Objective:To study the correlation of Claudins6 (CLDN6) gene expression in meningioma tissue with the expression of matrix metalloproteinases (MMPs)/tissue inhibitors of matrix metalloproteinase (TIMPs) and epithelial...Objective:To study the correlation of Claudins6 (CLDN6) gene expression in meningioma tissue with the expression of matrix metalloproteinases (MMPs)/tissue inhibitors of matrix metalloproteinase (TIMPs) and epithelial-mesenchymal transition (EMT) genes.Methods:Meningioma tissue samples that were surgically removed in Yibin First People's Hospital between April 2014 and May 2017 were selected, normal arachnoid tissue samples that were collected from decompressive craniectomy in Yibin First People's Hospital during the same period were selected, and the expression of CLDN6, MMPs/TIMPs and EMT genes in tissues were determined.Results: CLDN6 protein expression in meningioma tissue was significantly lower than that in normal arachnoid tissue;EMMPRIN, MMP2, MMP9, Vimentin and N-cadherin protein expression in meningioma tissue were significantly higher than those in normal arachnoid tissue while TIMP1, TIMP2, E-cadherin andα-catenin protein expression were significantly lower than those in normal arachnoid tissue;EMMPRIN, MMP2, MMP9, Vimentin and N-cadherin protein expression in meningioma tissue with higher CLDN6 expression were significantly lower than those in meningioma tissue with lower CLDN6 expression while TIMP1, TIMP2, E-cadherin andα-catenin protein expression were significantly higher than those in meningioma tissue with lower CLDN6 expression. Conclusion: Lowly expressed CLDN6 gene in meningioma tissue can increase the hydrolysis activity of MMPs, induce epithelial-mesenchymal transition and thus promote the invasive growth of meningioma.展开更多
Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-t...Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-target and multi-pathway mode of action.Material&Methods:This study investigates the protective mechanisms and benefits of PDMSCs in mitigating the effects of controlled cortical impact(CCI)in rats and glutamate-induced oxidative stress injury in HT22 cells in vitro.Our primary objective is to provide evidence supporting the clinical application of PDMSCs.Results:In the in vivo arm of our investigation,we observed a swift elevation of matrix metalloproteinase-9(MMP-9)in the proximal cortex of injured brain tissues after CCI.PDMSCs,distinguished by their heightened expression of metalloproteinase tissue inhibitors-1 and-2(TIMP-1 and TIMP-2):were intravenously administered via the caudal vein.This intervention yielded significant reductions in the permeability of the blood-brain barrier(BBB):the extent of brain edema,the levels of inflammatory cytokines IL-1βand TNF-αin damaged brain tissue,and the activation status of microglia in CCI-afflicted rats.In the realm of in vitro experiments,PDMSC-conditioned media demonstrated substantial reductions in mortality rates and cleaved caspase-3 levels in glutamate-induced HT22 cells compared with conventional media.Notably,this advantage was negated upon the introduction of neutralizing antibodies targeting TIMP-1 and TIMP-2.Conclusion:Collectively,our findings underscore the potential of PDMSCs in alleviating oxidative stress injury and secondary brain injury in the pathological process of TBI.展开更多
Objective:To study the correlation of extracellular matrix metalloproteinase inducer (EMMPRIN) expression with inflammatory response and matrix metalloproteinases (MMPs) /TIMPs in patients with myocardial infarction.M...Objective:To study the correlation of extracellular matrix metalloproteinase inducer (EMMPRIN) expression with inflammatory response and matrix metalloproteinases (MMPs) /TIMPs in patients with myocardial infarction.Methods: The patients who were diagnosed with acute myocardial infarction and the patients who were diagnosed with stable angina pectoris in the Second People's Hospital of Juancheng County between March 2014 and December 2017 were selected as the AMI group and SAP group respectively, and the healthy volunteers who received physical examination during the same period were selected as the control group. Peripheral blood was collected to detect the expression of EMMPRIN, and serum was collected to determine the contents of inflammatory cytokines and MMPs/TIMPs. Results: Peripheral blood EMMPRIN expression as well as serum ICAM1, VCAM1, IL-1β, IL-17, MMP2, MMP8 and MMP9 contents of AMI group and SAP group were significantly higher than those of control group whereas TGF-β1, sFGL-2, TIMP1 and TIMP2 contents were significantly lower than those of control group and the changes of above indexes in AMI group were more significant than those in SAP group. Serum ICAM1, VCAM1, IL-1β, IL-17, MMP2, MMP8 and MMP9 contents of AMI group of patients with high EMMPRIN expression were significantly higher than those of patients with low EMMPRIN expression whereas TGF-β1, sFGL-2, TIMP1 and TIMP2 contents were significantly lower than those of patients with low EMMPRIN expression.Conclusion:The high EMMPRIN expression in peripheral blood of patients with myocardial infarction can aggravate the inflammatory response and destroy the balance of MMPs/TIMPs.展开更多
