FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2889425610> ?p ?o ?g. }

• W2889425610 endingPage "143" @default.
• W2889425610 startingPage "133" @default.
• W2889425610 abstract "Adult mammalian hearts have a very limited regeneration capacity, due largely to a lack of cardiomyocyte (CM) proliferation. It was recently reported that epicardial, but not myocardial, follistatin-like 1 (Fstl1) activates CM proliferation and cardiac regeneration after myocardial infarction (MI). Furthermore, bacterially synthesized human FSTL 1 (hFSTL1) was found to induce CM proliferation, whereas hFSTL1 synthesized in mammals did not, suggesting that post-translational modifications (e.g., glycosylation) of the hFSTL1 protein affect its regenerative activity. We used modified mRNA (modRNA) technology to investigate the possible role of specific hFSTL1 N-glycosylation sites in the induction, by hFSTL1, of CM proliferation and cardiac regeneration. We found that the mutation of a single site (N180Q) was sufficient and necessary to increase the proliferation of rat neonatal and mouse adult CMs in vitro and after MI in vivo, respectively. A single administration of the modRNA construct encoding the N180Q mutant significantly increased cardiac function, decreased scar size, and increased capillary density 28 days post-MI. Overall, our data suggest that the delivery of N180Q hFSTL1 modRNA to the myocardium can mimic the beneficial effect of epicardial hFSTL1, triggering marked CM proliferation and cardiac regeneration in a mouse MI model. Adult mammalian hearts have a very limited regeneration capacity, due largely to a lack of cardiomyocyte (CM) proliferation. It was recently reported that epicardial, but not myocardial, follistatin-like 1 (Fstl1) activates CM proliferation and cardiac regeneration after myocardial infarction (MI). Furthermore, bacterially synthesized human FSTL 1 (hFSTL1) was found to induce CM proliferation, whereas hFSTL1 synthesized in mammals did not, suggesting that post-translational modifications (e.g., glycosylation) of the hFSTL1 protein affect its regenerative activity. We used modified mRNA (modRNA) technology to investigate the possible role of specific hFSTL1 N-glycosylation sites in the induction, by hFSTL1, of CM proliferation and cardiac regeneration. We found that the mutation of a single site (N180Q) was sufficient and necessary to increase the proliferation of rat neonatal and mouse adult CMs in vitro and after MI in vivo, respectively. A single administration of the modRNA construct encoding the N180Q mutant significantly increased cardiac function, decreased scar size, and increased capillary density 28 days post-MI. Overall, our data suggest that the delivery of N180Q hFSTL1 modRNA to the myocardium can mimic the beneficial effect of epicardial hFSTL1, triggering marked CM proliferation and cardiac regeneration in a mouse MI model." @default.
• W2889425610 created "2018-09-07" @default.
• W2889425610 creator A5029469019 @default.
• W2889425610 creator A5047702707 @default.
• W2889425610 creator A5063114684 @default.
• W2889425610 creator A5070867215 @default.
• W2889425610 creator A5072997986 @default.
• W2889425610 creator A5075899752 @default.
• W2889425610 date "2018-12-01" @default.
• W2889425610 modified "2023-10-01" @default.
• W2889425610 title "Ablation of a Single N-Glycosylation Site in Human FSTL 1 Induces Cardiomyocyte Proliferation and Cardiac Regeneration" @default.
• W2889425610 cites W1608549100 @default.
• W2889425610 cites W1788396114 @default.
• W2889425610 cites W1917974736 @default.
• W2889425610 cites W1969038150 @default.
• W2889425610 cites W1969210272 @default.
• W2889425610 cites W1976014395 @default.
• W2889425610 cites W1987648149 @default.
• W2889425610 cites W1992798588 @default.
• W2889425610 cites W2006836569 @default.
• W2889425610 cites W2016551011 @default.
• W2889425610 cites W2023012341 @default.
• W2889425610 cites W2054604628 @default.
• W2889425610 cites W2056880006 @default.
• W2889425610 cites W2070515279 @default.
• W2889425610 cites W2071765960 @default.
• W2889425610 cites W2078215784 @default.
• W2889425610 cites W2080632755 @default.
• W2889425610 cites W2095059099 @default.
• W2889425610 cites W2098419906 @default.
• W2889425610 cites W2106058491 @default.
• W2889425610 cites W2107696376 @default.
• W2889425610 cites W2122616632 @default.
• W2889425610 cites W2123219150 @default.
• W2889425610 cites W2126617656 @default.
• W2889425610 cites W2129466238 @default.
• W2889425610 cites W2135060727 @default.
• W2889425610 cites W2136928312 @default.
• W2889425610 cites W2139689863 @default.
• W2889425610 cites W2142190754 @default.
• W2889425610 cites W2152000585 @default.
• W2889425610 cites W2157671340 @default.
• W2889425610 cites W2167150144 @default.
• W2889425610 cites W2225099229 @default.
• W2889425610 cites W2226028872 @default.
• W2889425610 cites W2326092750 @default.
• W2889425610 cites W2546877739 @default.
• W2889425610 cites W2558656073 @default.
• W2889425610 cites W2572212643 @default.
• W2889425610 cites W2602505141 @default.
• W2889425610 cites W2621046444 @default.
• W2889425610 cites W2625547916 @default.
• W2889425610 cites W2740013291 @default.
• W2889425610 cites W2748490085 @default.
• W2889425610 doi "https://doi.org/10.1016/j.omtn.2018.08.021" @default.
• W2889425610 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6171324" @default.
• W2889425610 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30290305" @default.
• W2889425610 hasPublicationYear "2018" @default.
• W2889425610 type Work @default.
• W2889425610 sameAs 2889425610 @default.
• W2889425610 citedByCount "46" @default.
• W2889425610 countsByYear W28894256102019 @default.
• W2889425610 countsByYear W28894256102020 @default.
• W2889425610 countsByYear W28894256102021 @default.
• W2889425610 countsByYear W28894256102022 @default.
• W2889425610 countsByYear W28894256102023 @default.
• W2889425610 crossrefType "journal-article" @default.
• W2889425610 hasAuthorship W2889425610A5029469019 @default.
• W2889425610 hasAuthorship W2889425610A5047702707 @default.
• W2889425610 hasAuthorship W2889425610A5063114684 @default.
• W2889425610 hasAuthorship W2889425610A5070867215 @default.
• W2889425610 hasAuthorship W2889425610A5072997986 @default.
• W2889425610 hasAuthorship W2889425610A5075899752 @default.
• W2889425610 hasBestOaLocation W28894256101 @default.
• W2889425610 hasConcept C111566952 @default.
• W2889425610 hasConcept C126322002 @default.
• W2889425610 hasConcept C171056886 @default.
• W2889425610 hasConcept C207001950 @default.
• W2889425610 hasConcept C2777313579 @default.
• W2889425610 hasConcept C2778198053 @default.
• W2889425610 hasConcept C2778831791 @default.
• W2889425610 hasConcept C500558357 @default.
• W2889425610 hasConcept C54355233 @default.
• W2889425610 hasConcept C55493867 @default.
• W2889425610 hasConcept C62112901 @default.
• W2889425610 hasConcept C71924100 @default.
• W2889425610 hasConcept C86803240 @default.
• W2889425610 hasConcept C95444343 @default.
• W2889425610 hasConceptScore W2889425610C111566952 @default.
• W2889425610 hasConceptScore W2889425610C126322002 @default.
• W2889425610 hasConceptScore W2889425610C171056886 @default.
• W2889425610 hasConceptScore W2889425610C207001950 @default.
• W2889425610 hasConceptScore W2889425610C2777313579 @default.
• W2889425610 hasConceptScore W2889425610C2778198053 @default.
• W2889425610 hasConceptScore W2889425610C2778831791 @default.
• W2889425610 hasConceptScore W2889425610C500558357 @default.
• W2889425610 hasConceptScore W2889425610C54355233 @default.
• W2889425610 hasConceptScore W2889425610C55493867 @default.

• next