AIM:To demonstrate that CD14 + cells are an important source of the growth factor YKL40 in acute and chronic liver damage.METHODS:Rats were inoculated with one dose of CCl4 to induce acute damage.Liver biopsies were o...AIM:To demonstrate that CD14 + cells are an important source of the growth factor YKL40 in acute and chronic liver damage.METHODS:Rats were inoculated with one dose of CCl4 to induce acute damage.Liver biopsies were obtained at 0,6,12,24,48 and 72 h.For chronic damage,CCl4 was administered three days per week for 6 or 8 wk.Tissue samples were collected,and cellular populations were isolated by liver digestion and purified by cell sorting.YKL40 mRNA and protein expression were evaluated by realtime polymerase chain reaction and western blot.RESULTS:Acute liver damage induced a rapid increase of YKL40 mRNA beginning at 12 h.Expression peaked at 24 h,with a 26fold increase over basal levels.By 72 h however,YKL40 expression levels had nearly returned to control levels.On the other hand,chronic damage induced a sustained increase in YKL40 expression,with 7and 9fold higher levels at 6 and 8 wk,respectively.The pattern of YKL40 expression in different subpopulations showed that CD14+cells,which include Kupffer cells,are a source of YKL40 after acute damage at 72 h[0.09 relative expression units(REU)]as well as after chronic injury at 6 wk(0.11 REU).Hepatocytes,in turn,accounted for 0.06 and 0.01 REU after 72 h(acute)or 6 wk(chronic),respectively.The rest of the CD14cells(including T lymphocytes,B lymphocytes,natural killer and natural killer T cells) yielded 0.07 and 0.15 REU at 72 h and 6 wk,respectively.YKL40 protein expression in liver was detected at 72 h as well as 6 and 8 wk,with the highest expression relative to controls(11fold;P≤0.05)seen at 6 wk.Macrophages were stimulated by lipopolysaccharide.We demonstrate that under these conditions,these cells showed maximum expression of YKL40 at 12 h,with P<0.05 compared with controls.CONCLUSION:Hepatic CD14 + cells are an YKL40 mRNA and protein source in acute and chronic liver injury,with expression patterns similar to growth factors implicated in inflammationfibrogenesis.展开更多
To the Editor:Atherosclerosis is the main pathological feature of ischemic stroke,which remains a major cause of disability and death worldwide.[1]Vulnerable plaque,was characterized by ulceration,platelet activation,...To the Editor:Atherosclerosis is the main pathological feature of ischemic stroke,which remains a major cause of disability and death worldwide.[1]Vulnerable plaque,was characterized by ulceration,platelet activation,and thrombosis,potentially leading to emboli detachment and stroke.[2]Vascular smooth muscle cells(VSMCs),a major cellular component within lesions,can display pleiotropic phenotypes,including osteogenic or inammatory phenotypes,which may be harmful in maintaining advanced atherosclerotic plaque stability.[3]The modulation of the function of VSMCs,including proliferation,migration,and synthesizing the extracellular matrix(ECM)and matrix metalloproteinase(MMP),is thought to markedly affect plaque formation and vulnerability.[4]Therefore,it is of considerable signicance to drive harmful VSMCs toward VSMCs having benecial properties to strengthen plaque stability and retard plaque development.展开更多
基金Supported by Complementary support CONACyT 90361
文摘AIM:To demonstrate that CD14 + cells are an important source of the growth factor YKL40 in acute and chronic liver damage.METHODS:Rats were inoculated with one dose of CCl4 to induce acute damage.Liver biopsies were obtained at 0,6,12,24,48 and 72 h.For chronic damage,CCl4 was administered three days per week for 6 or 8 wk.Tissue samples were collected,and cellular populations were isolated by liver digestion and purified by cell sorting.YKL40 mRNA and protein expression were evaluated by realtime polymerase chain reaction and western blot.RESULTS:Acute liver damage induced a rapid increase of YKL40 mRNA beginning at 12 h.Expression peaked at 24 h,with a 26fold increase over basal levels.By 72 h however,YKL40 expression levels had nearly returned to control levels.On the other hand,chronic damage induced a sustained increase in YKL40 expression,with 7and 9fold higher levels at 6 and 8 wk,respectively.The pattern of YKL40 expression in different subpopulations showed that CD14+cells,which include Kupffer cells,are a source of YKL40 after acute damage at 72 h[0.09 relative expression units(REU)]as well as after chronic injury at 6 wk(0.11 REU).Hepatocytes,in turn,accounted for 0.06 and 0.01 REU after 72 h(acute)or 6 wk(chronic),respectively.The rest of the CD14cells(including T lymphocytes,B lymphocytes,natural killer and natural killer T cells) yielded 0.07 and 0.15 REU at 72 h and 6 wk,respectively.YKL40 protein expression in liver was detected at 72 h as well as 6 and 8 wk,with the highest expression relative to controls(11fold;P≤0.05)seen at 6 wk.Macrophages were stimulated by lipopolysaccharide.We demonstrate that under these conditions,these cells showed maximum expression of YKL40 at 12 h,with P<0.05 compared with controls.CONCLUSION:Hepatic CD14 + cells are an YKL40 mRNA and protein source in acute and chronic liver injury,with expression patterns similar to growth factors implicated in inflammationfibrogenesis.
基金Specifically Invited Professor of Oriental Scholar of Shanghai Colleges and Universities Tracking Program(No.GZ2016008)National Natural Science Foundation of China(No.81870347)
文摘To the Editor:Atherosclerosis is the main pathological feature of ischemic stroke,which remains a major cause of disability and death worldwide.[1]Vulnerable plaque,was characterized by ulceration,platelet activation,and thrombosis,potentially leading to emboli detachment and stroke.[2]Vascular smooth muscle cells(VSMCs),a major cellular component within lesions,can display pleiotropic phenotypes,including osteogenic or inammatory phenotypes,which may be harmful in maintaining advanced atherosclerotic plaque stability.[3]The modulation of the function of VSMCs,including proliferation,migration,and synthesizing the extracellular matrix(ECM)and matrix metalloproteinase(MMP),is thought to markedly affect plaque formation and vulnerability.[4]Therefore,it is of considerable signicance to drive harmful VSMCs toward VSMCs having benecial properties to strengthen plaque stability and retard plaque development.
