Methyl donor deficiency in H9c2 cardiomyoblasts induces ER stress as an important part of the proteome response

Autor: Jousse, Céline, Martinez, Emilie, Deval, Christiane, Mazur, Andrzej, Brachet, Patrick, Comte, Blandine
Přispěvatelé: Unité de Nutrition Humaine (UNH), Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université-Institut National de la Recherche Agronomique (INRA), Ministere de l'enseignement superieur et de la recherche (France), Unité de Nutrition Humaine - Clermont Auvergne (UNH), Institut National de la Recherche Agronomique (INRA)-Université Clermont Auvergne (UCA), Institut National de la Recherche Agronomique (INRA)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université
Jazyk: angličtina
Rok vydání: 2015
Předmět:
vascular endothelial-cell
Proteomics
endoplasmic-reticulum stress
Time Factors
Proteome
Intracellular Space
030204 cardiovascular system & hematology
Cell morphology
Biochemistry
homocysteine metabolism
cardiac-hypertrophy
0302 clinical medicine
Ubiquitin
disulfide-isomerase
oxidative stress
Electrophoresis
Gel
Two-Dimensional
Gene Regulatory Networks
Myocytes
Cardiac
Prohibitin
Homocysteine
[SDV.BDD]Life Sciences [q-bio]/Development Biology
ComputingMilieux_MISCELLANEOUS
0303 health sciences
Endoplasmic Reticulum Stress
[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM]
3. Good health
Cell biology
Vitamin B 12
Cardiomyoblasts
ER stress
Programmed cell death
Proteasome Endopeptidase Complex
Methyl donor deficiency
Cell Survival
Blotting
Western
heart
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Biology
Methylation
Cell Line
03 medical and health sciences
quality-control
Folic Acid
death
Extracellular
Animals
RNA
Messenger
030304 developmental biology
Cell Size
[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry
Molecular Biology/Molecular biology
[SDV.BDLR]Life Sciences [q-bio]/Reproductive Biology
Cell Biology
Rats
Gene Ontology
Unfolded protein response
biology.protein
ubiquitin-proteasome system
[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
Biomarkers
Densitometry
Zdroj: The International Journal of Biochemistry & Cell Biology
The International Journal of Biochemistry & Cell Biology, 2015, 59, pp.62-72. ⟨10.1016/j.biocel.2014.11.013⟩
2015, 59, pp.62-72. ⟨10.1016/j.biocel.2014.11.013⟩
ISSN: 1357-2725
Popis: International audience; Deficiency of methyl donors (MDs, folate, vitamin B12, and choline) causes increased plasma level of Hcy, a risk factor for cardiovascular diseases. Previously, we showed that maternal MD deprivation altered the cardiac proteome of rat pups. To better understand its impact on cardiac cells, we exposed rat H9c2 cardiomyoblasts to selectively a synthetic folate- or MD-deficient (FD or MDD) medium. We found that a 4-day exposure to the FD medium, unlike the MDD one, did not cause an abnormal extracellular release of Hcy relatively to similar exposure to the control complete (C) medium. Comparative analyses of the proteomes of FD, MDD, and C cells identified 7 and 6 proteins up- or downregulated by either deficiency, respectively. Most proteins were found interrelated in a single network dealing with "post-translational modification, protein folding and cell death/survival" (FD cells) or "DNA replication/recombination/repair and cell morphology/compromise" (MDD cells). Both deficiencies altered the protein and mRNA levels of the chaperones alpha-crystallin B, protein disulfide-isomerase A4, and prohibitin. This was concurrent with rapid induction of several key genes of the ER stress response, notably gadd153/chop, and increased expression of the E3 ubiquitin ligases, Hrdl, and MAFbx. In conclusion, the effects of folate and MD deficiencies on the cardiomyoblast proteome display some dissimilarities possibly related to different cellular production of Hcy. In both cases activation of the ER stress could occur in response to accumulation of ubiquitinated misfolded proteins.
Databáze: OpenAIRE
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