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Characteristic analysis of skin keratinocytes in patients with type 2 diabetes based on the single-cell levels

Chinese Medical Journal 2022年第20期135卷 2461-2466页

作者： Bingye Liao Qiuyi Ouyang Hongqin Song Ziqi Wang Jinhua Ou Jinxin Huang Liang Liu Department of Operating Room The First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510080China Wound Treatment Department Integrated Hospital of Traditional Chinese MedicineSouthern Medical UniversityGuangzhouGuangdong 510315China

Background: keratinocytes play an important role in wound healing;however, less is known about skin keratinocytes in patients with type 2 diabetes mellitus (T2DM). Therefore, this study aimed to search for the transcriptional characteristics of keratinocytes at the single-cell level from T2DM patients, and to provide experimental data for identifying the pathological mechanisms of keratinocytes under pathological conditions.Methods: We performed single-cell RNA sequencing on the skin tissue from two T2DM patients and one patient without diabetes-induced trauma using the BD Rhapsody^(TM) Single-Cell Analysis System. With the help of bioinformatics R-based single-cell analysis software, we analyzed the results of single-cell sequencing to identify the single-cell subsets and transcriptional characteristics of keratinocytes at the single-cell level, including Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analyzes.Results: In this study, we found specific highly expressed signature keratinocyte-related genes. We analyzed the transcriptome of keratinocytes from experimental and control groups and screened a total of 356 differential genes, which were subject to bioinformatics analysis. Enriched pathways included oxidative phosphorylation, antigen processing and presentation, prion and Huntingtons’ diseases, bacterial invasion of epithelial cells, thermogenesis, vasopressin-regulated water reabsorption, and protein processing in the endoplasmic reticulum.Conclusions: This study revealed the characteristics of keratinocytes at the single-cell level and screened a group of differentially expressed genes related to T2DM-associated keratinocytes, oxidative phosphorylation, cytokine receptor interactions, prion diseases, and other signaling pathways.

关键词： Diabetes mellitus,type 2 Gene Ontology keratinocytes Prion diseases Sequence analysis,RNA Single-cell analysis Transcriptome Wound healing

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FXYD3 enhances IL-17A signaling to promote psoriasis by competitively binding TRAF3 in keratinocytes

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Cellular & Molecular Immunology 2023年第3期20卷 292-304页

作者： Wenjuan Yang Rukun He Hao Qu Wenwen Lian Yue Xue Tao Wang Wenlong Lin Peishuo Zhu Meng Xia Lihua Lai Qingqing Wang Institute of Immunology Zhejiang University School of Medicine310058 HangzhouChina Liangzhu Laboratory Zhejiang University Medical Center1369 West Wenyi Road311121 HangzhouChina Department of Orthopedic Surgery The Second Affiliated HospitalZhejiang University School of Medicine310009 HangzhouChina Department of Pharmacology Zhejiang University School of Medicine310058 HangzhouChina

Psoriasis is a common chronic inflammatory skin disease characterized by inflammatory cell infiltration and epidermal hyperplasia.However,the regulatory complexity of cytokine and cellular networks still needs to be investigated.Here,we show that the expression of FXYD3,a member of the FXYD domain-containing regulators of Na+/K+ATPases family,is significantly increased in the lesional skin of psoriasis patients and mice with imiquimod(IMQ)-induced psoriasis.IL-17A,a cytokine important for the development of psoriatic lesions,contributes to FXYD3 expression in human primary keratinocytes.FXYD3 deletion in keratinocytes attenuated the psoriasis-like phenotype and inflammation in an IMQ-induced psoriasis model.Importantly,FXYD3 promotes the formation of the IL-17R-ACT1 complex by competing with IL-17R for binding to TRAF3 and then enhances IL-17A signaling in keratinocytes.This promotes the activation of the NF-κB and MAPK signaling pathways and leads to the expression of proinflammatory factors.Our results clarify the mechanism by which FXYD3 serves as a mediator of IL-17A signaling in keratinocytes to form a positive regulatory loop to promote psoriasis exacerbation.Targeting FXYD3 may serve as a potential therapeutic approach in the treatment of psoriasis.

