion abnormalities and display a transcriptional signature reminiscent of cells undergoing epithelial-mesenchymal transition(EMT),suggesting a role for EMT in keloid *** the current study,we further define the EMT-like phenotype of keloid scars and investigate regulation of EMT-related genes in ***:Primary keratinocytes from keloid scar and normal skin were cultured in the presence or absence of transforming growth factor beta 1(TGF-β1)+/-inhibitors of TGF-β1 and downstream signaling *** expression was measured using quantitative polymerase chain *** was analyzed using an in vitro wound healing *** in keloid scar and normal skin sections were localized by *** analyses utilized SigmaPlot(SyStat Software,San Jose,CA)or SAS?(SAS Institute,Cary,NC).Results:In keloid and normal keratinocytes,TGF-β1 regulated expression of EMT-related genes,including hyaluronan synthase 2,vimentin,cadherin-11,wingless-type MMTV integration site family,member 5A,frizzled 7,ADAM metallopeptidase domain 19,and *** of canonical TGF-β1 signaling in keloid keratinocytes significantly inhibited expression of these genes,and TGF-β1 stimulation of normal keratinocytes increased their *** inhibition of the extracellular signal-regulated kinase 1/2(ERK1/2)signaling pathway or the p38 mitogen-activated protein kinase pathway attenuated TGF-β1-induced expression of subsets of these *** of keloid keratinocytes,previously shown to be increased compared with normal keratinocytes,was significantly reduced by inhibition of TGF-β1 or E

关键词： Keloid keratinocyte Epithelial-mesenchymal transition Wound healing Scar Fibrosis

Construction and primary analysis of human keratinocyte model expressing anti-sense protein kinase Cζ

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Chinese Science Bulletin 1998年第18期43卷 1556-1562页

作者： Xiaoyan Zhang Huitu Liu Shengqing Ma State Key Laboratory of Cell Proliferation and Regulation Biology Department of Biology Beijing Normal University Beijing China Department of Dermatology The First Hospital Beijing Medical University Beijing China

Protein kinase C (PKC), which has a wide variety of functions, comprises at least twelve isoenzymes that have distinct roles respectively. Research in recent years indicates that PKCζ plays a pivotal role in the regulation of cell proliferation. In order to investigate its role in the regulation of keratinocyte proliferation, eukaryotic expression plasmid of anti_sense PKCζ is constructed and transfected into human keratinocyte line, Colo16. The human keratinocyte model expressing anti_sense PKCζ is established successfully, the growth properties of the cell model is analyzed by the detection of cell growth curve and cell cycle phase. The mechanism of the relationship between PKCζ and CyclinD1 is also investigated by the western blotting analysis of CyclinD1 protein.

关键词： PKCζ human keratinocyte proliferation.

Inhibiting Hyper-O-GlcNAcylation of c-Myc accelerate diabetic wound healing by alleviating keratinocyte dysfunction

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Burns & Trauma 2021年第1期9卷 170-183页

作者： Jie Zhang Peilang Yang Dan Liu Min Gao Jizhuang Wang Tianyi Yu Xiong Zhang Yan Liu Department of Burn Ruijin Hospital Affliated to Shanghai Jiao Tong University School of MedicineShanghai 200025China

Background:Diabetic foot ulcers characterized by delayed healing are one of the main complications of *** keratinocyte dysfunction has been found to play a pivotal role in the poor healing ability of diabetic *** this study,we aimed to explore the relationship between c-Myc and its O-linked N-acetylglucosamine(O-GlcNAc)glycosylation(O-GlcNAcylation)modification and keratinocyte dysfunction in diabetic ***:Clinical wound samples were collected and a full-thickness skin defect wound model of diabetic rats was ***-epithelialization of wounds was observed by H&E staining and expressions of proliferating cell nuclear antigen,transglutaminase 1,loricrin,c-Myc and O-GlcNAc were measured by *** functional changes of proliferation,migration and differentiation of human immortalized epidermal cells(HaCaT)cells after overexpression or knockdown of c-Myc were observed.O-GlcNAcylation of c-Myc was confirmed using immunoprecipitation and proximity ligation *** of the c-Myc protein was measured using *** healing was observed after topical application of compounds that inhibited c-Myc or O-GlcNAc on diabetic ***:keratinocytes at the diabetic wound margin were characterized by active proliferation and division,slow migration and poor *** phenomena were observed in HaCaT cells cultured in 30 mM glucose and keratinocytes at the wound margin of the diabetic *** expression of c-Myc was increased in keratinocytes at the wound margin of diabetic rats,patients,and in HaCaT cells cultured with 30 mM *** expression of c-Myc promoted the proliferation while inhibiting the migration and differentiation of the HaCaT cells,and inhibition of c-Myc promoted diabetic wound *** O-GlcNAcylation of c-Myc with 30mMglucose stabilized the c-Myc *** of O-GlcNAc ameliorated keratinocyte dysfunction and promoted diabetic wound ***

