Relevant bibliographies by topics / HaCaT

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'HaCaT'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'HaCaT.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "HaCaT"

1

Alexander, Eric T., Kelsey Mariner, Yelizaveta Borodyanskaya, Allyson Minton, and Susan K. Gilmour. "Polyamine-stimulation of arsenic-transformed keratinocytes." Carcinogenesis 40, no. 8 (June 12, 2019): 1042–51. http://dx.doi.org/10.1093/carcin/bgz115.

Full text
Abstract:
Abstract Tumor promotion is strongly associated with inflammation and increased polyamine levels. Our understanding of relevant mechanisms responsible for arsenic-induced cancer remains limited. Previous studies suggest that arsenic targets and dysregulates stem cell populations that remain dormant in the skin until promoted to be recruited out of the bulge stem cell region, thus giving rise to skin tumors. In this study, we explored a possible mechanism by which increased keratinocyte polyamine biosynthesis promotes tumorsphere formation and invasiveness of arsenic-transformed HaCaT keratinocytes (As-HaCaT). Unlike parental HaCaT cells, As-HaCaT cells were tumorigenic in athymic nude mice, and the CD45negative epithelial tumor cells had enriched expression of Toll-Like Receptor 4 (TLR4), CD34 and CXCR4 as did As-HaCaT tumorsphere cultures compared to As-HaCaT monolayer cultures. Ornithine decarboxylase (ODC) overexpressing keratinocytes (Ker/ODC) release increased levels of the alarmin high mobility group box 1 (HMGB1). Ker/ODC conditioned medium (CM) stimulated As-HaCaT but not parental HaCaT tumorsphere formation, and this was inhibited by glycyrrhizin, an inhibitor of HMGB1, and by TAK242, an inhibitor of the HMGB1 receptor TLR4. Compared to parental HaCaT cells, As-HaCaT cells demonstrated greater invasiveness across a Matrigel-coated filter using either fibroblast CM or SDF-1α as chemoattractants. Addition of Ker/ODC CM or HMGB1 dramatically increased As-HaCaT invasiveness. Glycyrrhizin and TAK242 inhibited this Ker/ODC CM-stimulated invasion of As-HaCaT cells but not HaCaT cells. These results show that polyamine-dependent release of HMGB1 promotes the expansion of stem cell-like subpopulations in arsenic-transformed keratinocytes while also increasing their invasiveness, suggesting that polyamines may be a potential therapeutic target for the prevention and treatment of arsenic-initiated skin cancers.
APA, Harvard, Vancouver, ISO, and other styles
2

Hamilton, Karina D., Daniel Czajkowski, Nicolas J. Kong, Trong D. Tran, Kirk R. Gustafson, Gary Pauly, Glen M. Boyle, et al. "Anti-Fibrotic Potential of Tomentosenol A, a Constituent of Cerumen from the Australian Native Stingless Bee, Tetragonula carbonaria." Antioxidants 11, no. 8 (August 19, 2022): 1604. http://dx.doi.org/10.3390/antiox11081604.

Full text
Abstract:
Bioactivity-guided fractionation was used to isolate two compounds, tomentosenol A (1) and torellianone A (2), from a cerumen extract from Tetragonula carbonaria. The anti-fibrotic activity of these compounds was examined using human cultured neonatal foreskin fibroblasts (NFF) and immortalised keratinocytes (HaCaTs). Tomentosenol A (1), inhibited NFF and HaCaT cell proliferation and prevented NFF and HaCaT scratch wound repopulation at 12.5–25 µM concentrations. These inhibitory effects were associated with reduced cell viability, determined by tetrazolium dye (MTT) and sulforhodamine B (SRB) assays. Compound 1 further inhibited transforming growth factor-β1 (TGF-β1)-stimulated, NFF-myofibroblast differentiation and soluble collagen production; and was an effective scavenger of the model oxidant, 2,2-diphenyl-1-picrylhydrazyl (DPPH·), with an EC50 value of 44.7 ± 3.1 µM. These findings reveal significant anti-fibrotic potential for cerumen-derived tomentosenol A (1).
APA, Harvard, Vancouver, ISO, and other styles
3

Pabuprapap, Wachirachai, Wongnapa Nakyai, Waraluck Chaichompoo, Nattharika Pheedee, Saowanee Phetkeereerat, Jarupa Viyoch, Boon-ek Yingyongnarongkul, et al. "Curcuma aromatica and Curcuma comosa Extracts and Isolated Constituents Provide Protection against UVB-Induced Damage and Attenuate Matrix Metalloproteinase-1 Expression in HaCaT Cells." Cosmetics 9, no. 1 (February 11, 2022): 23. http://dx.doi.org/10.3390/cosmetics9010023.

Full text
Abstract:
Ultraviolet-B (UVB) exposure is one of the primary extrinsic factors causing skin photoaging. It stimulates inflammatory responses and arrests the cell cycle. Matrix metalloproteinase-1 (MMP-1) secreted by keratinocytes is one of the important extracellular matrixes to attenuate UVB-induced skin aging via collagen degradation. Curcuma aromatica (CA) and Curcuma comosa (CC), the herbaceous plants in the Zingiberaceae family, are commonly used in Thai traditional women’s medicines. The present work was aimed to investigate the potential of the CA and CC extracts and their isolated compounds to attenuate UVB-induced MMP-1 and cell cycle arrest in HaCaT keratinocytes. Total phenolic contents and antioxidant capacities of the extracts were determined. CC extract contains more phenolic components and provides more potent antioxidant activities than CA extract. HaCaTs were pretreated with the extracts or their isolated constituents 1–4 for 24 h and then repeatedly exposed to UVB at 100 mJ/cm2 10 times. Both extracts and compounds 1–4 effectively reduce UVB-induced MMP-1 levels in HaCaT cells and restore cell cycle arrest. This is the first report on the potential of CA and CC extracts in reducing UVB-induced MMP-1 expression and regulating cell proliferation in HaCaT cells. Thus, CA and CC extracts might be used as alternative natural agents to prevent UVB-induced skin photoaging.
APA, Harvard, Vancouver, ISO, and other styles
4

Wang, Yongfang, Xinyu Li, Shasha Song, and Jianbo Wu. "Development of Basal-Like HaCaT Keratinocytes Containing the Genome of Human Papillomavirus (HPV) Type 11 for Screening of Anti-HPV Effects." Journal of Biomolecular Screening 19, no. 8 (May 29, 2014): 1154–63. http://dx.doi.org/10.1177/1087057114536987.

