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dc.contributor.authorKasnak, Gökhan
dc.contributor.authorGürsoy, Kahraman
dc.contributor.authorFıratlı, Halil Erhan
dc.contributor.authorFıratlı, Yiğit
dc.date.accessioned2022-07-04T15:39:37Z
dc.date.available2022-07-04T15:39:37Z
dc.identifier.citationFıratlı Y., Kasnak G., Fıratlı H. E. , Gürsoy K., "Localization and expression profiles of Gingival MCPIP-1 and MALT-1", Europerio 10, Kobenhavn, Danimarka, 15 - 18 Haziran 2022, cilt.49, sa.25, ss.152
dc.identifier.othervv_1032021
dc.identifier.otherav_bbf529df-dc24-416a-aecc-1ed97154615a
dc.identifier.urihttp://hdl.handle.net/20.500.12627/184445
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/epdf/10.1111/jcpe.13636
dc.identifier.urihttps://doi.org/10.1111/jcpe.13636
dc.description.abstractBackground and Aim: Monocyte chemoattractant protein-inducedprotein-1 (MCPIP-1) is a host inflammatory response cytokine RNaseand a suppressor of proinflammatory response. Mucosa associatedlymphoid tissue lymphoma translocation protein 1 (MALT-1) is a cys-teine protease that contributes to cleaving the negative regulation ofinflammatory signaling. Recent in vitro studies demonstrated thatMCPIP-1 is degraded byPorphyromonas gingivalisgingipains. Weaimed to localise MCPIP-1 and MALT-1 human gingival samples inrelation to periodontitis. Moreover, we tested the expression of theseproteins by gingival resident cells using a 3D-organotypic oral mucosamodel.Methods: Eight periodontitis patients and eight periodontally healthyindividuals were recruited. The study protocol was approved by theUniversity of Istanbul's Faculty of Dentistry's Ethics Committee inaccordance with the Helsinki Declaration (2017/41). Paraffin-embedded gingival samples were cut into 5μm-thick sections andplaced on slides for immunohistochemical analysis. The immunohisto-chemical stainings were evaluated under a light microscope and high-resolution images were captured to analyze signal intensities withImageJ immunohistochemistry analysis toolbox. Stainings' intensitieswere determined from epithelium and connective tissue. One-wayanalysis of variance (ANOVA) following Tukey's correction was usedin statistical analysis. A 3D-organotypic oral mucosa model was con-structed using gingival keratinocytes and gingival fibroblasts.MCPIP-1 and MALT-1 protein expressions were analyzedimmunohistochemically.Results: In human gingiva, MCPIP-1 was detectable in epithelium andconnective tissues, prominent around the blood vessel walls. MALT-1was detectable at all layers of gingival epithelium and especiallyaround the accumulated inflammatory cells in connective tissue. Nostatistical significance was detected between the periodontitis andcontrol groups. HMK cells of the 3D-organotypic oral mucosa modelhave been observed to express MCPIP-1 and MALT-1.Conclusions: This pilot study confirms the existence of MCPIP-1 andMALT-1 in gingival tissues both in periodontal health and in periodon-titis, and also confirms that the resident gingival cells can be a sourcefor these proteins.152ABSTRACTBackground and Aim: Monocyte chemoattractant protein-inducedprotein-1 (MCPIP-1) is a host inflammatory response cytokine RNaseand a suppressor of proinflammatory response. Mucosa associatedlymphoid tissue lymphoma translocation protein 1 (MALT-1) is a cys-teine protease that contributes to cleaving the negative regulation ofinflammatory signaling. Recent in vitro studies demonstrated thatMCPIP-1 is degraded byPorphyromonas gingivalisgingipains. Weaimed to localise MCPIP-1 and MALT-1 human gingival samples inrelation to periodontitis. Moreover, we tested the expression of theseproteins by gingival resident cells using a 3D-organotypic oral mucosamodel.Methods: Eight periodontitis patients and eight periodontally healthyindividuals were recruited. The study protocol was approved by theUniversity of Istanbul's Faculty of Dentistry's Ethics Committee inaccordance with the Helsinki Declaration (2017/41). Paraffin-embedded gingival samples were cut into 5μm-thick sections andplaced on slides for immunohistochemical analysis. The immunohisto-chemical stainings were evaluated under a light