Matches in SemOpenAlex for { <https://semopenalex.org/work/W4310758480> ?p ?o ?g. }
- W4310758480 endingPage "102574" @default.
- W4310758480 startingPage "102574" @default.
- W4310758480 abstract "Mice with ectopic expression of uncoupling protein-1 (UCP1) in skeletal muscle exhibit a healthy aging phenotype with increased longevity and resistance to impaired metabolic health. This may be achieved by decreasing protein glycation by the reactive metabolite, methylglyoxal (MG). We investigated protein glycation and oxidative damage in skeletal muscle of mice with UCP1 expression under control of the human skeletal actin promoter (HSA-mUCP1) at age 12 weeks (young) and 70 weeks (aged). We found both young and aged HSA-mUCP1 mice had decreased advanced glycation endproducts (AGEs) formed from MG, lysine-derived Nε(1-carboxyethyl)lysine (CEL) and arginine-derived hydroimidazolone, MG-H1, whereas protein glycation by glucose forming Nε-fructosyl-lysine (FL) was increased ca. 2-fold, compared to wildtype controls. There were related increases in FL-linked AGEs, Nε-carboxymethyl-lysine (CML) and 3-deoxylglucosone-derived hydroimidazolone 3DG-H, and minor changes in protein oxidative and nitration adducts. In aged HSA-mUCP1 mice, urinary MG-derived AGEs/FL ratio was decreased ca. 60% whereas there was no change in CML/FL ratio – a marker of oxidative damage. This suggests that, normalized for glycemic status, aged HSA-mUCP1 mice had a lower flux of whole body MG-derived AGE exposure compared to wildtype controls. Proteomics analysis of skeletal muscle revealed a shift to increased heat shock proteins and mechanoprotection and repair in HSA-mUCP1 mice. Decreased MG-derived AGE protein content in skeletal muscle of aged HSA-mUCP1 mice is therefore likely produced by increased proteolysis of MG-modified proteins and increased proteostasis surveillance of the skeletal muscle proteome. From this and previous transcriptomic studies, signaling involved in enhanced removal of MG-modified protein is likely increased HSPB1-directed HUWE1 ubiquitination through eIF2α-mediated, ATF5-induced increased expression of HSPB1. Decreased whole body exposure to MG-derived AGEs may be linked to increased weight specific physical activity of HSA-mUCP1 mice. Decreased formation and increased clearance of MG-derived AGEs may be associated with healthy aging in the HSA-mUCP1 mouse." @default.
- W4310758480 created "2022-12-17" @default.
- W4310758480 creator A5001547362 @default.
- W4310758480 creator A5021086938 @default.
- W4310758480 creator A5033433056 @default.
- W4310758480 creator A5034847939 @default.
- W4310758480 creator A5041180154 @default.
- W4310758480 creator A5049806586 @default.
- W4310758480 creator A5056708838 @default.
- W4310758480 date "2023-02-01" @default.
- W4310758480 modified "2023-10-14" @default.
- W4310758480 title "Decreased methylglyoxal-mediated protein glycation in the healthy aging mouse model of ectopic expression of UCP1 in skeletal muscle" @default.
- W4310758480 cites W1557253076 @default.
- W4310758480 cites W1609735481 @default.
- W4310758480 cites W1896619220 @default.
- W4310758480 cites W1898238965 @default.
- W4310758480 cites W1945607742 @default.
- W4310758480 cites W1964343416 @default.
- W4310758480 cites W1966012405 @default.
- W4310758480 cites W1968852002 @default.
- W4310758480 cites W1969653601 @default.
- W4310758480 cites W1970789531 @default.
- W4310758480 cites W1980536586 @default.
- W4310758480 cites W1983802110 @default.
- W4310758480 cites W1990591037 @default.
- W4310758480 cites W1994051814 @default.
- W4310758480 cites W2003648592 @default.
- W4310758480 cites W2006088447 @default.
- W4310758480 cites W2006297498 @default.
- W4310758480 cites W2006370393 @default.
- W4310758480 cites W2011064041 @default.
- W4310758480 cites W2011127981 @default.
- W4310758480 cites W2015556811 @default.
- W4310758480 cites W2015978398 @default.
- W4310758480 cites W2016949969 @default.
- W4310758480 cites W2018999183 @default.
- W4310758480 cites W2027974246 @default.
- W4310758480 cites W2031664391 @default.
- W4310758480 cites W2042363298 @default.
- W4310758480 cites W2045372182 @default.
- W4310758480 cites W2050748849 @default.
- W4310758480 cites W2060099568 @default.
- W4310758480 cites W2076944010 @default.
- W4310758480 cites W2076972400 @default.
- W4310758480 cites W2085250950 @default.
- W4310758480 cites W2087004359 @default.
- W4310758480 cites W2087543260 @default.
- W4310758480 cites W2107524932 @default.
- W4310758480 cites W2121491699 @default.
- W4310758480 cites W2121926883 @default.
- W4310758480 cites W2122612452 @default.
- W4310758480 cites W2125445685 @default.
- W4310758480 cites W2152366277 @default.
- W4310758480 cites W2155200626 @default.
- W4310758480 cites W2157796703 @default.
- W4310758480 cites W2157906022 @default.
- W4310758480 cites W2159416200 @default.
- W4310758480 cites W2169091672 @default.
- W4310758480 cites W2292256860 @default.
- W4310758480 cites W2391680777 @default.
- W4310758480 cites W2470810595 @default.
- W4310758480 cites W2513956585 @default.
- W4310758480 cites W2517358938 @default.
- W4310758480 cites W2734855412 @default.
- W4310758480 cites W2770372563 @default.
- W4310758480 cites W2784651532 @default.
- W4310758480 cites W2788820942 @default.
- W4310758480 cites W2938574745 @default.
- W4310758480 cites W2939723348 @default.
- W4310758480 cites W2944896292 @default.
- W4310758480 cites W2973932371 @default.
- W4310758480 cites W2989775132 @default.
- W4310758480 cites W2990526525 @default.
- W4310758480 cites W2990682862 @default.
- W4310758480 cites W3005109272 @default.
- W4310758480 cites W3007804840 @default.
- W4310758480 cites W3033596777 @default.
- W4310758480 cites W3095820202 @default.
- W4310758480 cites W3133695632 @default.
- W4310758480 cites W3134482301 @default.
- W4310758480 cites W3155251650 @default.
- W4310758480 cites W4206296686 @default.
- W4310758480 cites W4212966267 @default.
- W4310758480 cites W4294827450 @default.
- W4310758480 doi "https://doi.org/10.1016/j.redox.2022.102574" @default.
- W4310758480 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36521306" @default.
- W4310758480 hasPublicationYear "2023" @default.
- W4310758480 type Work @default.
- W4310758480 citedByCount "0" @default.
- W4310758480 crossrefType "journal-article" @default.
- W4310758480 hasAuthorship W4310758480A5001547362 @default.
- W4310758480 hasAuthorship W4310758480A5021086938 @default.
- W4310758480 hasAuthorship W4310758480A5033433056 @default.
- W4310758480 hasAuthorship W4310758480A5034847939 @default.
- W4310758480 hasAuthorship W4310758480A5041180154 @default.
- W4310758480 hasAuthorship W4310758480A5049806586 @default.
- W4310758480 hasAuthorship W4310758480A5056708838 @default.
- W4310758480 hasBestOaLocation W43107584801 @default.