FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2285680055> ?p ?o ?g. }

• W2285680055 endingPage "30529" @default.
• W2285680055 startingPage "30514" @default.
• W2285680055 abstract "Our laboratory previously reported that lecithin:cholesterol acyltransferase (LCAT) and LDL receptor double knock-out mice (Ldlr−/−xLcat−/− or DKO) spontaneously develop functioning ectopic brown adipose tissue (BAT) in skeletal muscle, putatively contributing to protection from the diet-induced obesity phenotype. Here we further investigated their developmental origin and the mechanistic role of LCAT deficiency. Gene profiling of skeletal muscle in DKO newborns and adults revealed a classical lineage. Primary quiescent satellite cells (SC) from chow-fed DKO mice, not in Ldlr−/−xLcat+/+ single-knock-out (SKO) or C57BL/6 wild type, were found to (i) express exclusively classical BAT-selective genes, (ii) be primed to express key functional BAT genes, and (iii) exhibit markedly increased ex vivo adipogenic differentiation into brown adipocytes. This gene priming effect was abrogated upon feeding the mice a 2% high cholesterol diet in association with accumulation of excess intracellular cholesterol. Ex vivo cholesterol loading of chow-fed DKO SC recapitulated the effect, indicating that cellular cholesterol is a key regulator of SC-to-BAT differentiation. Comparing adipogenicity of Ldlr+/+xLcat−/− (LCAT-KO) SC with DKO SC identified a role for LCAT deficiency in priming SC to express BAT genes. Additionally, we found that reduced cellular cholesterol is important for adipogenic differentiation, evidenced by increased induction of adipogenesis in cholesterol-depleted SC from both LCAT-KO and SKO mice. Taken together, we conclude that ectopic BAT in DKO mice is classical in origin, and its development begins in utero. We further showed complementary roles of LCAT deficiency and cellular cholesterol reduction in the SC-to-BAT adipogenesis. Our laboratory previously reported that lecithin:cholesterol acyltransferase (LCAT) and LDL receptor double knock-out mice (Ldlr−/−xLcat−/− or DKO) spontaneously develop functioning ectopic brown adipose tissue (BAT) in skeletal muscle, putatively contributing to protection from the diet-induced obesity phenotype. Here we further investigated their developmental origin and the mechanistic role of LCAT deficiency. Gene profiling of skeletal muscle in DKO newborns and adults revealed a classical lineage. Primary quiescent satellite cells (SC) from chow-fed DKO mice, not in Ldlr−/−xLcat+/+ single-knock-out (SKO) or C57BL/6 wild type, were found to (i) express exclusively classical BAT-selective genes, (ii) be primed to express key functional BAT genes, and (iii) exhibit markedly increased ex vivo adipogenic differentiation into brown adipocytes. This gene priming effect was abrogated upon feeding the mice a 2% high cholesterol diet in association with accumulation of excess intracellular cholesterol. Ex vivo cholesterol loading of chow-fed DKO SC recapitulated the effect, indicating that cellular cholesterol is a key regulator of SC-to-BAT differentiation. Comparing adipogenicity of Ldlr+/+xLcat−/− (LCAT-KO) SC with DKO SC identified a role for LCAT deficiency in priming SC to express BAT genes. Additionally, we found that reduced cellular cholesterol is important for adipogenic differentiation, evidenced by increased induction of adipogenesis in cholesterol-depleted SC from both LCAT-KO and SKO mice. Taken together, we conclude that ectopic BAT in DKO mice is classical in origin, and its development begins in utero. We further showed complementary roles of LCAT deficiency and cellular cholesterol reduction in the SC-to-BAT adipogenesis." @default.
• W2285680055 created "2016-06-24" @default.
• W2285680055 creator A5011857697 @default.
• W2285680055 creator A5011878659 @default.
• W2285680055 creator A5052502393 @default.
• W2285680055 creator A5055903100 @default.
• W2285680055 creator A5059130197 @default.
• W2285680055 creator A5086990168 @default.
• W2285680055 date "2015-12-01" @default.
• W2285680055 modified "2023-10-14" @default.
• W2285680055 title "Lecithin:Cholesterol Acyltransferase (LCAT) Deficiency Promotes Differentiation of Satellite Cells to Brown Adipocytes in a Cholesterol-dependent Manner" @default.
• W2285680055 cites W1528481598 @default.
• W2285680055 cites W1897745151 @default.
• W2285680055 cites W1965079305 @default.
• W2285680055 cites W1965754770 @default.
• W2285680055 cites W1966909881 @default.
• W2285680055 cites W1968200496 @default.
• W2285680055 cites W1970702544 @default.
• W2285680055 cites W1987229312 @default.
• W2285680055 cites W1992256913 @default.
• W2285680055 cites W1995253518 @default.
• W2285680055 cites W1996951495 @default.
• W2285680055 cites W2004803010 @default.
• W2285680055 cites W2005827500 @default.
• W2285680055 cites W2008301678 @default.
• W2285680055 cites W2013993866 @default.
• W2285680055 cites W2018124948 @default.
• W2285680055 cites W2023319900 @default.
• W2285680055 cites W2027753197 @default.
• W2285680055 cites W2039631030 @default.
• W2285680055 cites W2040328785 @default.
• W2285680055 cites W2047923192 @default.
• W2285680055 cites W2084581265 @default.
• W2285680055 cites W2084610235 @default.
• W2285680055 cites W2089053092 @default.
• W2285680055 cites W2089636232 @default.
• W2285680055 cites W2090891124 @default.
• W2285680055 cites W2104286517 @default.
• W2285680055 cites W2104827888 @default.
• W2285680055 cites W2107277218 @default.
• W2285680055 cites W2125996889 @default.
• W2285680055 cites W2143392718 @default.
• W2285680055 cites W2151064573 @default.
• W2285680055 cites W2159836929 @default.
• W2285680055 cites W2161615797 @default.
• W2285680055 cites W2170414800 @default.
• W2285680055 cites W2170874580 @default.
• W2285680055 doi "https://doi.org/10.1074/jbc.m115.676056" @default.
• W2285680055 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4683272" @default.
• W2285680055 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26494623" @default.
• W2285680055 hasPublicationYear "2015" @default.
• W2285680055 type Work @default.
• W2285680055 sameAs 2285680055 @default.
• W2285680055 citedByCount "6" @default.
• W2285680055 countsByYear W22856800552017 @default.
• W2285680055 countsByYear W22856800552018 @default.
• W2285680055 countsByYear W22856800552020 @default.
• W2285680055 countsByYear W22856800552023 @default.
• W2285680055 crossrefType "journal-article" @default.
• W2285680055 hasAuthorship W2285680055A5011857697 @default.
• W2285680055 hasAuthorship W2285680055A5011878659 @default.
• W2285680055 hasAuthorship W2285680055A5052502393 @default.
• W2285680055 hasAuthorship W2285680055A5055903100 @default.
• W2285680055 hasAuthorship W2285680055A5059130197 @default.
• W2285680055 hasAuthorship W2285680055A5086990168 @default.
• W2285680055 hasBestOaLocation W22856800551 @default.
• W2285680055 hasConcept C122927707 @default.
• W2285680055 hasConcept C126322002 @default.
• W2285680055 hasConcept C134018914 @default.
• W2285680055 hasConcept C171089720 @default.
• W2285680055 hasConcept C2778163477 @default.
• W2285680055 hasConcept C2780072125 @default.
• W2285680055 hasConcept C37002583 @default.
• W2285680055 hasConcept C43554185 @default.
• W2285680055 hasConcept C71924100 @default.
• W2285680055 hasConcept C86803240 @default.
• W2285680055 hasConceptScore W2285680055C122927707 @default.
• W2285680055 hasConceptScore W2285680055C126322002 @default.
• W2285680055 hasConceptScore W2285680055C134018914 @default.
• W2285680055 hasConceptScore W2285680055C171089720 @default.
• W2285680055 hasConceptScore W2285680055C2778163477 @default.
• W2285680055 hasConceptScore W2285680055C2780072125 @default.
• W2285680055 hasConceptScore W2285680055C37002583 @default.
• W2285680055 hasConceptScore W2285680055C43554185 @default.
• W2285680055 hasConceptScore W2285680055C71924100 @default.
• W2285680055 hasConceptScore W2285680055C86803240 @default.
• W2285680055 hasFunder F4320334506 @default.
• W2285680055 hasFunder F4320334604 @default.
• W2285680055 hasIssue "51" @default.
• W2285680055 hasLocation W22856800551 @default.
• W2285680055 hasLocation W22856800552 @default.
• W2285680055 hasLocation W22856800553 @default.
• W2285680055 hasOpenAccess W2285680055 @default.
• W2285680055 hasPrimaryLocation W22856800551 @default.
• W2285680055 hasRelatedWork W1575445194 @default.
• W2285680055 hasRelatedWork W1968960503 @default.
• W2285680055 hasRelatedWork W1976538330 @default.
• W2285680055 hasRelatedWork W1991751801 @default.

• next