Matches in SemOpenAlex for { <https://semopenalex.org/work/W2792597790> ?p ?o ?g. }
- W2792597790 endingPage "1470" @default.
- W2792597790 startingPage "1458" @default.
- W2792597790 abstract "Obesity is related to a dynamic extracellular matrix (ECM) remodeling, which involves the synthesis and degradation of different proteins, such as tenascin C (TNC) in the adipose tissue (AT). Given the functional relationship between leptin and inducible nitric oxide synthase (iNOS), our aim was to analyze the impact of the absence of the iNOS gene in AT inflammation and ECM remodeling in ob/ob mice. The expression of genes involved in inflammation and ECM remodeling was evaluated in 10-week-old male double knockout (DBKO) mice simultaneously lacking the ob and iNOS genes as well as in ob/ob mice classified into three groups [control, leptin-treated (1 mg kg−1 day−1) and pair-fed]. Leptin deficiency increased inflammation and fibrosis in AT. As expected, leptin treatment improved the obesity phenotype. iNOS deficiency in ob/ob mice improved insulin sensitivity, AT inflammation, and ECM remodeling, as evidenced by lower AT macrophage infiltration and collagen deposition, a downregulation of proinflammatory and profibrogenic genes Tnf, Emr1, Hif1a, Col6a1, Col6a3, and Tnc, as well as lower circulating TNC levels. Interestingly, leptin upregulated TNC expression and release in 3T3-L1 adipocytes, and iNOS knockdown in 3T3-L1 fat cells produced a significant decrease in basal and leptin-induced Tnc expression. Ablation of iNOS in leptin-deficient mice improved AT inflammation and ECM remodeling-related genes, attenuating fibrosis, and metabolic dysfunction. The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in adipocytes, suggesting an important role of this alarmin in the development of AT inflammation and fibrosis." @default.
- W2792597790 created "2018-03-29" @default.
- W2792597790 creator A5007732990 @default.
- W2792597790 creator A5016527523 @default.
- W2792597790 creator A5017864481 @default.
- W2792597790 creator A5027542066 @default.
- W2792597790 creator A5036389069 @default.
- W2792597790 creator A5050769816 @default.
- W2792597790 creator A5053231875 @default.
- W2792597790 creator A5060583904 @default.
- W2792597790 creator A5062747317 @default.
- W2792597790 creator A5067550012 @default.
- W2792597790 date "2018-02-15" @default.
- W2792597790 modified "2023-10-12" @default.
- W2792597790 title "Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C" @default.
- W2792597790 cites W1494780959 @default.
- W2792597790 cites W1502163633 @default.
- W2792597790 cites W1591600393 @default.
- W2792597790 cites W1675699936 @default.
- W2792597790 cites W1941545295 @default.
- W2792597790 cites W1967895142 @default.
- W2792597790 cites W1969409088 @default.
- W2792597790 cites W1987287108 @default.
- W2792597790 cites W1991374761 @default.
- W2792597790 cites W1993203791 @default.
- W2792597790 cites W1994809630 @default.
- W2792597790 cites W1996713062 @default.
- W2792597790 cites W1997196734 @default.
- W2792597790 cites W2002233417 @default.
- W2792597790 cites W2006433855 @default.
- W2792597790 cites W2010199313 @default.
- W2792597790 cites W2016662511 @default.
- W2792597790 cites W2021226385 @default.
- W2792597790 cites W2026497980 @default.
- W2792597790 cites W2044797498 @default.
- W2792597790 cites W2047442471 @default.
- W2792597790 cites W2049907045 @default.
- W2792597790 cites W2058314494 @default.
- W2792597790 cites W2059857175 @default.
- W2792597790 cites W2059946157 @default.
- W2792597790 cites W2061686058 @default.
- W2792597790 cites W2061873998 @default.
- W2792597790 cites W2062015016 @default.
- W2792597790 cites W2066528365 @default.
- W2792597790 cites W2068182431 @default.
- W2792597790 cites W2069237083 @default.
- W2792597790 cites W2072583314 @default.
- W2792597790 cites W2072747772 @default.
- W2792597790 cites W2072964420 @default.
- W2792597790 cites W2078575306 @default.
- W2792597790 cites W2084432666 @default.
- W2792597790 cites W2084802447 @default.
- W2792597790 cites W2090964555 @default.
- W2792597790 cites W2092721283 @default.
- W2792597790 cites W2093871599 @default.
- W2792597790 cites W2096015727 @default.
- W2792597790 cites W2101328621 @default.
- W2792597790 cites W2122486961 @default.
- W2792597790 cites W2123160276 @default.
- W2792597790 cites W2123333009 @default.
- W2792597790 cites W2124821727 @default.
- W2792597790 cites W2125500908 @default.
- W2792597790 cites W2126751653 @default.
- W2792597790 cites W2127865222 @default.
- W2792597790 cites W2129088717 @default.
- W2792597790 cites W2129316761 @default.
- W2792597790 cites W2138266804 @default.
- W2792597790 cites W2142431039 @default.
- W2792597790 cites W2145323170 @default.
- W2792597790 cites W2145697808 @default.
- W2792597790 cites W2149332882 @default.
- W2792597790 cites W2149512987 @default.
- W2792597790 cites W2155939449 @default.
- W2792597790 cites W2162397977 @default.
- W2792597790 cites W2163655812 @default.
- W2792597790 cites W2163691580 @default.
- W2792597790 cites W2254355725 @default.
- W2792597790 cites W2399693675 @default.
- W2792597790 cites W2408958960 @default.
- W2792597790 cites W2411779324 @default.
- W2792597790 cites W2571984714 @default.
- W2792597790 cites W2591981899 @default.
- W2792597790 cites W4205370185 @default.
- W2792597790 cites W4249727000 @default.
- W2792597790 doi "https://doi.org/10.1038/s41366-018-0005-5" @default.
- W2792597790 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29449623" @default.
- W2792597790 hasPublicationYear "2018" @default.
- W2792597790 type Work @default.
- W2792597790 sameAs 2792597790 @default.
- W2792597790 citedByCount "37" @default.
- W2792597790 countsByYear W27925977902018 @default.
- W2792597790 countsByYear W27925977902019 @default.
- W2792597790 countsByYear W27925977902020 @default.
- W2792597790 countsByYear W27925977902021 @default.
- W2792597790 countsByYear W27925977902022 @default.
- W2792597790 countsByYear W27925977902023 @default.
- W2792597790 crossrefType "journal-article" @default.
- W2792597790 hasAuthorship W2792597790A5007732990 @default.