关键词： FXYD3 TRAF3 IL-17signaling keratinocytes Psoriasis

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Reversibly immortalized keratinocytes(iKera)facilitate re-epithelization and skin wound healing:Potential applications in cell-based skin tissue engineering

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Bioactive Materials 2022年第3期7卷 523-540页

作者： Jiamin Zhong Hao Wang Ke Yang Huifeng Wang Chongwen Duan Na Ni Liqin An Yetao Luo Piao Zhao Yannian Gou Shiyan Sheng Deyao Shi Connie Chen William Wagstaff b Bryce Hendren-Santiago b Rex C.Haydon b Hue H.Luu b Russell R.Reid Sherwin HHo Guillermo A.Ameer Le Shen Tong-Chuan He Jiaming Fan Ministry of Education Key Laboratory of Diagnostic Medicine And Department of Clinical BiochemistrySchool of Laboratory MedicineChongqing Medical UniversityChongqing400016China Molecular Oncology Laboratory Department of Orthopaedic Surgery and Rehabilitation MedicineThe University of Chicago Medical CenterChicagoIL60637USA The Pediatric Research Institute The Children’s Hospital of Chongqing Medical UniversityChongqing400014China Biomedical Engineering Department Northwestern UniversityEvanstonIL60208USA Department of Orthopaedics Union Hospital of Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Surgery The University of Chicago Medical CenterChicagoIL60637USA Center for Advanced Regenerative Engineering(CARE) EvanstonIL60208USA Department of Surgery Northwestern University Feinberg School of MedicineChicagoIL60616USA

Skin injury is repaired through a multi-phase wound healing process of tissue granulation and re-epithelialization.Any failure in the healing process may lead to chronic non-healing wounds or abnormal scar formation.Although significant progress has been made in developing novel scaffolds and/or cell-based therapeutic strategies to promote wound healing,effective management of large chronic skin wounds remains a clinical challenge.keratinocytes are critical to re-epithelialization and wound healing.Here,we investigated whether exogenous keratinocytes,in combination with a citrate-based scaffold,enhanced skin wound healing.We first established reversibly immortalized mouse keratinocytes(iKera),and confirmed that the iKera cells expressed keratinocyte markers,and were responsive to UVB treatment,and were non-tumorigenic.In a proof-of-principle experiment,we demonstrated that iKera cells embedded in citrate-based scaffold PPCN provided more effective re-epithelialization and cutaneous wound healing than that of either PPCN or iKera cells alone,in a mouse skin wound model.Thus,these results demonstrate that iKera cells may serve as a valuable skin epithelial source when,combining with appropriate biocompatible scaffolds,to investigate cutaneous wound healing and skin regeneration.

关键词： keratinocytes Skin tissue engineering Reversible immortalization SV40 large T antigen PPCN Skin wound healing

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Transplantation of human induced pluripotent stem cell derived keratinocytes accelerates deep second-degree burn wound healing

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World Journal of Stem Cells 2023年第7期15卷 713-733页

作者： Li-Jun Wu Wei Lin Jian-Jiang Liu Wei-Xin Chen Wen-Jun He Yuan Shi Xiao Liu Ke Li Department of Plastic and Aesthetic Surgery The Second Affiliated Hospital of Soochow UniversitySuzhou 215004Jiangsu ProvinceChina Department of Burn and Plastic Surgery The First Affiliated Hospital of Soochow UniversitySuzhou 215006Jiangsu ProvinceChina