Full text
Abstract:
Condylomata acuminata (CA), induced by low-risk human papillomaviruses (HPVs), is one of the most common sexually transmitted diseases. The increasing incidence and the high recurrence rate of CA have significantly contributed to public health problems around the world. Because HPVs cannot be cultured in vitro for a long time, there has been little progress in the development of HPV-specific antiviral agents. In this study, we established an HPV11.HaCaT system by introducing the recircularized genome of HPV-11 into HaCaT keratinocytes with transfection techniques and cultured them in a special medium. The existence and replication of HPV-11 DNA were positively detected in established HPV11.HaCaT cells. The HPV-11 DNA in HPV11.HaCaT cells has been stably replicated in definite passages of cells. We preliminarily studied the anti–HPV-11 effects of recombinant human interferon α1b (rhIFN-α) and 13-hexyl-palmatine hydrochloride (HP-13) in HPV11.HaCaT cells. The results suggest that HP-13 significantly inhibited the proliferation of HPV11.HaCaT cells in a dose-dependent manner, whereas rhIFN-α did not. HP-13 and rhIFN-α inhibited the replication of HPV-11 DNA and the expression of E1∧E4 mRNA in HPV11.HaCaT cells. In conclusion, the established HPV11.HaCaT cells can provide us with a convenient and relatively stable tool for screening anti–HPV-11 agents.
APA, Harvard, Vancouver, ISO, and other styles
5

Lee, Hyo-Jung, Hyo-Jeong Lee, Eun Jung Sohn, Eun-Ok Lee, Jin-Hyoung Kim, Min-Ho Lee, and Sung-Hoon Kim. "Inhibition of Connexin 26/43 and Extracellular-Regulated Kinase Protein Plays a Critical Role in Melatonin Facilitated Gap Junctional Intercellular Communication in Hydrogen Peroxide-Treated HaCaT Keratinocyte Cells." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/589365.

Full text
Abstract:
Though melatonin was known to regulate gap junctional intercellular communication (GJIC) in chick astrocytes and mouse hepatocytes, the underlying mechanism by melatonin was not elucidated in hydrogen peroxide- (H2O2-) treated HaCaT keratinocyte cells until now. In the current study, though melatonin at 2 mM and hydrogen peroxide (H2O2) at 300 μM showed weak cytotoxicity in HaCaT keratinocyte cells, melatonin significantly suppressed the formation of reactive oxygen species (ROS) in H2O2-treated HaCaT cells compared to untreated controls. Also, the scrape-loading dye-transfer assay revealed that melatonin enhances the intercellular communication by introducing Lucifer Yellow into H2O2-treated cells. Furthermore, melatonin significantly enhanced the expression of connexin 26 (Cx26) and connexin 43 (Cx43) at mRNA and protein levels, but not that of connexin 30 (Cx30) in H2O2-treated HaCaT cells. Of note, melatonin attenuated the phosphorylation of extracellular signal-regulated protein kinases (ERKs) more than p38 MAPK or JNK in H2O2-treated HaCaT cells. Conversely, ERK inhibitor PD98059 promoted the intercellular communication in H2O2-treated HaCaT cells. Furthermore, combined treatment of melatonin (200 μM) and vitamin C (10 μg/mL) significantly reduced ROS production in H2O2-treated HaCaT cells. Overall, these findings support the scientific evidences that melatonin facilitates gap junctional intercellular communication in H2O2-treated HaCaT keratinocyte cells via inhibition of connexin 26/43 and ERK as a potent chemopreventive agent.
APA, Harvard, Vancouver, ISO, and other styles
6

Waterhouse, Miguel, Maria Themeli, Jurgen Finke, and Alexandros Spyridonidis. "Horizontal Gene Transfer through Apoptotic Bodies Confers a Possible Mechanism of Epithelial Chimerism after Allogeneic Hematopoietic Cell Transplantation." Blood 112, no. 11 (November 16, 2008): 2320. http://dx.doi.org/10.1182/blood.v112.11.2320.2320.

Full text
Abstract:
Abstract Animal and human studies have shown that after allogeneic hematopoietic cell transplantation (HCT) low percentage of epithelial cells containing donor-derived genome emerge. The mechanisms underlying this phenomenon are unclear. We investigated whether fusion or horizontal gene transfer between donor lymphocytes and recipient epithelial cells may explain epithelial chimerism after allo-HCT. In an in vitro model we analyzed whether and how genomic material could be transferred between cells. Briefly, keratinocyte HaCaT cells (Y-chromosome neg) were cocultivated with non-apoptotic Jurkat cells (Y+) or Jurkat cells in which apoptosis was induced with Camptothecin (4μM, 16h). Jurkat cells were labeled with CMFDA or BrdU in order to track the fate of genomic material. HaCaT cells co-cultivated with non-apoptotic Jurkat cells for 24–72h did not show any CMFDA, BrdU or FISH-Y chromosome signal, excluding fusion between cells in this experimental model. In contrast, co-cultivation of HaCaT cells with Jurkat apoptotic bodies for 48h resulted in CMFDA signal in 28% of the HaCaT cells, BrdU signal in about 5% and FISH Y-chromosome signal in about 3% of the cells. Importantly, the BrdU and the Y-chromosome signals were observed not only in the cytoplasm but also within the nucleus of the HaCaT cells as evaluated by confocal microscopy (Leica Confocal Microscope) and 3D analysis. Moreover, we obtained metaphases from the BrdU+ HaCaT cells and confirmed that the BrdU signal was located within the isolated chromosomes suggesting the creation of hybrid chromosomes. The incorporation of the transferred genomic material in the HaCaT host genome was inhibited by cytochalasin (inhibitor of phagocytosis) and increased 2-fold by bafylomicin (inhibitor of lysosomes) and aphidicolin (blocks the cell cycle in G1 phase). No transfer of genomic material was observed when the apoptotic bodies were separated from the HaCat cells by a semipermeable membrane in a transwell system. We isolated by a MoFlo FACS sorter the BrdU+ HaCaT cells bearing the Jurkat derived genomic material and found that 40% of them had an increased proliferating capacity (detected with CFSE labeling) as compared to untreated HaCaT cells. In order to evaluate expression of the horizontally transferred genomic material, we co-cultivated HacaT cells with intact or apoptotic GFP-transfected JvM cells. Cocultivation with non-apoptotic GFP+ cells resulted in no GFP expression n Hacat cells. In contrast, cocultivation of Hacat cells with GFP+ apoptotic bodies resulted in a 6-fold increase in the mean GFP fluorescence in HaCaT cells. When GFP+ apoptotic bodies were pretreated with DNase I no GFP expression in Hacat cells was observed indicating that the GFP expression of HaCaT cells after cocultivation with the apoptotic bodies was through horizontal transfer of DNA and not of mRNA material. Taken together, our in vitro model suggests horizontal gene transfer through apoptotic bodies as a possible mechanism explaining epithelial chimerism after allogeneic HCT. A possible scenario is that after allo-HCT apoptotic hematopoietic cells charge constantly the host environment with donor DNA which is phagocytated by epithelial cells. Part of this DNA could escape lysosomal degradation and integrate within the recipient DNA resulting in epithelial cells containing donor-derived genome.
APA, Harvard, Vancouver, ISO, and other styles
7