microscope and high-resolution images were captured to analyze signal intensities withImageJ immunohistochemistry analysis toolbox. Stainings' intensitieswere determined from epithelium and connective tissue. One-wayanalysis of variance (ANOVA) following Tukey's correction was usedin statistical analysis. A 3D-organotypic oral mucosa model was con-structed using gingival keratinocytes and gingival fibroblasts.MCPIP-1 and MALT-1 protein expressions were analyzedimmunohistochemically.Results: In human gingiva, MCPIP-1 was detectable in epithelium andconnective tissues, prominent around the blood vessel walls. MALT-1was detectable at all layers of gingival epithelium and especiallyaround the accumulated inflammatory cells in connective tissue. Nostatistical significance was detected between the periodontitis andcontrol groups. HMK cells of the 3D-organotypic oral mucosa modelhave been observed to express MCPIP-1 and MALT-1.Conclusions: This pilot study confirms the existence of MCPIP-1 andMALT-1 in gingival tissues both in periodontal health and in periodon-titis, and also confirms that the resident gingival cells can be a sourcefor these proteins.152ABSTRACTBackground and Aim: Monocyte chemoattractant protein-inducedprotein-1 (MCPIP-1) is a host inflammatory response cytokine RNaseand a suppressor of proinflammatory response. Mucosa associatedlymphoid tissue lymphoma translocation protein 1 (MALT-1) is a cys-teine protease that contributes to cleaving the negative regulation ofinflammatory signaling. Recent in vitro studies demonstrated thatMCPIP-1 is degraded byPorphyromonas gingivalisgingipains. Weaimed to localise MCPIP-1 and MALT-1 human gingival samples inrelation to periodontitis. Moreover, we tested the expression of theseproteins by gingival resident cells using a 3D-organotypic oral mucosamodel.Methods: Eight periodontitis patients and eight periodontally healthyindividuals were recruited. The study protocol was approved by theUniversity of Istanbul's Faculty of Dentistry's Ethics Committee inaccordance with the Helsinki Declaration (2017/41). Paraffin-embedded gingival samples were cut into 5μm-thick sections andplaced on slides for immunohistochemical analysis. The immunohisto-chemical stainings were evaluated under a light microscope and high-resolution images were captured to analyze signal intensities withImageJ immunohistochemistry analysis toolbox. Stainings' intensitieswere determined from epithelium and connective tissue. One-wayanalysis of variance (ANOVA) following Tukey's correction was usedin statistical analysis. A 3D-organotypic oral mucosa model was con-structed using gingival keratinocytes and gingival fibroblasts.MCPIP-1 and MALT-1 protein expressions were analyzedimmunohistochemically.Results: In human gingiva, MCPIP-1 was detectable in epithelium andconnective tissues, prominent around the blood vessel walls. MALT-1was detectable at all layers of gingival epithelium and especiallyaround the accumulated inflammatory cells in connective tissue. Nostatistical significance was detected between the periodontitis andcontrol groups. HMK cells of the 3D-organotypic oral mucosa modelhave been observed to express MCPIP-1 and MALT-1.Conclusions: This pilot study confirms the existence of MCPIP-1 andMALT-1 in gingival tissues both in periodontal health and in periodon-titis, and also confirms that the resident gingival cells can be a sourcefor these proteins.152ABSTRACT
dc.language.isoeng
dc.subjectOrthodontics
dc.subjectOral Surgery
dc.subjectDentistry (miscellaneous)
dc.subjectDental Hygiene
dc.subjectPeriodontics
dc.subjectDental Assisting
dc.subjectGeneral Dentistry
dc.subjectHealth Sciences
dc.subjectKlinik Bilimler
dc.subjectPeriodontoloji
dc.subjectDiş Hekimliği
dc.subjectSağlık Bilimleri
dc.subjectDİŞ HEKİMLİĞİ, ORAL CERRAHİ VE TIP
dc.subjectKlinik Tıp
dc.subjectKlinik Tıp (MED)
dc.titleLocalization and expression profiles of Gingival MCPIP-1 and MALT-1
dc.typeBildiri
dc.contributor.departmentİstanbul Üniversitesi , Diş Hekimliği Fakültesi , Klinik Bilimler Bölümü
dc.identifier.volume49
dc.contributor.firstauthorID3432654


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