BACKGROUND Current evidence shows that human induced pluripotent stem cells(hiPSCs)can effectively differentiate into keratinocytes(KCs),but its effect on skin burn healing has not been reported.AIM To observe the effects of hiPSCs-derived KCs transplantation on skin burn healing in mice and to preliminarily reveal the underlying mechanisms.METHODS An analysis of differentially expressed genes in burn wounds based on GEO datasets GSE140926,and GSE27186 was established.A differentiation medium containing retinoic acid and bone morphogenetic protein 4 was applied to induce hiPSCs to differentiate into KCs.The expression of KCs marker proteins was detected using immunofluorescence staining.A model of a C57BL/6 mouse with deep cutaneous second-degree burn was created,and then phosphate buffered saline(PBS),hiPSCs-KCs,or hiPSCs-KCs with knockdown of COL7A1 were injected around the wound surface.The wound healing,re-epithelialization,engraftment of hiPSCs-KCs into wounds,proinflammatory factor level,and the NF-κB pathway proteins were assessed by hematoxylin-eosin staining,carboxifluorescein diacetate succinimidyl ester(CFSE)fluorescence staining,enzyme linked immunosorbent assay,and Western blotting on days 3,7,and 14 after the injection,respectively.Moreover,the effects of COL7A1 knockdown on the proliferation and migration of hiPSCs-KCs were confirmed by immunohistochemistry,EdU,Transwell,and damage repair assays.RESULTS HiPSCs-KCs could express the hallmark proteins of KCs.COL7A1 was down-regulated in burn wound tissues and highly expressed in hiPSCs-KCs.Transplantation of hiPSCs-KCs into mice with burn wounds resulted in a significant decrease in wound area,an increase in wound re-epithelialization,a decrease in proinflammatory factors content,and an inhibition of NF-κB pathway activation compared to the PBS group.The in vitro assay showed that COL7A1 knockdown could rescue the inhibition of hiPSCs-KCs proliferation and migration,providing further evidence that COL7A1 speeds up burn wound healing by limiting cell

关键词： Induced pluripotent stem cell keratinocytes Cell transplantation Burn wound healing COL7A1

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Optimization of LPS-Induced Inflammation Model and Its Feasibility as a Fast Screening Model for Cosmetics

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Journal of Cosmetics, Dermatological Sciences and Applications 2024年第1期14卷 84-97页

作者： Fanghui Sun Xiaojie Song Nannan Liu Gang Huo R & D Center OSM Biology Co. Ltd. Huzhou China

Objectives: The existing inflammatory models are concentrated in relatively complex medical fields, and most of them use a single type of cell, and the induction conditions are not uniform, so the current LPS-induced inflammation model is less conducive to the study of skin inflammation. The aim of this research is to enhance the existing LPS-induced inflammation model and establish a skin inflammation model that is suitable for the swift screening of anti-inflammatory agents in the cosmetics industry. Methods: LPS was used to induce inflammatory responses in KC and THP-1 cells. Enzyme-linked immunosorbent assay (ELISA) was employed to assess the levels of IL-1α, IL-8, and TNF-α in the two cell types, while the DCFH-DA probe was utilized to label the levels of reactive oxygen species (ROS) in both cell types. Results: In KC cells, 10 μg/mL of LPS induced a significant upregulation of IL-8 but did not result in elevated expression of IL-1α. However, at 100 μg/mL of LPS, both IL-8 and IL-1α were highly expressed in KC cells. LPS concentrations ranging from 0.01 to 100 μg/mL failed to stimulate TNF-α production in KC cells but induced a gradient increase in ROS levels. In THP-1 cells, LPS concentrations from 0.01 to 100 μg/mL did not induce IL-1α production but significantly elevated IL-8 and led to a gradient increase in TNF-α and ROS. After treatment with 100 μg/mL of LPS, the cosmetic ingredient Rucika KGM mitigated the elevated levels of IL-1α, IL-8, and ROS in LPS-induced KC cells and IL-8 and ROS in THP-1 cells. Conclusion: This study has successfully developed an application-oriented model suitable for investigating skin inflammation, enabling the rapid and comprehensive screening of cosmetic ingredients with anti-inflammatory activity. .