Wang, Jun, Guanzhi Chen, Tongxin Shi, Yingying Wang, and Chengfei Guan. "Possible treatment for cutaneous lichen planus: An in vitro anti-inflammatory role of Angelica polysaccharide in human keratinocytes HaCaT." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841882183. http://dx.doi.org/10.1177/2058738418821837.

Full text
Abstract:
Cutaneous lichen planus (CLP) is an autoimmune disease. Angelica polysaccharide (AP) has been found to exert immunomodulation activity. In this study, we explored the roles of AP in lipopolysaccharide (LPS)-induced inflammatory injury of human keratinocytes (HaCaT cells), as well as the underlying mechanisms. LPS-induced cell injury was evaluated by alterations of cell viability, apoptosis, and expressions of proteins associated with apoptosis and inflammatory cytokines. Then, the protective effects of AP on LPS-induced cell injury were assessed. The protein expressions of sirtuin 1 (SIRT1) and key kinases in the Nrf2/HO-1 and nuclear factor κB (NF-κB) pathways were measured using western blotting. SIRT1 knockdown and overexpression were used to analyze whether AP affected HaCaT cells through regulating SIRT1. Finally, the possible inhibitory effects of AP on cell injury after LPS treatment were also evaluated. We found that LPS reduced HaCaT cell viability, enhanced apoptosis, and induced release of inflammatory cytokines. AP alleviated LPS-induced HaCaT cell inflammatory injury. The expression of SIRT1 was enhanced after AP treatment. AP activated Nrf2/HO-1 pathway while inhibited NF-κB pathway in HaCaT cells. The protective effects of AP on LPS-induced HaCaT cell injury were reversed by SIRT1 knockdown. Dysregulation of SIRT1 altered the activation of Nrf2/HO-1 and NF-κB pathways in LPS-treated HaCaT cells. Furthermore, AP also exerted inhibitory effects on HaCaT cell injury after LPS stimulation. In conclusion, AP could alleviate LPS-induced inflammatory injury of HaCaT cells through upregulating SIRT1 expression and then activating Nrf2/HO-1 pathway but inactivating NF-κB pathway. This study provided a possible therapeutic strategy for clinical CLP treatments.
APA, Harvard, Vancouver, ISO, and other styles
8

Zha, Weifeng, Bo Guo, Shuyue Chen, Junwei Lu, and Yunyun Shan. "MicroRNA-126-5p Regulates Proliferation and Apoptosis of IL-22-Stimulated Human Keratinocytes Through Regulating Caspase 1." Journal of Biomaterials and Tissue Engineering 11, no. 5 (May 1, 2021): 1010–16. http://dx.doi.org/10.1166/jbt.2021.2656.

Full text
Abstract:
Objective: The study was aimed to explore the roles of miR-126-5p in psoriasis and the underlying molecular mechanisms. Methods: In vitro cell model of psoriasis was established by IL-22 induction. CASP1, the target gene of miR-126-5p, was predicted by TargetScan and verified through the dual luciferase reporter gene system. qRT-PCR was used to measure the mRNA expression of miR-126-5p and CASP1 in IL-22 stimulated HaCaT cells. The protein expression of CASP1, cleaved-caspase3 and caspase3 were measured by Western blot analysis. MTT assay and flow cytometry analysis were performed to detect the cell proliferation and apoptosis. A Caspase3 Activity Assay kit was used to detect the activity of Caspase3. Results: miR-126-5p was high expressed in IL-22 stimulated HaCaT cells compared with normal HaCaT cells. We predicted and verified that CASP1 was a direct target of miR-126-5p, and the mRNA and protein expression of CASP1 were reduced in IL-22 stimulated HaCaT cells compared with the normal HaCaT cells. miR-126-5p inhibitor and CASP1-siRNA significantly decreased the expression of miR-126-5p and CASP1 in HaCaT cells respectively. miR-126-5p inhibitor up-regulated the expression of CASP1 in HaCaT cells, and the effect was reversed by the transfection with CASP1-siRNA. In comparison with the control group, miR-126-5p inhibitor decreased the cell proliferation, induced apoptosis, and improved the activity of Caspase3, enhanced cleaved-caspase3/caspase3 ratio in IL-22 stimulated HaCaT cells, and all the effects were reversed by down-regulating CASP1. Conclusion: We demonstrated that miR-126-5p inhibitor played a protective role in psoriasis by targeting CASP1, evidenced by inhibiting IL-22-induced HaCaT cell proliferation and inducing apoptosis.
APA, Harvard, Vancouver, ISO, and other styles
9

SUDBECK, Barry D., Petra BAUMANN, Gavin J. RYAN, Katja BREITKOPF, Roswitha NISCHT, Thomas KRIEG, and Cornelia MAUCH. "Selective loss of PMA-stimulated expression of matrix metalloproteinase 1 in HaCaT keratinocytes is correlated with the inability to induce mitogen-activated protein family kinases." Biochemical Journal 339, no. 1 (March 25, 1999): 167–75. http://dx.doi.org/10.1042/bj3390167.

