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ameliorates TNF-α induced meniscus degeneration in mature meniscal tissue in vitro.\nBACKGROUND: Joint inflammation causes meniscus degeneration and can exacerbate post-traumatic meniscus injuries by extracellular matrix degradation, cellular de-differentiation and cell death. The aim of this study was to examine whether anti-inflammatory interleukin-10 exerts protective effects in an in vitro model of TNF-α-induced meniscus degeneration.\nMETHODS: Meniscus tissue was harvested from the knees of adult cows. After 24 h of equilibrium explants were simultaneously treated with bovine TNF-α and IL-10. After an incubation time of 72 h cell death was measured histomorphometrically (nuclear blebbing, NB) and release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analysed. Transcription levels (mRNA) of matrix degrading enzymes, collagen type X (COL10A1) and nitric oxide synthetase 2 (NOS2) were measured by quantitative real time PCR. TNF-α-dependent formation of the aggrecanase-specific aggrecan neoepitope NITEGE was visualised by immunostaining. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test.\nRESULTS: Administration of IL-10 significantly prevented the TNF-α-related cell death (P .001), release of NO (P .003) and NOS2 expression (P .04). Release of GAG fragments (P .001), NITEGE formation and expression of MMP3 (P .007), -13 (P .02) and ADAMTS4 (P .001) were significantly reduced. The TNF-α-dependent increase in COL10A1 expression was also antagonized by IL-10 (P .02).\nCONCLUSION: IL-10 prevented crucial mechanisms of meniscal degeneration induced by a key cytokine of OA, TNF-α. Administration of IL-10 might improve the biological regeneration and provide a treatment approach in degenerative meniscus injuries and in conditions of post-traumatic sports injuries."}

    PubMed_Structured_Abstracts

    {"project":"PubMed_Structured_Abstracts","denotations":[{"id":"T1","span":{"begin":102,"end":447},"obj":"BACKGROUND"},{"id":"T2","span":{"begin":457,"end":1193},"obj":"METHODS"},{"id":"T3","span":{"begin":1203,"end":1577},"obj":"RESULTS"},{"id":"T4","span":{"begin":1590,"end":1875},"obj":"CONCLUSION"}],"text":"IL-10 ameliorates TNF-α induced meniscus degeneration in mature meniscal tissue in vitro.\nBACKGROUND: Joint inflammation causes meniscus degeneration and can exacerbate post-traumatic meniscus injuries by extracellular matrix degradation, cellular de-differentiation and cell death. The aim of this study was to examine whether anti-inflammatory interleukin-10 exerts protective effects in an in vitro model of TNF-α-induced meniscus degeneration.\nMETHODS: Meniscus tissue was harvested from the knees of adult cows. After 24 h of equilibrium explants were simultaneously treated with bovine TNF-α and IL-10. After an incubation time of 72 h cell death was measured histomorphometrically (nuclear blebbing, NB) and release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analysed. Transcription levels (mRNA) of matrix degrading enzymes, collagen type X (COL10A1) and nitric oxide synthetase 2 (NOS2) were measured by quantitative real time PCR. TNF-α-dependent formation of the aggrecanase-specific aggrecan neoepitope NITEGE was visualised by immunostaining. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test.\nRESULTS: Administration of IL-10 significantly prevented the TNF-α-related cell death (P .001), release of NO (P .003) and NOS2 expression (P .04). Release of GAG fragments (P .001), NITEGE formation and expression of MMP3 (P .007), -13 (P .02) and ADAMTS4 (P .001) were significantly reduced. The TNF-α-dependent increase in COL10A1 expression was also antagonized by IL-10 (P .02).\nCONCLUSION: IL-10 prevented crucial mechanisms of meniscal degeneration induced by a key cytokine of OA, TNF-α. Administration of IL-10 might improve the biological regeneration and provide a treatment approach in degenerative meniscus injuries and in conditions of post-traumatic sports injuries."}