关键词： c-Myc O-GlcNAc diabetes wound healing keratinocyte glucose

Chemerin Exacerbates Psoriasis by Stimulating keratinocyte Proliferation and Cytokine Production

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Current Medical Science 2023年第2期43卷 399-408页

作者： Shu-min KONG Xiao-yan SUN Wen-ya CUI Yu-chun CAO Department of Dermatology Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan430030China

Objective Psoriasis is often combined with metabolic abnormalities,such as obesity and *** upregulation of chemerin,which is an essential protein produced primarily from white fat,is strongly correlated to the development of ***,there is no clarification on its exact function and mechanism in disease *** present study aims to determine its function and mechanism in disease *** The present study used a psoriasislike inflammatory cell model and imiquimod(IMQ)-induced mouse model to confirm whether chemerin is upregulated in psoriasis *** Chemerin enhanced the keratinocyte proliferation,inflammatory cytokine secretion,and activation of the MAPK signaling ***,the intraperitoneal injection of neutralizing anti-chemerin antibody(ChAb)diminished the epidermal proliferation and inflammation in the IMQ-induced mouse *** The present results indicate that chemerin promotes keratinocyte proliferation,and enhances the production of inflammatory cytokines,thereby aggravating the ***,chemerin can be a prospective target for the treatment of psoriasis.

关键词： psoriasis keratinocyte chemerin proliferation inflammation

Role of gap junctions between keratinocyte and melanocyte in melanogenesis

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Frontiers in Biology 2015年第6期10卷 495-502页

作者： Divya Padma Kapaettu Satyamoorthy Kumar M.R. Bhat Division of Biotechnology School of Life Sciences Manipal University Manipal-576104 India Department of Anatomy Kasturba Medical College Manipal University Manipal-5 76104 India

The process ofmelanogenesis in melanocytes and the transport of melanin in the form ofmelanosomes to the neighboring keratinocytes are the key steps in human skin pigmentation. keratinocytes and melanocytes interact in intricate manner to maintain the homeostasis. The present study was designed to understand the role of cell-cell interaction through the gap junctions between melanocytes and keratinocytes on melanogenesis. We show that, inhibition of the gap junctional activity between human keratinocytes and melanocytes in a coculture system using gap junction blocker lowers the expression of key regulatory genes of melanogenesis such as tyrosinase and microphthalmia- associated transcription factor （MITF）. This was followed by concurrent decrease in tyrosinase protein levels and activity. Our results show the preliminary evidence for the regulation of melanogenesis in melanocytes through direct gap junctional communication by keratinocytes. Deciphering the mechanism and factors involved in the process would uncover the significance of gap junctions in melanogenesis.

关键词： melanocyte keratinocyte melanogenesis gap junctions cell communication

Cultured keratinocyte grafting on various biologic matrices

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第二军医大学学报 1998年第S1期19卷 5-12页

作者： Stark GB△ Horch RE Voigt M Kopp J Saied S Jiao XY Guest professor of Second Military Medical University From the Department of Plastic and Hand Surgery and Tissue Engineering Lab. and valley TEC University of Freiburg Medical Center Freiburg Germany Department of Plastic Surgery Changhai Hospital Second Military Medical University Shanghai 200433

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关键词： keratinocyte culture tissue engineering skin substitute burns biomaterials

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Journal of Medical Colleges of PLA(China) 2008年第3期23卷 167-175页

作者： Xie Shaoqiong Liao Wanqing Yao Zhirong Wang Zhidong Department of Dermatology Shangai Skin Disease and STD Shanghai 200050 China Department of Dermatology Changzheng Hospital Second Military Medical University Shanghai 200003 China