关键词： Cell Culture Anti-Inflammatory Lipopolysaccharide keratinocytes THP-1 Inflammatory Factors

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Transcription and Secretion of Interleukin-1β and HMGB1 in keratinocytes Exposed to Stimulations Mimicking Common Inflammatory Damages

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International Journal of Dermatology and Venereology 2023年第3期6卷 121-129页

作者： Xue-Cui Wei Yu-Jie Chen Fang-Yuan Long Shan-Shan Yu Song Xu Xu Chen School of Public Health Nanjing Medical UniversityNanjingJiangsu 211166China Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs Hospital for Skin Diseases(Institute of Dermatology)Chinese Academy of Medical Sciences&Peking Union Medical CollegeNanjingJiangsu 210042China Key Laboratory of Basic and Translational Research on Immune-Mediated Skin Diseases Hospital for Skin Diseases(Institute of Dermatology)Chinese Academy of Medical Sciences&Peking Union Medical CollegeNanjingJiangsu 210042China

Objective:Interleukin-1β(IL-1β)and high-mobility group box 1(HMGB1)are widely known damage-associated molecular patterns(DAMPs).However,their expression and secretion in different skin diseases,especially in inflammatory skin disorders,remain to be further elucidated.This study was performed to explore and compare the transcriptional and secretory levels of IL-1β and HMGB1 in keratinocytes under 3 types of stimulation:ultraviolet B(UVB)irradiation;co-stimulation by tumor necrosis factor-α(TNF-α)and interferon-γ(IFN-γ)(simulation of T helper 1 cell inflammatory challenge);and psoriasis-like stimulation by M5,a mixture of 5 proinflammatory cytokines.Methods:We used quantitative reverse-transcription polymerase chain reaction to determine the transcription levels of IL-1β and HMGB1.Western blotting and enzyme-linked immunosorbent assay were used to detect the secretion levels of IL-1β and HMGB1.The results were statistically analyzed by t test.Results:A rapid transcriptional and secretory response of IL-1β from keratinocytes occurred in all 3 types of stimulation mimicking common inflammatory environments(Pkeratinocytes in inflammatory responses.In this study,keratinocytes restrained transcription of HMGB1 when the secretion of HMGB1 was induced in certain stimulations(eg,by UVB exposure or stimulation by TNF-α and IFN-γ).

关键词： damage-associated molecular patterns interleukin-1β high-mobility group box 1 keratinocytes inflammatory skin disorders

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keratinocytes costimulate naive human T cells via CD2: a potential target to prevent the development of proinflammatory Th1 cells in the skin

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Cellular & Molecular Immunology 2020年第4期17卷 380-394页

作者： Christian Orlik Daniel Deibel Johanna Küblbeck Emre Balta Sabina Ganskih Jüri Habicht Beate Niesler Jutta Schröder-Braunstein Knut Schäkel Guido Wabnitz Yvonne Samstag Institute of Immunology Section Molecular ImmunologyHeidelberg UniversityIm Neuenheimer Feld 30569120 HeidelbergGermany Institute of Human Genetics Department of Human Molecular Geneticsand nCounter Core FacilityHeidelberg UniversityIm Neuenheimer Feld 36669120 HeidelbergGermany Department of Dermatology Heidelberg UniversityIm Neuenheimer Feld 44069120 HeidelbergGermany

