FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W657304069> ?p ?o ?g. }

• W657304069 endingPage "15511" @default.
• W657304069 startingPage "15496" @default.
• W657304069 abstract "Studies in human populations have shown a significant correlation between procollagen C-endopeptidase enhancer protein 2 (PCPE2) single nucleotide polymorphisms and plasma HDL cholesterol concentrations. PCPE2, a 52-kDa glycoprotein located in the extracellular matrix, enhances the cleavage of C-terminal procollagen by bone morphogenetic protein 1 (BMP1). Our studies here focused on investigating the basis for the elevated concentration of enlarged plasma HDL in PCPE2-deficient mice to determine whether they protected against diet-induced atherosclerosis. PCPE2-deficient mice were crossed with LDL receptor-deficient mice to obtain LDLr−/−, PCPE2−/− mice, which had elevated HDL levels compared with LDLr−/− mice with similar LDL concentrations. We found that LDLr−/−, PCPE2−/− mice had significantly more neutral lipid and CD68+ infiltration in the aortic root than LDLr−/− mice. Surprisingly, in light of their elevated HDL levels, the extent of aortic lipid deposition in LDLr−/−, PCPE2−/− mice was similar to that reported for LDLr−/−, apoA-I−/− mice, which lack any apoA-I/HDL. Furthermore, LDLr−/−, PCPE2−/− mice had reduced HDL apoA-I fractional clearance and macrophage to fecal reverse cholesterol transport rates compared with LDLr−/− mice, despite a 2-fold increase in liver SR-BI expression. PCPE2 was shown to enhance SR-BI function by increasing the rate of HDL-associated cholesteryl ester uptake, possibly by optimizing SR-BI localization and/or conformation. We conclude that PCPE2 is atheroprotective and an important component of the reverse cholesterol transport HDL system.Background:Extracellular matrix protein PCPE2 is linked to alterations in HDL size and concentration.Results:PCPE2 protects against diet-induced atherosclerosis by promoting HDL catabolism, reverse cholesterol transport, and SR-BI-mediated uptake of HDL-cholesteryl ester.Conclusion:PCPE2 mediates HDL function by reducing lipid and immune cell accumulation in the artery.Significance:These findings establish a role for the extracellular matrix glycoprotein PCPE2 in SR-BI-mediated HDL function and the prevention of atherosclerosis. Studies in human populations have shown a significant correlation between procollagen C-endopeptidase enhancer protein 2 (PCPE2) single nucleotide polymorphisms and plasma HDL cholesterol concentrations. PCPE2, a 52-kDa glycoprotein located in the extracellular matrix, enhances the cleavage of C-terminal procollagen by bone morphogenetic protein 1 (BMP1). Our studies here focused on investigating the basis for the elevated concentration of enlarged plasma HDL in PCPE2-deficient mice to determine whether they protected against diet-induced atherosclerosis. PCPE2-deficient mice were crossed with LDL receptor-deficient mice to obtain LDLr−/−, PCPE2−/− mice, which had elevated HDL levels compared with LDLr−/− mice with similar LDL concentrations. We found that LDLr−/−, PCPE2−/− mice had significantly more neutral lipid and CD68+ infiltration in the aortic root than LDLr−/− mice. Surprisingly, in light of their elevated HDL levels, the extent of aortic lipid deposition in LDLr−/−, PCPE2−/− mice was similar to that reported for LDLr−/−, apoA-I−/− mice, which lack any apoA-I/HDL. Furthermore, LDLr−/−, PCPE2−/− mice had reduced HDL apoA-I fractional clearance and macrophage to fecal reverse cholesterol transport rates compared with LDLr−/− mice, despite a 2-fold increase in liver SR-BI expression. PCPE2 was shown to enhance SR-BI function by increasing the rate of HDL-associated cholesteryl ester uptake, possibly by optimizing SR-BI localization and/or conformation. We conclude that PCPE2 is atheroprotective and an important component of the reverse cholesterol transport HDL system. Extracellular matrix protein PCPE2 is linked to alterations in HDL size and concentration. PCPE2 protects against diet-induced atherosclerosis by promoting HDL catabolism, reverse cholesterol transport, and SR-BI-mediated uptake of HDL-cholesteryl ester. PCPE2 mediates HDL function by reducing lipid and immune cell accumulation in the artery." @default.
• W657304069 created "2016-06-24" @default.
• W657304069 creator A5005935544 @default.
• W657304069 creator A5009724431 @default.
• W657304069 creator A5012217431 @default.
• W657304069 creator A5042284627 @default.
• W657304069 creator A5047166527 @default.
• W657304069 creator A5051180703 @default.
• W657304069 creator A5058164261 @default.
• W657304069 creator A5059518260 @default.
• W657304069 creator A5059884166 @default.
• W657304069 creator A5065306258 @default.
• W657304069 creator A5069677443 @default.
• W657304069 creator A5072376448 @default.
• W657304069 creator A5084285774 @default.
• W657304069 date "2015-06-01" @default.
• W657304069 modified "2023-10-15" @default.
• W657304069 title "Procollagen C-endopeptidase Enhancer Protein 2 (PCPE2) Reduces Atherosclerosis in Mice by Enhancing Scavenger Receptor Class B1 (SR-BI)-mediated High-density Lipoprotein (HDL)-Cholesteryl Ester Uptake" @default.
• W657304069 cites W1523684025 @default.
• W657304069 cites W1775749144 @default.
• W657304069 cites W1964734943 @default.
• W657304069 cites W1964786421 @default.
• W657304069 cites W1971338943 @default.
• W657304069 cites W1973858093 @default.
• W657304069 cites W1974784535 @default.
• W657304069 cites W1974864595 @default.
• W657304069 cites W1981535135 @default.
• W657304069 cites W1981798265 @default.
• W657304069 cites W1986524045 @default.
• W657304069 cites W1989249306 @default.
• W657304069 cites W1991504286 @default.
• W657304069 cites W1991879363 @default.
• W657304069 cites W1993730942 @default.
• W657304069 cites W1994456824 @default.
• W657304069 cites W1996895583 @default.
• W657304069 cites W2000703690 @default.
• W657304069 cites W2001614649 @default.
• W657304069 cites W2006155006 @default.
• W657304069 cites W2007211958 @default.
• W657304069 cites W2009979715 @default.
• W657304069 cites W2019797368 @default.
• W657304069 cites W2022619537 @default.
• W657304069 cites W2025155898 @default.
• W657304069 cites W2027927035 @default.
• W657304069 cites W2028858008 @default.
• W657304069 cites W2030380897 @default.
• W657304069 cites W2032274963 @default.
• W657304069 cites W2035996489 @default.
• W657304069 cites W2041966195 @default.
• W657304069 cites W2050966312 @default.
• W657304069 cites W2055502077 @default.
• W657304069 cites W2055661201 @default.
• W657304069 cites W2055823448 @default.
• W657304069 cites W2056887926 @default.
• W657304069 cites W2057470641 @default.
• W657304069 cites W2061613731 @default.
• W657304069 cites W2062160450 @default.
• W657304069 cites W2063755332 @default.
• W657304069 cites W2067064472 @default.
• W657304069 cites W2070060517 @default.
• W657304069 cites W2072470057 @default.
• W657304069 cites W2074358822 @default.
• W657304069 cites W2076947779 @default.
• W657304069 cites W2077723075 @default.
• W657304069 cites W2079330956 @default.
• W657304069 cites W2082781916 @default.
• W657304069 cites W2083281877 @default.
• W657304069 cites W2085649019 @default.
• W657304069 cites W2086014282 @default.
• W657304069 cites W2087250632 @default.
• W657304069 cites W2088800437 @default.
• W657304069 cites W2093099491 @default.
• W657304069 cites W2093395445 @default.
• W657304069 cites W2096772522 @default.
• W657304069 cites W2098296263 @default.
• W657304069 cites W2104130684 @default.
• W657304069 cites W2107001681 @default.
• W657304069 cites W2108563210 @default.
• W657304069 cites W2109251589 @default.
• W657304069 cites W2109429564 @default.
• W657304069 cites W2114343361 @default.
• W657304069 cites W2117349394 @default.
• W657304069 cites W2117622925 @default.
• W657304069 cites W2121244624 @default.
• W657304069 cites W2124091270 @default.
• W657304069 cites W2132017466 @default.
• W657304069 cites W2134027848 @default.
• W657304069 cites W2135806933 @default.
• W657304069 cites W2135888652 @default.
• W657304069 cites W2136468897 @default.
• W657304069 cites W2139787160 @default.
• W657304069 cites W2149718877 @default.
• W657304069 cites W2155406689 @default.
• W657304069 cites W2158174974 @default.
• W657304069 cites W2160979649 @default.
• W657304069 cites W2161649596 @default.
• W657304069 cites W2161925559 @default.
• W657304069 cites W2163320658 @default.

• next