文摘Objective:To study the correlation of Claudins6 (CLDN6) gene expression in meningioma tissue with the expression of matrix metalloproteinases (MMPs)/tissue inhibitors of matrix metalloproteinase (TIMPs) and epithelial-mesenchymal transition (EMT) genes.Methods:Meningioma tissue samples that were surgically removed in Yibin First People's Hospital between April 2014 and May 2017 were selected, normal arachnoid tissue samples that were collected from decompressive craniectomy in Yibin First People's Hospital during the same period were selected, and the expression of CLDN6, MMPs/TIMPs and EMT genes in tissues were determined.Results: CLDN6 protein expression in meningioma tissue was significantly lower than that in normal arachnoid tissue;EMMPRIN, MMP2, MMP9, Vimentin and N-cadherin protein expression in meningioma tissue were significantly higher than those in normal arachnoid tissue while TIMP1, TIMP2, E-cadherin andα-catenin protein expression were significantly lower than those in normal arachnoid tissue;EMMPRIN, MMP2, MMP9, Vimentin and N-cadherin protein expression in meningioma tissue with higher CLDN6 expression were significantly lower than those in meningioma tissue with lower CLDN6 expression while TIMP1, TIMP2, E-cadherin andα-catenin protein expression were significantly higher than those in meningioma tissue with lower CLDN6 expression. Conclusion: Lowly expressed CLDN6 gene in meningioma tissue can increase the hydrolysis activity of MMPs, induce epithelial-mesenchymal transition and thus promote the invasive growth of meningioma.
基金financially supported by the Key Research Projects of Ningxia Hui Autonomous Region of China under Grant No.2018BCG01002(to HCX).
文摘Background:As a form of biological therapy,placenta-derived mesenchymal stem cells(PDMSCs)exhibit considerable promise in addressing the complex pathological processes of traumaticbrain injury(TBI)due to their multi-target and multi-pathway mode of action.Material&Methods:This study investigates the protective mechanisms and benefits of PDMSCs in mitigating the effects of controlled cortical impact(CCI)in rats and glutamate-induced oxidative stress injury in HT22 cells in vitro.Our primary objective is to provide evidence supporting the clinical application of PDMSCs.Results:In the in vivo arm of our investigation,we observed a swift elevation of matrix metalloproteinase-9(MMP-9)in the proximal cortex of injured brain tissues after CCI.PDMSCs,distinguished by their heightened expression of metalloproteinase tissue inhibitors-1 and-2(TIMP-1 and TIMP-2):were intravenously administered via the caudal vein.This intervention yielded significant reductions in the permeability of the blood-brain barrier(BBB):the extent of brain edema,the levels of inflammatory cytokines IL-1βand TNF-αin damaged brain tissue,and the activation status of microglia in CCI-afflicted rats.In the realm of in vitro experiments,PDMSC-conditioned media demonstrated substantial reductions in mortality rates and cleaved caspase-3 levels in glutamate-induced HT22 cells compared with conventional media.Notably,this advantage was negated upon the introduction of neutralizing antibodies targeting TIMP-1 and TIMP-2.Conclusion:Collectively,our findings underscore the potential of PDMSCs in alleviating oxidative stress injury and secondary brain injury in the pathological process of TBI.
文摘Objective:To study the correlation of extracellular matrix metalloproteinase inducer (EMMPRIN) expression with inflammatory response and matrix metalloproteinases (MMPs) /TIMPs in patients with myocardial infarction.Methods: The patients who were diagnosed with acute myocardial infarction and the patients who were diagnosed with stable angina pectoris in the Second People's Hospital of Juancheng County between March 2014 and December 2017 were selected as the AMI group and SAP group respectively, and the healthy volunteers who received physical examination during the same period were selected as the control group. Peripheral blood was collected to detect the expression of EMMPRIN, and serum was collected to determine the contents of inflammatory cytokines and MMPs/TIMPs. Results: Peripheral blood EMMPRIN expression as well as serum ICAM1, VCAM1, IL-1β, IL-17, MMP2, MMP8 and MMP9 contents of AMI group and SAP group were significantly higher than those of control group whereas TGF-β1, sFGL-2, TIMP1 and TIMP2 contents were significantly lower than those of control group and the changes of above indexes in AMI group were more significant than those in SAP group. Serum ICAM1, VCAM1, IL-1β, IL-17, MMP2, MMP8 and MMP9 contents of AMI group of patients with high EMMPRIN expression were significantly higher than those of patients with low EMMPRIN expression whereas TGF-β1, sFGL-2, TIMP1 and TIMP2 contents were significantly lower than those of patients with low EMMPRIN expression.Conclusion:The high EMMPRIN expression in peripheral blood of patients with myocardial infarction can aggravate the inflammatory response and destroy the balance of MMPs/TIMPs.