    Goldhamster2_Cellosaurus

    {"project":"Goldhamster2_Cellosaurus","denotations":[{"id":"T1","span":{"begin":390,"end":392},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T2","span":{"begin":390,"end":392},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T3","span":{"begin":523,"end":527},"obj":"CVCL_8262|Cancer_cell_line|Homo sapiens"},{"id":"T4","span":{"begin":615,"end":617},"obj":"CVCL_8754|Cancer_cell_line|Homo sapiens"},{"id":"T5","span":{"begin":615,"end":617},"obj":"CVCL_H241|Cancer_cell_line|Homo sapiens"},{"id":"T6","span":{"begin":629,"end":633},"obj":"CVCL_0047|Telomerase_immortalized_cell_line|Homo sapiens"},{"id":"T7","span":{"begin":930,"end":934},"obj":"CVCL_3351|Cancer_cell_line|Homo sapiens"},{"id":"T8","span":{"begin":930,"end":934},"obj":"CVCL_T747|Cancer_cell_line|Homo sapiens"},{"id":"T9","span":{"begin":971,"end":975},"obj":"CVCL_0047|Telomerase_immortalized_cell_line|Homo sapiens"},{"id":"T10","span":{"begin":1145,"end":1146},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T11","span":{"begin":1147,"end":1150},"obj":"CVCL_Z424|Spontaneously_immortalized_cell_line|Ostrinia nubilalis"},{"id":"T12","span":{"begin":1166,"end":1167},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T13","span":{"begin":1281,"end":1287},"obj":"CVCL_JT24|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T14","span":{"begin":1317,"end":1321},"obj":"CVCL_3351|Cancer_cell_line|Homo sapiens"},{"id":"T15","span":{"begin":1317,"end":1321},"obj":"CVCL_T747|Cancer_cell_line|Homo sapiens"},{"id":"T16","span":{"begin":1368,"end":1374},"obj":"CVCL_JT24|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T17","span":{"begin":1452,"end":1458},"obj":"CVCL_JT24|Induced_pluripotent_stem_cell|Homo sapiens"},{"id":"T18","span":{"begin":1661,"end":1662},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"},{"id":"T19","span":{"begin":1768,"end":1769},"obj":"CVCL_6479|Finite_cell_line|Mus musculus"}],"text":"IL-10 ameliorates TNF-α induced meniscus degeneration in mature meniscal tissue in vitro.\nBACKGROUND: Joint inflammation causes meniscus degeneration and can exacerbate post-traumatic meniscus injuries by extracellular matrix degradation, cellular de-differentiation and cell death. The aim of this study was to examine whether anti-inflammatory interleukin-10 exerts protective effects in an in vitro model of TNF-α-induced meniscus degeneration.\nMETHODS: Meniscus tissue was harvested from the knees of adult cows. After 24 h of equilibrium explants were simultaneously treated with bovine TNF-α and IL-10. After an incubation time of 72 h cell death was measured histomorphometrically (nuclear blebbing, NB) and release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analysed. Transcription levels (mRNA) of matrix degrading enzymes, collagen type X (COL10A1) and nitric oxide synthetase 2 (NOS2) were measured by quantitative real time PCR. TNF-α-dependent formation of the aggrecanase-specific aggrecan neoepitope NITEGE was visualised by immunostaining. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test.\nRESULTS: Administration of IL-10 significantly prevented the TNF-α-related cell death (P .001), release of NO (P .003) and NOS2 expression (P .04). Release of GAG fragments (P .001), NITEGE formation and expression of MMP3 (P .007), -13 (P .02) and ADAMTS4 (P .001) were significantly reduced. The TNF-α-dependent increase in COL10A1 expression was also antagonized by IL-10 (P .02).\nCONCLUSION: IL-10 prevented crucial mechanisms of meniscal degeneration induced by a key cytokine of OA, TNF-α. Administration of IL-10 might improve the biological regeneration and provide a treatment approach in degenerative meniscus injuries and in conditions of post-traumatic sports injuries."}