Full text
Abstract:
Many cell types, including fibroblasts and primary keratinocytes, increase matrix metalloproteinase 1 (MMP-1) production in response to agonists such as growth factors and phorbol esters. However, the spontaneously transformed human keratinocyte cell line HaCaT, although it increases MMP-1 production in response to epidermal growth factor (EGF), does not respond similarly to stimulation with PMA. This phenomenon occurs even though HaCaT cells remain proliferatively responsive to both agonists, suggesting a HaCaT-specific defect in a PMA-mediated signal transduction pathway. Using an inside-out approach to elucidate the source of this defect, we found that EGF, but not PMA, stimulated MMP-1 promoter activity in transiently transfected HaCaT keratinocytes. In addition, an assessment of fibroblast and HaCaT c-fos and c-jun gene expression after exposure to EGF and PMA showed that although both agonists increased the expression of c-fos and c-jun mRNA in fibroblasts, only EGF did so in HaCaT keratinocytes. Finally, we looked at the activation of mitogen-activated protein (MAP) family kinases after stimulation with EGF or PMA and found that both agonists increased the phosphorylation and activation of fibroblast extracellular signal-regulated protein kinase and c-Jun N-terminal kinase, but only EGF activated the same kinase activities in HaCaT cells. Further, the EGF-mediated increase in MMP-1 gene expression was inhibited by the MAP kinase/ERK kinase (MEK)-specific inhibitor PD98059 and the p38 kinase-specific inhibitor SB203580. Our evidence indicates that although HaCaT MAP kinases are functional, they are not properly regulated in response to the activation of protein kinase C, and that the defect that bars HaCaT MMP-1 expression in response to stimulation with PMA lies before MAP kinase activation.
APA, Harvard, Vancouver, ISO, and other styles
10

Yuan, Keyu, Yi Sun, and Yu Ji. "MicroRNA-485-5p reduces keratinocyte proliferation and migration by regulating ITGA5 expression in skin wound healing." Tropical Journal of Pharmaceutical Research 19, no. 12 (March 15, 2021): 2553–57. http://dx.doi.org/10.4314/tjpr.v19i12.10.

Full text
Abstract:
Purpose: To determine the effect of miR-485-5p on keratinocyte proliferation and migration.Methods: Human primary keratinocytes (HaCaT cells) were treated with different concentrations of transforming growth factor-β1 (TGF)-β1. miR-485-5p expression levels were determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). MTT (3-[4,5-dimethylthiazol-2- yl]-2,5 diphenyl tetrazolium bromide) and wound healing assays were performed to investigate the regulatory effects of miR-485-5p on cell viability and migration of HaCaT cells. Downstream target gene expression of miR-485-5p was determined using a luciferase activity assay.Results: In HaCaT cells, miR-485-5p was time- and dose-dependently downregulated by TGF-β1 treatment (p < 0.05). Forced expression of miR-485-5p decreased cell viability and migration of HaCaT cells (p < 0.05). Knockdown of miR-485-5p enhanced HaCaT cell viability and migration. Integrin subunit alpha-5 (ITGA5) was predicted and verified to be a downstream target of miR-485-5p in HaCaT cells. Overexpression of ITGA5 attenuated the miR-485-5p-induced decrease of HaCaT cell viability and migration (p < 0.05).Conclusion: MiR-485-5p reduces cell proliferation and migration of keratinocytes through the regulation of ITGA5. This mechanism provides a potential therapeutic strategy for skin wound healing. Keywords: ITGA5, Keratinocyte, Cell migration, MiR-485-5p, Cell proliferation, Wound healing
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "HaCaT"

1

Martynova, E. "HACAT AS A MODEL FOR KERATINOCYTESTRANSFORMATION." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/221055.

Full text
Abstract:
Mutations of the tumor suppressor gene p53 occur in more than 50% of human malignancies and lead to the loss of suppressor activity. Moreover frequently p53 mutants gain novel, oncogenic properties by transcriptional activation of the genes, involved in cellular proliferation, cell survival and angiogenesis. Today’s challenge is to understand mechanisms underlying the gain-of-function of mutant p53 proteins. By the example of KLF4 promoter we demonstrate that mutant p53 can carries out its gain-of-function by interaction with another p53 family member, transcription factor p63. In the first report we provide strong evidence that KLF4 is negatively controlled by p63 in normal skin in the presence of physiological levels of wild type p53 (wtp53) and that this regulation is subverted by oncogenic mutations of p53, establishing a direct link between these TFs, commonly overexpressed in squamous cell carcinoma (SCC). These results inspired us to investigate the mechanisms of mutant p53 gain-of-function on the genome scale. In the second manuscript we demonstrate that mutant p53 HaCaT alleles are pro-growth and mutp53 have thousands of binding sites in the human genome; they affect gene expression profoundly, both by binding with p63 to consensus elements and by being tethered by other TFs to their locations. Although 2 mutant p53 alleles are definitely gain-of-function in the HaCaT, they are not sufficient to render these cells malignant. Based on the sphere-forming assay we developed novel model for the tumorigenic conversion of the HaCaT cells: while immortalized keratinocytes display transformed phenotype in vitro and not tumorigenic upon injection into nude mice, HaCaTderived spheres give rise to the SCC in vivo. Thus, this simple model can be 3 useful for the future studies of the genetic and phenotypic signatures during SCC initiation and development. There is an indication that mutant p53 can execute its gain-of-function via interaction with NF-Y transcription factor. Ongoing study is devoted to the investigation of NF-YA subunit role in the processes of cellular proliferation and apoptosis in the cells with different p53 status.
APA, Harvard, Vancouver, ISO, and other styles
2

Hansen, Kari Ellen. "Utvidet studie av PLA2-uttrykk i HaCaT-keratinocytter :." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for biologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-13203.