Objective:To examine the level of expression of anti skin aging gene of Ganoderma lucidum polysacchayides and clarify its mechanism with anti aging of this ancient Chinese ***:HacaT cell of keratinocytes lines were cultured and treated with the *** total RNA was extracted with Trizol reagent and cDNA was synthesized by reverse *** obtained cDNAs were then fluorescently labeled with cy3 and cy5 respectively and hybridized with gene expressing pedigree cDNA *** images were scanned and analyzed with special *** scan data were analyzed with software and checked by real time ***:Among total 18 346 human genes,the expression of 103 ones was up-regulated and 378 ones *** was demonstrated evidently that Ganoderma lucidum polysaccharides affected the expression of genes of anti skin *** ways are ***:it is concluded by analysis of function of these up-regulation and down-regulation genes that Ganoderma lucidum polysaccharides may play an important role in boosting cell growth and against skin *** shows that the results of gene array reliable by real time PCR.

关键词： Ganoderma lucidum polysaccharides Skin aging Gene chip keratinocyte

The expression of P63 protein in some keratinocyte original tissues and cells

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Journal of Nanjing Medical University 2007年第6期21卷 402-407页

作者： Rong Cui Jie Feng Xin Zhang Xi Zhou Haozhe Cao Xiaoning Yan Department of Dermatology the Second Affiliated Hospital Medical School of Xi＇ an Jiaotong University Xi＇ an 710004 Shanxi Province China Cancer Stem Cell Research Center Xi＇an Jiaotong University Xi＇an 710061 Shanxi Province China

Objective： To examine the expression patterns of p63 in tissues of particular keratinocyte original hyperproliferate diseases and variety cell types for determining if P63 is the marker of proliferative potential keratinocytes. Methods： P63 protein was detected and analyzed by immunoreactivity method and Western blot in biopsy specimens of keratinocyte original disorders including squamous cell carcinomas SCC, basal cell carcinomas BCC, Bowen＇ s disease and other tissues or cells, such as psoriasis vulgaris, normal skin tissues, primary cultured keratinocytes, immortal HaCaT cells, and epidermoid carcinoma cells A431. Results： P63 protein was expressed in the nuclei of basal and suprabasal layer of the epidermis, germinative cells of sebaceous glands in normal epidermal. P63 was strongly and diffusely detected in the majority of tumor cells in BCC and poorly-differentiated SCC. In Bowen＇ s disease, p63 expresses are remarkable in all cell layers. In the psoriasis plaque epidermal, p63 expressed mainly in basal cells and part of spinous cells. P63 expressed more strongly in primary cultured keratinocytes than in A431 cells or HaCaT cells. Conclusion： P63 is a nuclei marker of undifferentiated keratinocytes with the proliferative potential and may disrupt the terminal differentiation. The overexpression of p63 reflects immaturity of the tumor cells. The immunohistochemical staining of p63 may be useful for investigating the origin and differentiation of tumor cells.

关键词： protein keratinocyte carcinoma, skin psoriasis

Curcumin down-regulates PCNA,cyclin D1 and Bcl-X_L expression in human keratinocyte cell lines

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Journal of Medical Colleges of PLA(China) 2010年第6期25卷 321-330页

作者： Yang Zhengsheng Li Xiaoli Peng Zhenhui Song Jianwen Ren Jianwen Department of Dermatology Second Affiliated Hospital Xi 'an Jiaotong University Xi 'an 710004 China

Objective：To evaluate the effects of curcumin on regulating the proliferation,cell cycle distribution,apoptosis and relevant mechanisms in keratinocyte cell ***：The human immortalized human keratinocyte lines（HaCaT cells） were treated with different doses of *** effects of curcumin on cell viability were measured by MTT assay,and the cell cycle distribution and apoptosis determined by flow *** mRNA expression changes of proliferating cell nuclear antigen（PCNA）,cyclin D1 and Bcl-xL were from real-time PCR analysis and the protein levels were detected by Western ***：Data obtained in the study showed that curcumin could cause significantly inhibitory effect on proliferation in HaCaT cells in a time- and dose-dependent *** arrest at G1/S phase and significant apoptosis were observed after being treated with curcumin for 24 *** association with these,the expression of PCNA,cyclin D1 and Bcl-xL were decreased both at mRNA and protein levels for the same ***：Curcumin can inhibit proliferation,induce cell arrest at G1/S phase and cause apoptosis in HaCaT *** decreased expression of PCNA,cyclin D1 and Bcl-xL induced by curcumin contributes to the above effects in vitro.

关键词： Curcumin keratinocyte Proliferating cell nuclear antigen Cyclin D1 Bcl-XL