    Inflammaging

    {"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":89},"obj":"Sentence"},{"id":"T2","span":{"begin":90,"end":101},"obj":"Sentence"},{"id":"T3","span":{"begin":102,"end":282},"obj":"Sentence"},{"id":"T4","span":{"begin":283,"end":447},"obj":"Sentence"},{"id":"T5","span":{"begin":448,"end":456},"obj":"Sentence"},{"id":"T6","span":{"begin":457,"end":516},"obj":"Sentence"},{"id":"T7","span":{"begin":517,"end":608},"obj":"Sentence"},{"id":"T8","span":{"begin":609,"end":815},"obj":"Sentence"},{"id":"T9","span":{"begin":816,"end":980},"obj":"Sentence"},{"id":"T10","span":{"begin":981,"end":1095},"obj":"Sentence"},{"id":"T11","span":{"begin":1096,"end":1193},"obj":"Sentence"},{"id":"T12","span":{"begin":1194,"end":1202},"obj":"Sentence"},{"id":"T13","span":{"begin":1203,"end":1341},"obj":"Sentence"},{"id":"T14","span":{"begin":1342,"end":1487},"obj":"Sentence"},{"id":"T15","span":{"begin":1488,"end":1577},"obj":"Sentence"},{"id":"T16","span":{"begin":1578,"end":1689},"obj":"Sentence"},{"id":"T17","span":{"begin":1690,"end":1875},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":89},"obj":"Sentence"},{"id":"T2","span":{"begin":90,"end":101},"obj":"Sentence"},{"id":"T3","span":{"begin":102,"end":282},"obj":"Sentence"},{"id":"T4","span":{"begin":283,"end":447},"obj":"Sentence"},{"id":"T5","span":{"begin":448,"end":456},"obj":"Sentence"},{"id":"T6","span":{"begin":457,"end":516},"obj":"Sentence"},{"id":"T7","span":{"begin":517,"end":608},"obj":"Sentence"},{"id":"T8","span":{"begin":609,"end":815},"obj":"Sentence"},{"id":"T9","span":{"begin":816,"end":980},"obj":"Sentence"},{"id":"T10","span":{"begin":981,"end":1095},"obj":"Sentence"},{"id":"T11","span":{"begin":1096,"end":1193},"obj":"Sentence"},{"id":"T12","span":{"begin":1194,"end":1202},"obj":"Sentence"},{"id":"T13","span":{"begin":1203,"end":1341},"obj":"Sentence"},{"id":"T14","span":{"begin":1342,"end":1487},"obj":"Sentence"},{"id":"T15","span":{"begin":1488,"end":1577},"obj":"Sentence"},{"id":"T16","span":{"begin":1578,"end":1689},"obj":"Sentence"},{"id":"T17","span":{"begin":1690,"end":1875},"obj":"Sentence"}],"text":"IL-10 ameliorates TNF-α induced meniscus degeneration in mature meniscal tissue in vitro.\nBACKGROUND: Joint inflammation causes meniscus degeneration and can exacerbate post-traumatic meniscus injuries by extracellular matrix degradation, cellular de-differentiation and cell death. The aim of this study was to examine whether anti-inflammatory interleukin-10 exerts protective effects in an in vitro model of TNF-α-induced meniscus degeneration.\nMETHODS: Meniscus tissue was harvested from the knees of adult cows. After 24 h of equilibrium explants were simultaneously treated with bovine TNF-α and IL-10. After an incubation time of 72 h cell death was measured histomorphometrically (nuclear blebbing, NB) and release of glycosaminoglycans (GAG, DMMB assay) and nitric oxide (NO, Griess-reagent) were analysed. Transcription levels (mRNA) of matrix degrading enzymes, collagen type X (COL10A1) and nitric oxide synthetase 2 (NOS2) were measured by quantitative real time PCR. TNF-α-dependent formation of the aggrecanase-specific aggrecan neoepitope NITEGE was visualised by immunostaining. Differences between groups were calculated using a one-way ANOVA with a Bonferroni post hoc test.\nRESULTS: Administration of IL-10 significantly prevented the TNF-α-related cell death (P .001), release of NO (P .003) and NOS2 expression (P .04). Release of GAG fragments (P .001), NITEGE formation and expression of MMP3 (P .007), -13 (P .02) and ADAMTS4 (P .001) were significantly reduced. The TNF-α-dependent increase in COL10A1 expression was also antagonized by IL-10 (P .02).\nCONCLUSION: IL-10 prevented crucial mechanisms of meniscal degeneration induced by a key cytokine of OA, TNF-α. Administration of IL-10 might improve the biological regeneration and provide a treatment approach in degenerative meniscus injuries and in conditions of post-traumatic sports injuries."}