Full text
Abstract:
I denne masteroppgaven har det blitt utviklet primerpar for 17 humane PLA2-isotyper. Ved hjelp av primerene har vi påvist uttrykk av 17 PLA2-isotyper i HaCaT-keratinocytter, hvorav 11 av disse representerer førstegangspåvisninger i HaCaT. Funnene representerer økt kunnskap om PLA2-familien og viser at HaCaT uttrykker et mangfold av PLA2-isotyper. Primerene ble også benyttet til å kartlegge PLA2-uttrykk gjennom keratinocytters differensiering. Resultatene viser at 13 av 17 isotyper uttrykkes gjennom hele differensieringsprosessen, som indikerer at PLA2-enzymer spiller sentrale roller i lipidmetabolisme i human epidermis. PLA2G2A viste, som den eneste av de studerte isotypene, sterk oppregulering under differensieringen, som vitner om at enzymet kan spille en viktig rolle i de øvre strata i epidermis.Sammendrag Under utviklingen av primerparene ble human postnatal placenta tatt i bruk som antatt positiv kontroll for uttrykk av samtlige PLA2-isotyper. 8 av 17 primerpar detekterte mRNA i placenta, hvorav PLA2 gruppe 2D, 4C, 4D og 10 representerer førstegangspåvisninger i human placenta. Sammendrag Primerene utgjør et verktøy som gjør det mulig å kartlegge PLA2-uttrykk i alle humane celler og vev. Da diverse PLA2-isotyper har blitt vist å spille en sentral rolle i inflammasjonssykdommer ved å katalysere hydrolysen av arakidonsyre fra glyserofosfolipider, vil det være intressant å kartlegge PLA2-uttrykk i friskt vev versus betent vev. Primerene vil legge grunnlaget for økt forståelse av de mange PLA2-enzymenes funksjoner i inflammasjonssammenheng, og potensielt legge grunnlag for utvikling av målrettede medisiner mot kronisk inflammatoriske sykdommer.
APA, Harvard, Vancouver, ISO, and other styles
3

Oehme, Martina. "Veränderte Wachstumsfaktorexpression in Spätstadien der Tumorprogression von HaCaT-ras-Zellen /." Heidelberg, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000259538.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Goltz, Gerit. "Charakterisierung von Ceramidase-Inhibitoren an der humanen Keratinozyten-Zellinie HaCaT." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/180/index.html.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Kors, Christian. "Regulation der Freisetzung von SCF aus proliferierenden versus differenzierenden Keratinozyten/HaCaT." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2006. http://dx.doi.org/10.18452/15499.

Full text
Abstract:
Der humane Stammzellfaktor (SCF) ist ein zentraler Wachstumsfaktor für Mastzellen in der Dermis und für Melanozyten in den Basalzellschichten der Epidermis. Er wird u. a. von Keratinozyten produziert. In dieser Arbeit wurde die mögliche Regulation der Expression von SCF aus Keratinozyten durch All-Trans-Retinsäure (RA) und Dexamethason in vitro an Hand der HaCaT-Zelllinie untersucht. Die HaCaT-Zellen wurden mit den beiden o. g. Substanzen (10 hoch -5 M bis 10 hoch -9 M) über 24 Stunden und 11 Tage inkubiert. Die Auswertung der HaCaT-Zellzahl, des Gesamt-Proteins SCF, dessen Splicevarianten (mSCF, sSCF) und der Rezeptoren von RA (RAR-alpha, -beta, -gamma) und von Dexamethason (GR-alpha, -beta) erfolgte mittels ELISA und RT-PCR. Dabei ergaben sich folgende Resultate: RA bewirkt einen Anstieg von SCF, Dexamethason bewirkt bei Kurzinkubation eine deutliche Zunahme von SCF, bei Dauerinkubation einen starken Abfall. Die RA-Rezeptoren RA-alpha und -gamma waren nach Inkubation mit RA verstärkt nachzuweisen; die Glukokortikoid-Rezeptoren GR-alpha und -beta zeigten nach Inkubation mit Dexamethason ebenfalls eine vermehrte Expression. Die Expression des Mastzellwachstumsfaktors SCF könnte deshalb unter physiologischen, pathologischen und therapeutischen Bedingungen durch Retinoide und Glukokortikoide reguliert sein.
The human stem cell factor (SCF) is a crucial growth factor for mast cells in the dermis and for the melanocytes in the basal layers of the epidermis. SCF is produced, among others, by keratinocytes. This study examines the possible regulation of the expression of SCF from keratinocytes by all-trans retinoic acid (RA) and dexamethasone in vitro by the keratinocyte cell line HaCaT. The HaCaT-cells were incubated for 24 hours or 11 days, respectively, with one of the above mentioned substances (10 to the power of -5 M to 10 to the power of -9 M). The analysis of the number of HaCaT-cells, of the total SCF protein, its splice variants (mSCF, sSCF), the receptors of RA (RAR-alpha, -beta, -gamma), and of the dexamethasone (GR-alpha, -beta) was done by ELISA and RT-PCR. The following results were found: RA induces an increase of SCF, dexamethasone at a short incubation period a considerable increase of SCF, and at long-term incubation a strong decrease. The RA-receptors RA-alpha und -gamma expression is increased after incubation with RA, and the glucocorticoid-receptors GR-alpha and -beta after the incubation with dexamethasone. Therefore, it is probable that the increase of the mast cell growth factor SCF under physiological, pathological and therapeutic conditions could be regulated by retinoic acid and glucocorticoids.
APA, Harvard, Vancouver, ISO, and other styles
6

Elbadawy, Hossein Mostafa. "Studies on the start family of lipid trafficking proteins in HaCaT keratinocytes." Thesis, Glasgow Caledonian University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.554307.

