In order to select improved varieties, a study on the fine individual selection was carried out in Pengshui County, Chongqing Province. For 14 fine individuals with high and stable yield preliminarily screened, eight ...In order to select improved varieties, a study on the fine individual selection was carried out in Pengshui County, Chongqing Province. For 14 fine individuals with high and stable yield preliminarily screened, eight factors(fruit height, fruit diameter, pericarp thickness, fresh fruit weight, fresh seed weight, dry seed weight, dry seed yield and fresh seed yield) related to yield were selected to perform principal component analysis, and based on comprehensive scores and oil contents, five fine individuals(Longshe Town 7, 8, 12, 17 and Shaoqing Street 2) of Camellia pitardii were determined. These fine individuals have a better performance.展开更多
METRNL is a recently identified secreted protein with emerging functions.This study is to find major cellular source of circulating METRNL and to determine METRNL novel function.Here,we show METRNL is abundant in huma...METRNL is a recently identified secreted protein with emerging functions.This study is to find major cellular source of circulating METRNL and to determine METRNL novel function.Here,we show METRNL is abundant in human and mouse vascular endothelium and released by endothelial cells using endoplasmic reticulum-Golgi apparatus pathway.By creating endothelial cell-specific Metrnl knockout mice,combined with bone marrow transplantation to produce bone marrow-specific deletion of Metrnl,we demonstrate that most of circulating METRNL(approximately 75%)originates from the endothelial cells.Both endothelial and circulating METRNL decrease in atherosclerosis mice and patients.By generating endothelial cell-specific Metrnl knockout in apolipoprotein E-deficient mice,combined with bone marrow-specific deletion of Metrnl in apolipoprotein E-deficient mice,we further demonstrate that endothelial METRNL deficiency accelerates atherosclerosis.Mechanically,endothelial METRNL deficiency causes vascular endothelial dysfunction including vasodilation impairment via reducing eNOS phosphorylation at Ser1177 and inflammation activation via enhancing NFκB pathway,which promotes the susceptibility of atherosclerosis.Exogenous METRNL rescues METRNL deficiency induced endothelial dysfunction.These findings reveal that METRNL is a new endothelial substance not only determining the circulating METRNL level but also regulating endothelial function for vascular health and disease.METRNL is a therapeutic target against endothelial dysfunction and atherosclerosis.展开更多
基金Supported by Chongqing Copyright Administration Key Scientific and Technological Project
文摘In order to select improved varieties, a study on the fine individual selection was carried out in Pengshui County, Chongqing Province. For 14 fine individuals with high and stable yield preliminarily screened, eight factors(fruit height, fruit diameter, pericarp thickness, fresh fruit weight, fresh seed weight, dry seed weight, dry seed yield and fresh seed yield) related to yield were selected to perform principal component analysis, and based on comprehensive scores and oil contents, five fine individuals(Longshe Town 7, 8, 12, 17 and Shaoqing Street 2) of Camellia pitardii were determined. These fine individuals have a better performance.
基金supported by grants from the National Natural Science Foundation of China Major Project(Nos.81730098 and 82030110)National Natural Science Foundation of China Young Program(No.82104165)+2 种基金Shanghai Science and Technology Commission Project(No.201409004600,China)Shanghai Sailing Program(No.21YF1457600,China)Medical Innovation Project(Nos.16CXZ009,16QNP087 and 2018-CGPZ-A03,China)。
文摘METRNL is a recently identified secreted protein with emerging functions.This study is to find major cellular source of circulating METRNL and to determine METRNL novel function.Here,we show METRNL is abundant in human and mouse vascular endothelium and released by endothelial cells using endoplasmic reticulum-Golgi apparatus pathway.By creating endothelial cell-specific Metrnl knockout mice,combined with bone marrow transplantation to produce bone marrow-specific deletion of Metrnl,we demonstrate that most of circulating METRNL(approximately 75%)originates from the endothelial cells.Both endothelial and circulating METRNL decrease in atherosclerosis mice and patients.By generating endothelial cell-specific Metrnl knockout in apolipoprotein E-deficient mice,combined with bone marrow-specific deletion of Metrnl in apolipoprotein E-deficient mice,we further demonstrate that endothelial METRNL deficiency accelerates atherosclerosis.Mechanically,endothelial METRNL deficiency causes vascular endothelial dysfunction including vasodilation impairment via reducing eNOS phosphorylation at Ser1177 and inflammation activation via enhancing NFκB pathway,which promotes the susceptibility of atherosclerosis.Exogenous METRNL rescues METRNL deficiency induced endothelial dysfunction.These findings reveal that METRNL is a new endothelial substance not only determining the circulating METRNL level but also regulating endothelial function for vascular health and disease.METRNL is a therapeutic target against endothelial dysfunction and atherosclerosis.