The interplay between keratinocytes and immune cells,especially T cells,plays an important role in the pathogenesis of chronic inflammatory skin diseases.During psoriasis,keratinocytes attract T cells by releasing chemokines,while skin-infiltrating selfreactive T cells secrete proinflammatory cytokines,e.g.,IFN γand IL-17A,that cause epidermal hyperplasia.Similarly,in chronic graftversus-host disease,allogenic IFN γ-producing Th1/Tc1 and IL-17-producing Th17/Tc17 cells are recruited by keratinocyte-derived chemokines and accumulate in the skin.However,whether keratinocytes act as nonprofessional antigen-presenting cells to directly activate naive human T cells in the epidermis remains unknown.Here,we demonstrate that under proinflammatory conditions,primary human keratinocytes indeed activate naive human T cells.This activation required cell contact and costimulatory signaling via CD58/CD2 and CD54/LFA-1.Naive T cells costimulated by keratinocytes selectively differentiated into Th1 and Th17 cells.In particular,keratinocyte-initiated Th1 differentiation was dependent on costimulation through CD58/CD2.The latter molecule initiated STAT1 signaling and IFN γproduction in T cells.Costimulation of T cells by keratinocytes resulting in Th1 and Th17 differentiation represents a new explanation for the local enrichment of Th1 and Th17 cells in the skin of patients with a chronic inflammatory skin disease.Consequently,local interference with T cell–keratinocyte interactions may represent a novel strategy for the treatment of Th1 and Th17 cell-driven skin diseases.

关键词： keratinocytes inflammatory skin diseases psoriasis human T cells costimulation CD2 LFA-1 nonprofessional antigenpresenting cells Th1 cells Th17 cells

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Laminin 332-functionalized coating to regulate the behavior of keratinocytes and gingival mesenchymal stem cells to enhance implant soft tissue sealing

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Regenerative Biomaterials 2022年第1期9卷 724-738页

作者： Lipeng Liu Jing Wang Ying Li Bing Liu Wei Zhang Weikang An Qing Wang Boya Xu Lingzhou Zhao Chufan Ma State Key Laboratory of Military Stomatology&National Clinical Research Center for Oral Diseases&Shaanxi Key Laboratory of Stomatology Department of ProsthodonticsSchool of StomatologyThe Fourth Military Medical UniversityXi’anShaanxi 710032China Department of Stomatology Air Force Medical CenterThe Fourth Military Medical UniversityBeijing 100142China

Peri-implant epithelial sealing is the first line of defense against external pathogens or stimuli;hence,an essential process to prevent peri-implantitis.Laminin 332(LN332)is the main component of the internal basal lamina and participates in peri-implant epithelial sealing by forming hemidesmosomes(HDs)with integrinα6β4.In thiswork,poly(D,L-lactide)(PDLLA)-LN332 composite coating was successfully constructed by a method similar to layer-by-layer assembly,displaying staged LN332 release for as long as 28days.The PDLLA-LN332 composite coating can activate the intracellular PI3K-Akt pathway via binding to cellular integrinα6β4,which can promote adhesion,migration and proliferation of HaCaT cells and further enhance the expression of keratinocyte HD-related molecules,including integrinα6β4,LN332 and plectin.Furthermore,the PDLLA-LN332 composite coating can promote the adhesion,spreading and proliferation of gingival mesenchymal stem cells and accelerate their epithelial differentiation.Therefore,the PDLLA-LN332 composite coating can enhance implant soft tissue sealing,warranting further in vivo study.

关键词： PDLLA laminin 332 keratinocytes gingival mesenchymal stem cells soft tissue sealing

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Effect of RNA Interference Targeting STAT3 Gene Combined with Ultrasonic Irradiation and SonoVue Microbubbles on Proliferation and Apoptosis in keratinocytes of Psoriatic Lesions

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Chinese Medical Journal 2018年第17期131卷 2097-2104页

作者： Li-Wei Ran Hao Wang Dong Lan Hong-Xia Jia Si-Si Yu Department of DermatolocIy Jinqxi Campus Beijing Chaoyang Hospital Capital Medical University Beijing 100043 China Department of Dermatology The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an Shaanxi 710004 China