Full text
Abstract:
Terminally differentiating keratinocytes actively synthesize and accumulate lipids to maintain the production of lipid lamellae and an effective epidermal barrier. This thesis explored the role of steroidogenic acute regulatory (StAR) related-lipid transfer (START) proteins in the immortalized HaCaT keratinocyte cell line. Differing cell culture conditions were used to study differentiation of HaCaT keratinocytes, including the 'calcium switch' model, studied over a period of 21 days. Gene expression of five 'markers' of keratinocyte differentiation, KRTI, KRTIO, KRTI4, INVand LOR, was used to define progression of this process, revealing a dependency on calcium concentration, and increasing confluency. We then investigated gene expression of the START family of lipid trafficking proteins in HaCaT keratinocytes, compared with primary human keratinocytes. The same nine members of the family, STARDI, STARD2, STARD3, STARD4, STARD5, STARD7, STARDIO, STARD11 and STARDI2 were expressed in both cell types, although levels of STARD2, STARD5 and STARDI2 mRNA proved higher in HaCaT cells than in primary keratinocytes, and gene expression of STARD4 was lower in HaCaT cells compared with primary cells. During HaCaT differentiation, marked changes in gene expression of this family of proteins were noted, reflecting changes in lipid metabolism occurring during this process, the most notable being an increase in cholesterol mass after 21 days in cells exposed to I.4mM calcium compared with cells cultured in calcium depleted media. Steady state levels of mRNA encoding STARDI, D3, D2, D7, DID and Dll tended to increase during keratinocyte differentiation, while STARD4 and STARD5 showed a more complex pattern of expression, with decreased expression observed in the presence of I.4mM calcium. In order to investigate the function of the cytosolic cholesterol binding proteins, STARD4 and STARD5, in HaCaT cells, transient transfections were performed (48h) with pCMV6 vector encoding full length STARD4 or STARD5. Confocal microscopy confirmed the cytosolic location of both proteins, while in 3-D organotypic cultures STARD5 eo-localised with Keratin 10 rather than Loricrin, suggesting a locale in the spinous layer of these cultures. While both cholesterol trafficking proteins repressed cholesterol and cholesteryl ester biosynthesis from [I 4C] acetate, consistent with their proposed role as directional sterol transporters, these changes were associated with distinct gene expression patterns. Overexpression of ST ARD4 was associated with induction of Loricrin mRNA and protein, while STARD5 overexpression repressed gene expression of keratin 1, indicating that altered intracellular cholesterol transport can influence keratinocyte differentiation status. Further, ST ARD4 overexpression was associated with induction of SREBF2 and ABCG4, and repression of ABCAI, while overexpression of STARD5 resulted in induction of PPARD, PPARG and ABCAI, and repression of SREBF2 and LDLR. These findings confirm the impact of these cytosolic sterol transporters on keratinocyte lipid metabolism, and may suggest that ST ARD5 may be more efficient in this regard. In conclusion, manipulation of intracellular lipid transport proteins may therefore provide novel therapeutic strategies for the treatment of lipid-related skin disorders.
APA, Harvard, Vancouver, ISO, and other styles
7

Szkoda, Blake E. "THE EFFECTS OF CITRAL ON CASPASE-3 ACTIVATION IN M624 AND HaCaT CELLS." Marietta College Honors Theses / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=marhonors1463566418.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Bretland, Amanda Jane. "Growth, survival and cell death in the epithelial cell lines HaCaT, HT29 and SW742." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286914.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Zanoni, Thalita Boldrin. "Avaliação do perfil de citotoxicidade, mutagenicidade e genotoxicidade dos corantes Basic Red 51, Basic Yellow 57 e P-Fenilenodiamina usados na tintura de cabelo em células da pele." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-31102014-144039/.

Full text
Abstract:
O processo de coloração de cabelos é um dos métodos de tintura mais antigos. No século XIX, iniciou-se a produção de corantes sintéticos, a partir do desenvolvimento da pfenilenodiamina (PPD). Os corantes de cabelo são classificados de acordo com seu mecanismo de ação. Os corantes permanentes são classificados por mecanismos oxidativos, enquanto os corantes diretos colorem a fibra capilar por mecanismos não oxidativos. A investigação sobre os possíveis danos á saúde humana, que podem ser resultantes da exposição de corantes de cabelos, têm sido um tema de enorme desafio para a comunidade cientifica. Particularmente, devido à enorme discrepância dos estudos epidemiológicos e estudos que empregam metodologias in vitro. Neste trabalho, foram investigadas a capacidade citotóxica de um composto representante de cada classe de tinturas de cabelo, um corante temporário (Basic Yellow 57 (BY57), um semi-temporário (Basic Red 51(BR51) e um ingrediente permanente p-fenilinodiamina (PPD) em linhagens de células de pele humana. As linhagens normais da pele humana estudadas foram os queratinócitos imortalizados humanos (HaCaT) e fibroblastos primários, utilizou-se também melanoma SK-Mel-103. Posteriormente, após caracterização do corante mais tóxico, foi investigado o tipo de morte celular, as possíveis alterações destes compostos no ciclo celular, a capacidade de geração de espécies reativas de oxigênio (EROs) e aplicação em cultura tridimensional de pele artificial. Posteriormente, foi avaliada a capacidade de cada corante em induzir estresse oxidativo em queratinócitos humanos (HaCaT), que são a primeira via de exposição de corantes de cabelos. Em seguida, o corante elegido mais tóxico foi aplicado em pele humana provenientes de cirurgia. Finalmente, o potencial de mutagenicidade dos corantes BY57 e BR51 foram avaliados.
The process involving hair dyes is one of the oldest methods of coloring. The use of synthetic hair dyes started in the nineteenth century, after the development of p-phenylenodiamine (PPD). The hair dyes are classified according to their mechanism of action. The permanent hair dyes are classified by oxidative mechanisms, while direct dyes color the hair fiber by non-oxidative mechanisms. Research regarding the potential damage of hair dyes to human health has been an enormous challenge for the scientific community. Particularly due to the large discrepancy of epidemiological studies involving in vitro methodologies. In this study, we evaluated the cytotoxic potential of a compound representative from each of the class of hair dyes, a temporary dye (Basic Yellow 57 (BY57), a semi temporary (Basic Red 51 (BR51) and a permanent hair dyes p-phenylenodiamine (PPD) in human skin cells. The studied skin cell lines where, immortalized human keratinocytes (HaCaT) primary fibroblasts, we also used melanoma SK-Mel-103. Subsequently, after characterization of the most toxic dye, we investigated specific mechanisms of cell death, changes in cell cycle and the ability to generate reactive oxygen species (ROS) followed by the evaluation of three-dimensional artificial skin. In addition, we assessed the ability of each dye in inducing oxidative stress in immortalized human keratinocytes (HaCaT) this is the primary route of exposure of hair dyes. Then, the most toxic compound was tested in human skin explants. Finally the mutagenic potential of the dyes BY57 and BR51 were evaluated.
APA, Harvard, Vancouver, ISO, and other styles
10

