Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Przeglądasz jako GOŚĆ
Tytuł pozycji:

Fetal Programming by Methyl Donor Deficiency Produces Pathological Remodeling of the Ascending Aorta.

Tytuł :
Fetal Programming by Methyl Donor Deficiency Produces Pathological Remodeling of the Ascending Aorta.
Autorzy :
Balint B; UMR Inserm 1256 N-GERE (Nutrition, Génetique et Exposition aux Risques Environmentaux) (B.B., S.H., R.-M.G.-R., J.-L.G.).
Hergalan S; UMR Inserm 1256 N-GERE (Nutrition, Génetique et Exposition aux Risques Environmentaux) (B.B., S.H., R.-M.G.-R., J.-L.G.).
Camadro JM; Université de Lorraine, France. Mass Spectrometry Laboratory, Institut Jacques Monod, UMR 7592, Université Paris Diderot, CNRS, Sorbonne Paris Cité, France (J.-M.C., L.L.).
Blaise S; UMR CNRS (S.B., L.V.).
Vanalderwiert L; UMR CNRS (S.B., L.V.).
Lignières L; Université de Lorraine, France. Mass Spectrometry Laboratory, Institut Jacques Monod, UMR 7592, Université Paris Diderot, CNRS, Sorbonne Paris Cité, France (J.-M.C., L.L.).
Guéant-Rodriguez RM; UMR Inserm 1256 N-GERE (Nutrition, Génetique et Exposition aux Risques Environmentaux) (B.B., S.H., R.-M.G.-R., J.-L.G.).; Department of Molecular Medicine and National Center of Inborn Errors of Metabolism, University Hospital Center (R.-M.G.-R., J.-L.G.).
Guéant JL; UMR Inserm 1256 N-GERE (Nutrition, Génetique et Exposition aux Risques Environmentaux) (B.B., S.H., R.-M.G.-R., J.-L.G.).; Department of Molecular Medicine and National Center of Inborn Errors of Metabolism, University Hospital Center (R.-M.G.-R., J.-L.G.).
Pokaż więcej
Źródło :
Arteriosclerosis, thrombosis, and vascular biology [Arterioscler Thromb Vasc Biol] 2021 Apr 08, pp. ATVBAHA120315587. Date of Electronic Publication: 2021 Apr 08.
Publication Model :
Ahead of Print
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: 1998- : Baltimore, Md. : Lippincott Williams & Wilkins
Original Publication: Dallas, TX : American Heart Association, c1995-
Contributed Indexing :
Keywords: aorta; blood pressure; extracellular matrix; homocysteine; vinculin
Entry Date(s) :
Date Created: 20210408 Latest Revision: 20210408
Update Code :
20210408
DOI :
10.1161/ATVBAHA.120.315587
PMID :
33827257
Czasopismo naukowe
Objective: Deficiency in vitamin B12/folate (methyl donor deficiency [MDD]) produces cardiovascular outcomes during aging and fetal programming effects in newborns of MDD mothers. Whether fetal programming provokes long-term effects on aorta remains largely unknown. Approach and Results: We investigated the impact of fetal programming on ascending aorta of aged rats born from mothers subjected to MDD during gestation/lactation. We performed morphological and molecular examinations of ascending aorta in 21 days- and 400 days-aged rats with initial MDD fetal programming (initial MDD) compared with control matched rats. Initial MDD induces remodeling of ascending aorta in aged rats, with collagen deposition ( P =0.0008), decreased thickness of elastin ( P <0.0001), and 8.7-fold increase of elastin breaks ( P =0.0002). Proteomic analyses, Western blotting, and immunohistochemical examination revealed decreased expression of α-smooth muscle actin, vinculin, SM22α (smooth muscle 22α), and N-cadherin and increased expression of TGF (transforming growth factor) β1. Elastin breaks were correlated to increased neutrophil elastase ( P =0.0002), cathepsin-K ( P =0.0002), cathepsin-S ( P <0.0001), and MMP (matrix metalloproteinase) 9, and MMP2 ( P <0.0001 and P =0.02). Proximity Duolink ligation assay showed homocysteinylation of actin-associated and extracellular matrix proteins, including SM22α ( P =0.01), N-cadherin ( P =0.0008), and vinculin ( P =0.001), which was associated with elastin breaks ( P =0.002) and increased expression of MARS (methionyl-tRNA synthetase; involved in irreversible protein homocysteinylation). Furthermore, we observed an inverse relationship between elastin breaks and blood pressure (systolic, P =0.004 and diastolic, P =0.0007).
Conclusions: MDD fetal programming produced altered integrity and remodeling of ascending aorta during aging and irreversible MARS-associated homocysteinylation of key proteins of extracellular matrix and elastin homeostasis. This contributes to understanding why homocysteine-lowering vitamin B supplementation fails to relieve vascular complications in adulthood.

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies