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  • 1. Jimbo, Ryo
    et al.
    Ivarsson, Mikael
    Örebro University, School of Health and Medical Sciences.
    Koskela, Anita
    Örebro University, School of Health and Medical Sciences.
    Sul, Young-Taeg
    Johansson, Carina B.
    Örebro University, School of Health and Medical Sciences.
    Protein adsorption to surface chemistry and crystal structure modification of titanium surfaces2010In: Journal of oral & maxillofacial research, ISSN 2029-283X, Vol. 1, no 3, p. e3-Article in journal (Refereed)
    Abstract [en]

    Objectives: To observe the early adsorption of extracellular matrix and blood plasma proteins to magnesium-incorporated titanium oxide surfaces, which has shown superior bone response in animal models.

    Material and Methods: Commercially pure titanium discs were blasted with titanium dioxide (TiO2) particles (control), and for the test group, TiO2 blasted discs were further processed with a micro-arc oxidation method (test). Surface morphology was investigated by scanning electron microscopy, surface topography by optic interferometry, characterization by X-ray photoelectron spectroscopy (XPS), and by X-ray diffraction (XRD) analysis. The adsorption of 3 different proteins (fibronectin, albumin, and collagen type I) was investigated by an immunoblotting technique.

    Results: The test surface showed a porous structure, whereas the control surface showed a typical TiO2 blasted structure. XPS data revealed magnesium-incorporation to the anodic oxide film of the surface. There was no difference in surface roughness between the control and test surfaces. For the protein adsorption test, the amount of albumin was significantly higher on the control surface whereas the amount of fibronectin was significantly higher on the test surface. Although there was no significant difference, the test surface had a tendency to adsorb more collagen type I.

    Conclusions: The magnesium-incorporated anodized surface showed significantly higher fibronectin adsorption and lower albumin adsorption than the blasted surface. These results may be one of the reasons for the excellent bone response previously observed in animal studies.

  • 2.
    Koskela, Anita
    et al.
    Clinical Research Center, University Hospital, Örebro, Sweden; Örebro Life Science Center, University Hospital Örebro, Örebro, Sweden.
    Engström, Kristina
    Department of Otolaryngology, Örebro University Hospital, Örebro, Sweden.
    Hakelius, Malin
    Department of Surgical Sciences, Plastic Surgery Unit, Uppsala University, Uppsala, Sweden.
    Nowinski, Daniel
    Department of Surgical Sciences, Plastic Surgery Unit, Uppsala University, Uppsala, Sweden.
    Ivarsson, Mikael
    Clinical Research Center, Örebro University Hospital, Örebro, Sweden; Örebro Life Science Center, University Hospital Örebro, Örebro, Sweden.
    Regulation of fibroblast gene expression by keratinocytes in organotypic skin culture provides possible mechanisms for the antifibrotic effect of reepithelialization.2010In: Wound Repair and Regeneration, ISSN 1067-1927, E-ISSN 1524-475X, Vol. 18, no 5, p. 452-459Article in journal (Refereed)
    Abstract [en]

    To investigate the mechanisms behind the antifibrotic effect associated with epidermal regeneration, the expression of 12 fibroblast genes important for the modulation of the extracellular matrix (ECM), as well as α-smooth muscle actin, was studied in a keratinocyte-fibroblast organotypic skin culture model. The study was performed over time during epidermal generation and in the presence or absence of the profibrotic factor transforming growth factor-β. the Presence of epidermal differentiation markers in the model was essentially coherent with that of native skin. Fibroblast gene expression was analyzed with real-time polymerase chain reaction after removal of the epidermal layer. After 2 days of air-exposed culture, 11 out of the 13 genes studied were significantly regulated by keratinocytes in the absence or presence of transforming growth factor-β. The regulation of connective tissue growth factor, collagen I and III, fibronectin, plasmin system regulators, matrix metalloproteinases and their inhibitors as well as α-smooth muscle actin was consistent with a suppression of ECM formation or contraction. Overall, the results support a view that keratinocytes regulate fibroblasts to act catabolically on the ECM in epithelialization processes. This provides possible mechanisms for the clinical observations that reepithelialization and epidermal wound coverage counteract excessive scar formation.

  • 3.
    Koskela, Anita
    et al.
    Örebro University, School of Health and Medical Sciences.
    Nilsdotter-Augustinsson, A.
    Persson, Lennart
    Söderquist, Bo
    Örebro University, School of Health and Medical Sciences.
    Prevalence of the ica operon and insertion sequence IS256 among Staphylococcus epidermidis prosthetic joint infection isolates2009In: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 28, no 6, p. 655-660Article in journal (Refereed)
    Abstract [en]

    Joint replacement surgery has improved the quality of life for hundreds of thousands of patients. However, the infection of a joint implant is an important and serious complication, though the prevalence is low. Staphylococcus epidermidis is the most important pathogen involved in foreign-body infections. S. epidermidis is also a commensal that comprises a substantial part of the normal skin flora of humans. The possibility to demonstrate potential specific virulence markers may facilitate the interpretation of the bacteriological findings, as well as the clinical decision. The prevalence of the ica locus and insertion sequence IS256 by using polymerase chain reaction (PCR) among 32 clinical S. epidermidis isolates from prosthetic joint infections (PJIs) and 24 commensal isolates from nares and skin was investigated. Sixteen (50%) of the 32 PJI isolates harbored the ica operon compared with one-third of the commensal isolates obtained from the samples of the skin and nares of healthy individuals. The IS256 was demonstrated in 26 (81%) out of 32 PJI isolates. By contrast, IS256 was found in one of 24 commensal isolates. In conclusion, IS256 may be superior to the ica operon as a marker of the invasive capacity of S. epidermidis, since it was found in most of the PJI isolates, but rarely among commensals.

  • 4.
    Koskela von Sydow, Anita
    Örebro University, School of Medical Sciences.
    Regulation of fibroblast activity by keratinocytes, TGF-β and IL-1α: studies in two- and three dimensional in vitro models2016Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Dysregulated wound healing is commonly associated with excessive fibrosis. Connective tissue growth factor (CTGF/CCN2) is characteristically overexpressed in fibrotic diseases and stimulated by transforming growth factor-β (TGF-β) in dermal fibroblasts. Reepithelialisation and epidermal wound coverage counteract excessive scar formation. We have previously shown that interleukin-1α (IL-1α) derived from keratinocytes conteracts TGF-β-stimulated CTGF-expression. The aim of this thesis was to further explore the effects of keratinocytes and IL-1α on gene and protein expression, as well as pathways, in TGF-β stimulated fibroblasts. Fibroblasts were studied in vitro by conventional two dimensional cell culture models and in a three dimensional keratinocyte-fibroblast organotypic skin culture model.

    The results showed that IL-1 suppresses basal and TGF-β-induced CTGF mRNA and protein, involving a possible TAK1 mechanism. Keratinocytes regulate the expression of fibroblast genes important for the turnover of the extracellular matrix. Most of the genes analysed (11/13) were regulated by TGF-β and counter regulated by keratinocytes. The overall results support a view that keratinocytes regulate fibroblasts to act catabolically (anti-fibrotic) on the extracellular matrix.

    Transcriptional microarray and gene set enrichment analysis showed that antagonizing effects of IL-1α on TGF-β were much more prominent than the synergistic effects. The most confident of these pathways was the interferon signaling, which were inhibited by TGF-β and activated by IL-1α. A proteomics study confirmed that IL-1α preferentially conteracts TGF-β effects. Six new fibroblast proteins involved in synthesis/ regulation were identified, being regulated by TGF-β and antagonized by IL-1α. Pathway analysis confirmed counter-regulation of interferon signaling by the two cytokines. These findings have implications for understanding the role of fibroblasts for inflammatory responses and development of fibrosis in the skin.

    List of papers
    1. Inhibition of Connective Tissue Growth Factor/CCN2 Expression in Human Dermal Fibroblasts by Interleukin-1 alpha and beta
    Open this publication in new window or tab >>Inhibition of Connective Tissue Growth Factor/CCN2 Expression in Human Dermal Fibroblasts by Interleukin-1 alpha and beta
    Show others...
    2010 (English)In: Journal of Cellular Biochemistry, ISSN 0730-2312, E-ISSN 1097-4644, Vol. 110, no 5, p. 1226-1233Article in journal (Refereed) Published
    Abstract [en]

    Connective tissue growth factor (CTGF/CCN2) is a matricellular protein induced by transforming growth factor (TGF)-beta and intimately involved with tissue repair and overexpressed in various fibrotic conditions We previously showed that keratmocytes in vitro downregulate TGF-beta-induced expression of CTGF in fibroblasts by an interleukin (IL)-1 alpha-dependent mechanism. Here, we investigated further the mechanisms of this downregulation by both IL-1 alpha and beta Human dermal fibroblasts and NIH 3T3 cells were treated with IL-1 alpha or beta in presence or absence of TGF-beta 1. IL-1 suppressed basal and TGF-beta-induced CTGF mRNA and protein expression. IL-1 alpha and beta inhibited TGF-beta-stimulated CTGF promoter activity, and the activity of a synthetic minimal promoter containing Smad 3-binding CAGA elements Furthermore. IL-1 alpha and beta inhibited TGF-beta-stimulated Smad 3 phosphorylation, possibly linked to an observed increase in Smad 7 mRNA expression. In addition. RNA interference suggested that TGF-beta activated kinase1 (TAK1) is necessary for IL-1 inhibition of TGF-beta-stimulated CTGF expression. These results add to the understanding of how the expression of CTGF in human dermal fibroblasts is regulated, which in turn may have implications for the pathogenesis of fibrotic conditions involving the skin. J. Cell Biochem. 110: 1226-1233, 2010. (C) 2010 Wiley-Liss. Inc

    Keywords
    interleukin-1, connective tissue growth factor, transforming growth factor-beta, smad 3, tak1
    National Category
    Cell Biology Biochemistry and Molecular Biology
    Research subject
    Cell Research
    Identifiers
    urn:nbn:se:oru:diva-28379 (URN)10.1002/jcb.22637 (DOI)000280435900021 ()20544797 (PubMedID)2-s2.0-77954894569 (Scopus ID)
    Available from: 2013-03-26 Created: 2013-03-14 Last updated: 2018-04-24Bibliographically approved
    2. Regulation of fibroblast gene expression by keratinocytes in organotypic skin culture provides possible mechanisms for the antifibrotic effect of reepithelialization.
    Open this publication in new window or tab >>Regulation of fibroblast gene expression by keratinocytes in organotypic skin culture provides possible mechanisms for the antifibrotic effect of reepithelialization.
    Show others...
    2010 (English)In: Wound Repair and Regeneration, ISSN 1067-1927, E-ISSN 1524-475X, Vol. 18, no 5, p. 452-459Article in journal (Refereed) Published
    Abstract [en]

    To investigate the mechanisms behind the antifibrotic effect associated with epidermal regeneration, the expression of 12 fibroblast genes important for the modulation of the extracellular matrix (ECM), as well as α-smooth muscle actin, was studied in a keratinocyte-fibroblast organotypic skin culture model. The study was performed over time during epidermal generation and in the presence or absence of the profibrotic factor transforming growth factor-β. the Presence of epidermal differentiation markers in the model was essentially coherent with that of native skin. Fibroblast gene expression was analyzed with real-time polymerase chain reaction after removal of the epidermal layer. After 2 days of air-exposed culture, 11 out of the 13 genes studied were significantly regulated by keratinocytes in the absence or presence of transforming growth factor-β. The regulation of connective tissue growth factor, collagen I and III, fibronectin, plasmin system regulators, matrix metalloproteinases and their inhibitors as well as α-smooth muscle actin was consistent with a suppression of ECM formation or contraction. Overall, the results support a view that keratinocytes regulate fibroblasts to act catabolically on the ECM in epithelialization processes. This provides possible mechanisms for the clinical observations that reepithelialization and epidermal wound coverage counteract excessive scar formation.

    Place, publisher, year, edition, pages
    The Wound Healing Society, 2010
    National Category
    Other Basic Medicine
    Identifiers
    urn:nbn:se:oru:diva-48462 (URN)10.1111/j.1524-475X.2010.00605.x (DOI)000282263500004 ()20731800 (PubMedID)2-s2.0-77956625499 (Scopus ID)
    Available from: 2016-02-22 Created: 2016-02-22 Last updated: 2018-05-02Bibliographically approved
    3. IL-1α Counteract TGF-β Regulated Genes and Pathways in Human Fibroblasts
    Open this publication in new window or tab >>IL-1α Counteract TGF-β Regulated Genes and Pathways in Human Fibroblasts
    Show others...
    2016 (English)In: Journal of Cellular Biochemistry, ISSN 0730-2312, E-ISSN 1097-4644, Vol. 117, no 7, p. 1622-1632Article in journal (Refereed) Published
    Abstract [en]

    Dysregulated wound healing is commonly associated with excessive fibrosis. Connective tissue growth factor (CTGF/CCN2) is characteristically overexpressed in fibrotic diseases and stimulated by transforming growth factor-β (TGF-β) in dermal fibroblasts. We previously showed that interleukin-1 (IL-1α) counteracts TGF-β-stimulated CTGF mRNA and protein expression in these cells. The aim of this study was to explore the effects of IL-1α on further genes and pathways in TGF-β regulated fibroblasts. Transcriptional microarray and multiple comparison analysis showed that the antagonizing effects of IL-1α was much more prominent than the synergistic effects, both with respect to number of genes and extent of changes in gene expression. Moreover, comparing canonical pathways by gene set enrichment analysis and the Ingenuity Pathway Analysis tool revealed that IL-1α counteracted TGF-β in the top six most confident pathways regulated by both cytokines. Interferon and IL-1 signaling, as well as two pathways involved in apoptosis signaling were suppressed by TGF-β and activated by IL-1α. Pathways involving actin remodeling and focal adhesion dynamics were activated by TGF-β and suppressed by IL-1α. Analyzing upstream regulators in part corroborate the comparison of canonical pathways and added cell cycle regulators as another functional group regulated by IL-1α. Finally, gene set enrichment analysis of fibrosis-related genes indicated that IL-1 moderately counteracts the collective effect of TGF-β on these genes. Microarray results were validated by qPCR. Taken together, the results indicate prominent antagonistic effects of IL-1α on TGF-β regulated interferon signaling, as well as on a wide variety of other genes and pathways in fibroblasts. This article is protected by copyright. All rights reserved.

    Place, publisher, year, edition, pages
    Hoboken, USA: Wiley-Blackwell, 2016
    Keywords
    Connective tissue growth factor, transforming growth factor-beta, interleukin-1, interferon, fibroblast, fibrosis and ingenuity pathway analysis
    National Category
    Other Basic Medicine Cell Biology Biochemistry and Molecular Biology
    Research subject
    Cell Research
    Identifiers
    urn:nbn:se:oru:diva-48463 (URN)10.1002/jcb.25455 (DOI)000375916800014 ()26629874 (PubMedID)2-s2.0-84964773875 (Scopus ID)
    Note

    Funding Agencies:

    Örebro County Council Research Committee of the Örebro University Hospital OLL-550071

    Nyckelfonden AE56340

    Available from: 2016-02-22 Created: 2016-02-22 Last updated: 2019-03-26Bibliographically approved
    4. IL-1α counteracts TGF-β regulated protein expression in human dermal fibroblasts
    Open this publication in new window or tab >>IL-1α counteracts TGF-β regulated protein expression in human dermal fibroblasts
    (English)Manuscript (preprint) (Other academic)
    National Category
    Other Basic Medicine
    Identifiers
    urn:nbn:se:oru:diva-48464 (URN)
    Available from: 2016-02-22 Created: 2016-02-22 Last updated: 2018-01-10Bibliographically approved
  • 5.
    Koskela von Sydow, Anita
    et al.
    Örebro University, School of Health Sciences.
    Janbaz, Chris
    Department of Plastic and Reconstructive Surgery Clinic, School of Medical Science, Örebro University SE 70182, Örebro, Sweden.
    Bergemalm, Daniel
    Örebro University, School of Health Sciences. Department of Internal Medicine, Division of Gastroenterology.
    Ivarsson, Mikael
    Örebro University, School of Health Sciences.
    IL-1α counteracts TGF-β regulated protein expression in human dermal fibroblastsManuscript (preprint) (Other academic)
  • 6.
    Koskela von Sydow, Anita
    et al.
    Department of Clinical Research Laboratory, Örebro University Hospital, Örebro, Sweden.
    Janbaz, Chris
    Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Plastic and Reconstructive Surgery, Örebro University Hospital, Örebro, Sweden .
    Kardeby, Caroline
    Örebro University, School of Medical Sciences.
    Repsilber, Dirk
    Örebro University, School of Medical Sciences.
    Ivarsson, Mikael
    Örebro University, School of Health Sciences.
    IL-1α Counteract TGF-β Regulated Genes and Pathways in Human Fibroblasts2016In: Journal of Cellular Biochemistry, ISSN 0730-2312, E-ISSN 1097-4644, Vol. 117, no 7, p. 1622-1632Article in journal (Refereed)
    Abstract [en]

    Dysregulated wound healing is commonly associated with excessive fibrosis. Connective tissue growth factor (CTGF/CCN2) is characteristically overexpressed in fibrotic diseases and stimulated by transforming growth factor-β (TGF-β) in dermal fibroblasts. We previously showed that interleukin-1 (IL-1α) counteracts TGF-β-stimulated CTGF mRNA and protein expression in these cells. The aim of this study was to explore the effects of IL-1α on further genes and pathways in TGF-β regulated fibroblasts. Transcriptional microarray and multiple comparison analysis showed that the antagonizing effects of IL-1α was much more prominent than the synergistic effects, both with respect to number of genes and extent of changes in gene expression. Moreover, comparing canonical pathways by gene set enrichment analysis and the Ingenuity Pathway Analysis tool revealed that IL-1α counteracted TGF-β in the top six most confident pathways regulated by both cytokines. Interferon and IL-1 signaling, as well as two pathways involved in apoptosis signaling were suppressed by TGF-β and activated by IL-1α. Pathways involving actin remodeling and focal adhesion dynamics were activated by TGF-β and suppressed by IL-1α. Analyzing upstream regulators in part corroborate the comparison of canonical pathways and added cell cycle regulators as another functional group regulated by IL-1α. Finally, gene set enrichment analysis of fibrosis-related genes indicated that IL-1 moderately counteracts the collective effect of TGF-β on these genes. Microarray results were validated by qPCR. Taken together, the results indicate prominent antagonistic effects of IL-1α on TGF-β regulated interferon signaling, as well as on a wide variety of other genes and pathways in fibroblasts. This article is protected by copyright. All rights reserved.

  • 7. Nilsdotter-Augustinsson, Åsa
    et al.
    Koskela, Anita
    Öhman, Lena
    Söderquist, Bo
    Örebro University, School of Health and Medical Sciences.
    Characterization of coagulase-negative staphylococci isolated from patients with infected hip prostheses: use of phenotypic and genotypic analyses, including tests for the presence of the ica operon2007In: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 26, no 4, p. 255-65Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to investigate phenotypic and/or genotypic heterogeneity in coagulase-negative staphylococci (CoNS) obtained from multiple tissue samples taken perioperatively during exchange surgery from each of 19 patients with clinically and/or microbiologically proven hip prosthesis infections. CoNS are important pathogens in prosthetic hip joint infections. Several virulence factors have been suggested for CoNS, such as phenotypic variation, yet the pathogenic processes that are involved remain unclear. The PhenePlate system (PhPlate AB, Stockholm Sweden) was used for phenotyping and pulsed-field gel electrophoresis for genotyping of polymorphisms in isolates of CoNS. Furthermore, polymerase chain reaction was used to determine the presence of the icaADB gene complex in the isolates. Some patients were infected with CoNS and other species, some were infected with multiple CoNS species, although infections with Staphylococcus epidermidis alone were most common, and some were infected with different S. epidermidis clones. Phenotypic variation was found among isolates both from the same tissue sample and from different samples from the same patient, and in some cases such variation represented the presence of different clones. One-third of the patients infected with S. epidermidis carried the icaADB genes. CoNS isolates showing phenotypic and/or genotypic heterogeneity were identified in tissue samples from half of the patients. The presence of the intercellular adhesion (ica) operon does not seem to be a prerequisite for establishing infection with CoNS.

  • 8.
    Nowinski, D.
    et al.
    Dept Surg Sci, Plast Surg Unit, Uppsala Univ, Uppsala, Sweden.
    Koskela, Anita
    Örebro University, School of Health and Medical Sciences. Örebro University Hospital, Örebro, Sweden.
    Kiwanuka, E.
    Dept Surg Sci, Plast Surg Unit, Uppsala Univ, Uppsala, Sweden.
    Boström, M.
    Dept Surg Sci, Plast Surg Unit, Uppsala Univ, Uppsala, Sweden.
    Gerdin, B.
    Dept Surg Sci, Plast Surg Unit,Uppsala Univ, Uppsala, Sweden.
    Ivarsson, Mikael
    Örebro University, School of Health and Medical Sciences. Örebro University Hospital, Örebro, Sweden.
    Inhibition of Connective Tissue Growth Factor/CCN2 Expression in Human Dermal Fibroblasts by Interleukin-1 alpha and beta2010In: Journal of Cellular Biochemistry, ISSN 0730-2312, E-ISSN 1097-4644, Vol. 110, no 5, p. 1226-1233Article in journal (Refereed)
    Abstract [en]

    Connective tissue growth factor (CTGF/CCN2) is a matricellular protein induced by transforming growth factor (TGF)-beta and intimately involved with tissue repair and overexpressed in various fibrotic conditions We previously showed that keratmocytes in vitro downregulate TGF-beta-induced expression of CTGF in fibroblasts by an interleukin (IL)-1 alpha-dependent mechanism. Here, we investigated further the mechanisms of this downregulation by both IL-1 alpha and beta Human dermal fibroblasts and NIH 3T3 cells were treated with IL-1 alpha or beta in presence or absence of TGF-beta 1. IL-1 suppressed basal and TGF-beta-induced CTGF mRNA and protein expression. IL-1 alpha and beta inhibited TGF-beta-stimulated CTGF promoter activity, and the activity of a synthetic minimal promoter containing Smad 3-binding CAGA elements Furthermore. IL-1 alpha and beta inhibited TGF-beta-stimulated Smad 3 phosphorylation, possibly linked to an observed increase in Smad 7 mRNA expression. In addition. RNA interference suggested that TGF-beta activated kinase1 (TAK1) is necessary for IL-1 inhibition of TGF-beta-stimulated CTGF expression. These results add to the understanding of how the expression of CTGF in human dermal fibroblasts is regulated, which in turn may have implications for the pathogenesis of fibrotic conditions involving the skin. J. Cell Biochem. 110: 1226-1233, 2010. (C) 2010 Wiley-Liss. Inc

  • 9. Olsson, Emma
    et al.
    Friberg, Örjan
    Venizelos, Nikolaos
    Örebro University, School of Health and Medical Sciences.
    Koskela, Anita
    Örebro University, School of Health and Medical Sciences.
    Källman, Jan
    Söderquist, Bo
    Örebro University, School of Health and Medical Sciences.
    Coagulase-negative staphylococci isolated from sternal wound infections after cardiac surgery: attachment to and accumulation on sternal fixation stainless steel wires2007In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 115, no 2, p. 142-151Article in journal (Refereed)
    Abstract [en]

    Sternal wound infection (SWI) is a serious complication after cardiac surgery. Coagulase-negative staphylococci (CoNS) have been found to be the most common pathogen involved in this postoperative infection related to implanted foreign materials, i.e. sternal fixation wires made from stainless steel. In this study a rapid and simple assay was developed for studying attachment and accumulation of CoNS on stainless steel wires in vitro using [(3)H] thymidine. The method showed a potential to detect differences in the dynamics of the adherence patterns among various CoNS isolates. However, no differences in attachment and accumulation were found between isolates causing deep SWI after cardiac surgery and contaminant isolates. In addition, there were no differences in the distribution of the ica operon between the two groups, as determined by polymerase chain reaction (PCR). Nevertheless, the ability to produce biofilm was found to be present significantly more frequently among SWI isolates than among contaminants.

  • 10.
    Siekmann, Wiebke
    et al.
    Örebro University, School of Medical Sciences. Department of Anesthesiology and Intensive Care.
    Tina, Elisabet
    Örebro University, School of Medical Sciences. Department of Clinical Research Laboratory,.
    Koskela von Sydow, Anita
    Örebro University, School of Medical Sciences. Department of Clinical Research Laboratory.
    Gupta, Anil
    Department of Physiology and Pharmacology, Karolinska Institute and Karolinska University Hospital, Stockholm; School of Medical Sciences, Örebro University, Örebro, Sweden.
    Effect of lidocaine and ropivacaine on primary (SW480) and metastatic (SW620) colon cancer cell lines2019In: Oncology Letters, ISSN 1792-1074, E-ISSN 1792-1082, Vol. 18, no 1, p. 395-401Article in journal (Refereed)
    Abstract [en]

    Regional anesthesia may prolong survival following surgery for different types of cancers. The mechanisms behind this are unclear but direct effects on cancer cells by local anesthetics (LA) have been suggested. The aim of this study was to investigate if lidocaine or ropivacaine have a dose-dependent effect on the cell viability and proliferation of a primary and a secondary colon carcinoma cell line in vitro. The colon cancer cell lines SW480 derived from primary tumor and SW620 from a metastatic site in the same patient were exposed to increasing concentrations of lidocaine and ropivacaine (5-1,000 mu M). Cell viability was measured using CellTiter-Blue((R)) and cell proliferation by PKH67 after exposure for up to 72 h. Cell viability was significantly reduced by ropivacaine at the highest concentration (1,000 mu M) after 48 and 72 h in the cell line SW480 and at 72 h in SW620. Exposure to lidocaine did not show any significant reduction in cell viability. Notably, low concentrations of both lidocaine and ropivacaine significantly increased cell viability after 48 and 72 h in SW620. Cell proliferation was significantly reduced by 1,000 mu M lidocaine in SW480 and by 1,000 mu M ropivacaine in SW620. In summary, both lidocaine and ropivacaine showed an anti-proliferative effect in the colon cancer cell lines at high concentrations and after prolonged exposure to LA in vitro. Our findings also indicate that lower concentrations promote cell viability in the metastatic cell line.

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