Raithel, Kerstin. "Effekt von S-Lost in HaCaT-Zellkulturen : Induktion der Apoptose und Effekt eines PARP-Inhibitors /." München, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254372.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "HaCaT"

1

Fadel, Hayat Abu. Hayat. Beirut: Riad El Rayess, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kır, Evren. Hayat. İstanbul: Cinius Yayınları, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hayat bilgisi. Yenibosna, İstanbul: Etkileşim, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Gasparyan, Norek. Havat Artsʻakhi. Erevan: "Nairi", 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Pakistan), Balochi Academy (Quetta, ed. Hapat talār. Koʼiṭah: Balocī Ikaiḍamī, 2015.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Azad, M. H. Abe hayat. Mirpur: Arsalan Books, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Yeni hayat. Cağaloğlu, İstanbul: İletişim, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Neclâ, Feroğlu, ed. Sevdalım hayat. 2nd ed. Etiler, İstanbul: Remzi Kitabevi, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Yardım, Mehmet Nuri. Bâbıâli'de hayat. Istanbul: Çağrı, 2014.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Şemo, Ereb. Mutlu hayat. Istanbul: Mirza Basım Yayım, 2021.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "HaCaT"

1

Wilson, Van G. "Growth and Differentiation of HaCaT Keratinocytes." In Methods in Molecular Biology, 33–41. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/7651_2013_42.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Reichrath, J., U. Hügel, G. Klaus, N. E. Fusenig, and E. W. Rauterberg. "Modulation of 1,25-Dihydroxyvitamin D3 Receptor Expression in HaCaT Keratinocytes." In Cell and Tissue Culture Models in Dermatological Research, 37–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77817-9_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Scharffetter-Kochanek, K., G. Heinen, S. Lange, K. Kirchberg, G. Goerz, N. E. Fusenig, and G. Plewig. "Collagen Type-I Is Chemoattractive for the Human Keratinocyte Cell Line (HaCaT)." In Cell and Tissue Culture Models in Dermatological Research, 208–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77817-9_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Breitkreutz, D., H. J. Stark, M. Baur, and N. E. Fusenig. "Differentielle Veränderungen epidermaler Integrinmuster in Modellepithelien transformierter benigner und maligner Keratinozyten (HACAT-RAS)." In Wundheilung — Wundverschluß, 37–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-79173-4_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wells, Julie, and Xing Dai. "Using siRNA Knockdown in HaCaT Cells to Study Transcriptional Control of Epidermal Proliferation Potential." In Methods in Molecular Biology, 107–25. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-380-0_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Nagy, Gábor, Melinda Turáni, Katalin Éva Kovács, and Gáspár Bánfalvi. "Chromatin Changes upon Silver Nitrate Treatment in Human Keratinocyte HaCaT and K562 Erythroleukemia Cells." In Cellular Effects of Heavy Metals, 195–217. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0428-2_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Meineke, Viktor, Carolina Pfaffendorf, Michaela Schinn, Wolfgang Tilgen, Artur Mayerhofer, Nicola Dimitrijevic, Dirk van Beuningen, and Jörg Reichrath. "Modulation of X-ray-Induced Apoptosis in Human Keratinocytes (HaCaT) by 1,25-Dihydroxyvitamin D3." In Recent Results in Cancer Research, 427–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55580-0_31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Avezov, K., A. Z. Reznick, and D. Aizenbud. "Time and Dose Effects of Cigarette Smoke and Acrolein on Protein Carbonyl Formation in HaCaT Keratinocytes." In Advances in Experimental Medicine and Biology, 57–64. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/5584_2014_91.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Hoh, A., and K. Maier. "Comparative Cytotoxicity Test with Human Keratinocytes, HaCaT Cells, and Skin Fibroblasts to Investigate Skin-Irritating Substances." In Cell and Tissue Culture Models in Dermatological Research, 341–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77817-9_38.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Koren Carmi, I., R. Haj, H. Yehuda, S. Tamir, and A. Z. Reznick. "The Role of Oxidation in FSL-1 Induced Signaling Pathways of an Atopic Dermatitis Model in HaCaT Keratinocytes." In Advances in Experimental Medicine and Biology, 1–10. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/5584_2014_98.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "HaCaT"

1

Selvaag, Edgar, Anita B. Petersen, Robert Gniadecki, Tine Thorn, and Hans Christian Wulf. "Antidiabetics and diuretics show phototoxicity in HaCaT cells." In European Conference on Biomedical Optics, edited by Reginald Birngruber and Hubert van den Bergh. SPIE, 2001. http://dx.doi.org/10.1117/12.446520.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

ElMasri, Wafic M., Minshu Yu, Victoria M. Virador, and Elise C. Kohn. "Abstract 3389: SLPI promotes EMT in HaCaT cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3389.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Selvaag, Edgar, Anita B. Petersen, Robert Gniadecki, Tine Thorn, and Hans Christian Wulf. "Antidiabetics and diuretics show phototoxicity in HaCaT cells." In European Conference on Biomedical Optics. Washington, D.C.: Optica Publishing Group, 2001. http://dx.doi.org/10.1364/ecbo.2001.4433_158.

