FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2067602009> ?p ?o ?g. }

• W2067602009 endingPage "341" @default.
• W2067602009 startingPage "332" @default.
• W2067602009 abstract "ObjectiveThe ABCA2 transporter shares high structural homology to ABCA1, which is crucial for the removal of excess cholesterol from macrophages and, by extension, in atherosclerosis. It has been suggested that ABCA2 sequesters cholesterol inside the lysosomes, however, little is known of the macrophage-specific role of ABCA2 in regulating lipid homeostasis in vivo and in modulating susceptibility to atherosclerosis.MethodsChimeras with dysfunctional macrophage ABCA2 were generated by transplantation of bone marrow from ABCA2 knockout (KO) mice into irradiated LDL receptor (LDLr) KO mice.ResultsInterestingly, lack of ABCA2 in macrophages resulted in a diminished lesion size in the aortic root (−24.5%) and descending thoracic aorta (−36.6%) associated with a 3-fold increase in apoptotic cells, as measured by both caspase 3 and TUNEL. Upon oxidized LDL exposure, macrophages from wildtype (WT) transplanted animals developed filipin-positive droplets in lysosomal-like compartments, corresponding to free cholesterol (FC) accumulation. In contrast, ABCA2-deficient macrophages displayed an abnormal diffuse distribution of FC over peripheral regions. The accumulation of neutral sterols in lipid droplets was increased in ABCA2-deficient macrophages, but primarily in cytoplasmic clusters and not in lysosomes. Importantly, apoptosis of oxLDL loaded macrophages lacking ABCA2 was increased 2.7-fold, probably as a consequence of the broad cellular distribution of FC.ConclusionsLack of functional ABCA2 generates abnormalities in intracellular lipid distribution/trafficking in macrophages consistent with its lysosomal sequestering role, leading to an increased susceptibility to apoptosis in response to oxidized lipids and reduced atherosclerotic lesion development." @default.
• W2067602009 created "2016-06-24" @default.
• W2067602009 creator A5000848861 @default.
• W2067602009 creator A5002460140 @default.
• W2067602009 creator A5007621291 @default.
• W2067602009 creator A5011849370 @default.
• W2067602009 creator A5024327405 @default.
• W2067602009 creator A5024733637 @default.
• W2067602009 creator A5040422403 @default.
• W2067602009 creator A5048849311 @default.
• W2067602009 creator A5054806342 @default.
• W2067602009 creator A5057079657 @default.
• W2067602009 creator A5066244900 @default.
• W2067602009 creator A5068656271 @default.
• W2067602009 creator A5069864602 @default.
• W2067602009 creator A5091661590 @default.
• W2067602009 date "2012-08-01" @default.
• W2067602009 modified "2023-10-02" @default.
• W2067602009 title "Macrophage ABCA2 deletion modulates intracellular cholesterol deposition, affects macrophage apoptosis, and decreases early atherosclerosis in LDL receptor knockout mice" @default.
• W2067602009 cites W1551340735 @default.
• W2067602009 cites W1908587496 @default.
• W2067602009 cites W1967502002 @default.
• W2067602009 cites W1973363980 @default.
• W2067602009 cites W1986439388 @default.
• W2067602009 cites W2013465063 @default.
• W2067602009 cites W2021437904 @default.
• W2067602009 cites W2023345325 @default.
• W2067602009 cites W2031205796 @default.
• W2067602009 cites W2033909730 @default.
• W2067602009 cites W2034109847 @default.
• W2067602009 cites W2038446516 @default.
• W2067602009 cites W2045518664 @default.
• W2067602009 cites W2048561509 @default.
• W2067602009 cites W2051844149 @default.
• W2067602009 cites W2056452930 @default.
• W2067602009 cites W2057330104 @default.
• W2067602009 cites W2058555221 @default.
• W2067602009 cites W2069540409 @default.
• W2067602009 cites W2071006116 @default.
• W2067602009 cites W2072568946 @default.
• W2067602009 cites W2076546793 @default.
• W2067602009 cites W2085764346 @default.
• W2067602009 cites W2098562504 @default.
• W2067602009 cites W2103714932 @default.
• W2067602009 cites W2105761603 @default.
• W2067602009 cites W2108572753 @default.
• W2067602009 cites W2111528756 @default.
• W2067602009 cites W2115457290 @default.
• W2067602009 cites W2116409647 @default.
• W2067602009 cites W2124980568 @default.
• W2067602009 cites W2125448572 @default.
• W2067602009 cites W2128738849 @default.
• W2067602009 cites W2140187466 @default.
• W2067602009 cites W2146791011 @default.
• W2067602009 cites W2147865480 @default.
• W2067602009 cites W2158531928 @default.
• W2067602009 cites W2160123988 @default.
• W2067602009 cites W2187715873 @default.
• W2067602009 cites W4241939777 @default.
• W2067602009 cites W4249417358 @default.
• W2067602009 cites W4253702721 @default.
• W2067602009 cites W4256475235 @default.
• W2067602009 doi "https://doi.org/10.1016/j.atherosclerosis.2012.05.039" @default.
• W2067602009 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22748276" @default.
• W2067602009 hasPublicationYear "2012" @default.
• W2067602009 type Work @default.
• W2067602009 sameAs 2067602009 @default.
• W2067602009 citedByCount "14" @default.
• W2067602009 countsByYear W20676020092014 @default.
• W2067602009 countsByYear W20676020092015 @default.
• W2067602009 countsByYear W20676020092016 @default.
• W2067602009 countsByYear W20676020092018 @default.
• W2067602009 countsByYear W20676020092021 @default.
• W2067602009 countsByYear W20676020092022 @default.
• W2067602009 countsByYear W20676020092023 @default.
• W2067602009 crossrefType "journal-article" @default.
• W2067602009 hasAuthorship W2067602009A5000848861 @default.
• W2067602009 hasAuthorship W2067602009A5002460140 @default.
• W2067602009 hasAuthorship W2067602009A5007621291 @default.
• W2067602009 hasAuthorship W2067602009A5011849370 @default.
• W2067602009 hasAuthorship W2067602009A5024327405 @default.
• W2067602009 hasAuthorship W2067602009A5024733637 @default.
• W2067602009 hasAuthorship W2067602009A5040422403 @default.
• W2067602009 hasAuthorship W2067602009A5048849311 @default.
• W2067602009 hasAuthorship W2067602009A5054806342 @default.
• W2067602009 hasAuthorship W2067602009A5057079657 @default.
• W2067602009 hasAuthorship W2067602009A5066244900 @default.
• W2067602009 hasAuthorship W2067602009A5068656271 @default.
• W2067602009 hasAuthorship W2067602009A5069864602 @default.
• W2067602009 hasAuthorship W2067602009A5091661590 @default.
• W2067602009 hasBestOaLocation W20676020091 @default.
• W2067602009 hasConcept C134018914 @default.
• W2067602009 hasConcept C185592680 @default.
• W2067602009 hasConcept C190283241 @default.
• W2067602009 hasConcept C202751555 @default.
• W2067602009 hasConcept C2777895019 @default.
• W2067602009 hasConcept C2778163477 @default.
• W2067602009 hasConcept C2779244956 @default.

• next