Background： Signal transducer and activator of transcription 3 （STAT3） was strongly expressed and activated in psoriatic keratinocytes （KCs） and correlated with the severity of psoriasis. The study aimed to investigate the effects of STAT3 small interfering RNA （siRNA） combined with ultrasonic irradiation and SonoVue microbubbles on the proliferation and apoptosis in KCs of psoriatic lesions and the relative mechanisms. Methods： Psoriatic KCs were transfected under four experimental conditions：（1） STA T3 siRNA carried by Lipofectamine 3000 combined with ultrasonic irradiation and SonoVue microbubbles （LUS group）; （2） STA T3 siRNA only carried by Lipofectamine 3000 （L group）; （3） the negative control ofsiRNA carried by Lipofectamine 3000 combined with ultrasonic irradiation and SonoVue microbubbles （siRNA-NC）; （4） not treated as Blank. Cell Counting Kit-8 assay was used to evaluate the cell proliferation. Cell cycle analysis was detected with cycle test Plus DNA reagent kit associated with flow cytometer. FITC Annexin V apoptosis detection kit associated with flow cytometer was applied for apoptosis analysis. Fluo calcium indicator associated with flow cytometer was used to analyze intracellular free calcium concentration （[Ca^2＋）. The expressions of cyclin D1 and Bcl-xL were detected both at the mRNA level by real-time reverse transcription-polymerase chain reaction （RT-PCR） and at the protein level by Western blotting. The obtained data were statistically evaluated by two-way analysis of variance. Results： STAT3 siRNA inhibited the growth of KCs in a time-dependent manner showing the highest proliferation inhibition in LUS group with proliferation ratio of 45.38% ± 5.85% at 72h （P 〈 0.05 vs. L group, siRNA-NC, or Blank）. STAT3 siRNA induced an altered cell cycle distribution of KCs showing the highest increases in G2/M-phase population up to 18.06% ± 0.36% in LUS group （P 〈 0.05 vs. L group, siRNA-NC, or Blank）. ST,4 T3 siRNA induced late apoptosis of KCs with the highest late apoptosis percentage of 22.87% ± 1

关键词： Apoptosis Cell Proliferation keratinocytes Microbubbles Psoriasis RNA Interference Small Interfering RNA STAT3 Transcription Factor

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Efficacy of horse oil on lipopolysaccharide-induced inflammation in human keratinocytes

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Journal of Traditional Chinese Medicine 2021年第3期41卷 355-359页

作者： In Wook Kim Hyo-Soon Jeong Hye-Young Yun Kwang Jin Baek Nyoun Soo Kwon Dong-Seok Kim Department of Biochemistry Chung-Ang University College of MedicineSeoul 06974Republic of Korea

OBJECTIVE: To investigate the efficacy of horse oil on lipopolysaccharide(LPS)-induced inflammation in human keratinocytes.METHODS: Western blot analysis was performed to measure the expression of cyclooxygenase-2(COX-2) and IκBα. ELISA was used to analyze prostaglandin E2(PGE2) levels.RESULTS: Horse oil decreased LPS-induced COX-2 and PGE2 levels in a dose-dependent manner. Nuclear factor-kappa B(NF-κB) plays a key role in the expression of inflammatory cytokines and mediators. Therefore, we investigated the influence of horse oil on the NF-κB signaling pathways. Horse oil inhibited translocation of NF-κB from the cytosol to the nucleus. Furthermore, LPS-induced degradation of IκBα was recovered by horse oil. The activation of p38 mitogen-activated protein kinase(MAPK) reportedly induces degradation of IκBα In agreement with this, LPS activated p38 MAPK and caused IκBα degradation. Conversely, horse oil inhibited LPS-induced p38 MAPK activation and IκBαdegradation. In addition, a specific p38 MAPK inhibitor, SB203580, blocked IκBα degradation.CONCLUSION: Horse oil decreased COX-2 and PGE2 by inhibiting p38 MAPK activation, IκBα degradation, and the translocation of NF-κB.

关键词： horse oil inflammation keratinocytes NF-kappa B cyclooxygenase 2 mitogen-activated protein kinase lipopolysaccharides dinoprostone

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