Full text
Abstract:
The antidiabetics tolbutamide, glibenclamide, and glipizide, and the diuretics bendroflumethiazide, butizide, furosemide, hydrochlorothiazide, and trichlormethiazide were investigated for potential phototoxicity in the HaCaT cell line. The cells were incubated with the drugs and then exposed to UVA1 irradiation. The effects of the antioxidants L-ascorbic acid, and α-tocopherol on oxidative DNA damage were assessed. Bendroflumethiazide, furosemide, hydrochlorothiazide, trichlormethiazide, or tolbutamide induced dose-dependent phototoxicity. Cells incubated with bendroflumethiazide, tolbutamide, and glibenclamide, and irradiated with UVA1 demonstrated an increased oxidative DNA damage. Pre-treatment with L-ascorbic acid, or α-tocopherol, suppressed the UVA-induced DNA damage in cells incubated with 1 mM of bendroflumethiazide, furosemide, glibenclamide, glipizide, tolbutamide, and trichloromethiazide, further implying the involvement of reactive oxygen species in the phototoxic DNA damage. These results may indicate a link between phototoxic and photocancerogenic potential of the sulfonamide-derived oral antidiabetic and diuretic drugs, as it has previously been recognized for psoralen, chlorpromazine, and fluoroquinolones. Excessive exposure to UV light may be deleterious for patients treated with these drugs.
APA, Harvard, Vancouver, ISO, and other styles
4

Azevedo, Isa Maria Ferreira, Renally Barbosa Da Silva, Aryane De Azevedo Pinheiro, Rômulo Farias Carneiro, and Luiz Gonzaga Do Nascimento Neto. "AVALIAÇÃO DA ATIVIDADE ANTITUMORAL DA LECTINA ISOLADA DA ESPONJA MARINHA CHONDRILLA CARIBENSIS." In II Congresso Brasileiro de Ciências Biológicas On-line. Revista Multidisciplinar de Educação e Meio Ambiente, 2021. http://dx.doi.org/10.51189/rema/1270.

Full text
Abstract:
Introdução: O câncer é o nome dado a um conjunto de mais de 100 doenças que tem em comum o crescimento desordenado de células, as quais podem, inclusive, invadir outros tecidos, ocasionando alto índice de mortalidade, assim sendo estabelecido como um importante problema de saúde pública. Células tumorais apresentam alterações significativas na expressão de glicoproteínas em suas superfícies e sua detecção precoce é uma etapa definitiva para a cura durante o tratamento. Na busca por novas moléculas com potencial biotecnológico, vários estudos de prospecção têm sido realizados em habitats marinhos. Lectinas oriundas dos habitats marinhos demonstram relevante potencial biotecnológico, na qual várias atividades biológicas estão descritas na literatura. Tendo em vista a frequente expressão de padrões aberrantes de glicosilação nas células tumorais, as lectinas por serem proteínas com capacidade de ligação seletiva a carboidratos surgem como promissores agentes antineoplásicos. Objetivo: Este trabalho objetivou avaliar a atividade antitumoral da lectina isolada da esponja marinha Chondrilla caribensis (CCL) sobre células de carcinoma de próstata (LNCaP), bem como analisar o perfil de citotoxicidade da CCL sobre a linhagem de queratinócitos normais (HaCaT). Material e Métodos: O efeito citotóxico da CCL foi avaliado através do ensaio de viabilidade celular usando o método colorimétrico do sal tetrazolium MTS para as células das linhagens LNCaP e HaCaT. As linhagens celulares foram expostas a concentrações de 500 a 7,8 µg.ml-1 de CCL por 48 h. Resultados: Os resultados mostraram uma redução de 76,71% na viabilidade de LNCaP nas concentrações de 500, 250 e 125 µg.ml-1 (IC50 = 44,31 µg.ml-1). Para a linhagem celular HaCaT, o tratamento com CCL nas concentrações de 500, 250 e 125 µg.ml-1 resultou na redução da viabilidade em 28,64 %; 12,24 % e 0,76 %, respectivamente, onde 71,36 % ± 0,588 das células HaCaT permaneceram viáveis após 48 h de tratamento. Conclusão: Em conclusão, os resultados sugerem que a CCL possui maior seletividade para a linhagem LNCaP, e em contrapartida apresentou toxicidade reduzida sobre queratinócitos humanos saudáveis. Estudos adicionais devem ser realizados para investigar o mecanismo de ação da CCL sobre as células utilizadas no estudo.
APA, Harvard, Vancouver, ISO, and other styles
5

Wahyudi, Lilik Duwi, Jiwon Jeong, Heejung Yang, and Jung-Hwan Kim. "Abstract 5428: Effect of amentoflavone on Nrf2 signaling in HaCaT cells." 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.am2018-5428.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Corradi, E., N. Schmidt, N. Räber, M. De Mieri, M. Hamburger, O. Potterat, and V. Butterweck. "Metabolite profile and antiproliferative effects in HaCaT cells of a Salix reticulata extract." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608182.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Neza, E., and M. Centini. "Effects of different essential oils on HaCaT keratinocytes against hydrogen peroxide induced oxidative stress." In 67th International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA) in cooperation with the French Society of Pharmacognosy AFERP. © Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3400028.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Szeimies, Rolf-Markus, Wolfgang Baeumler, Sigrid Karrer, and Michael Landthaler. "Wavelength-dependent photodynamic inactivation of HaCaT human keratinocytes after preincubation with 5-aminolevulinic acid." In Fifth International Photodynamic Association Biennial Meeting, edited by Denis A. Cortese. SPIE, 1994. http://dx.doi.org/10.1117/12.203421.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Junco, Jacob, Piotr Kowalczyk, Magdalena Kowalczyk, Olga Tolstykh, Margaret Hanausek, Zbigniew Walaszek, and Thomas J. Slaga. "Abstract 5657: Ursolic acid prevents activation of oncogenic factors in UV-treated HaCaT cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5657.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Tong, Lingying, and Shiyong Wu. "Abstract 3011: Correlation of PERK activation with increased GRP78-binding in UVB-irradiated HaCaT cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3011.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'HaCaT' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography