We are analyzing https://link.springer.com/article/10.1007/s00395-009-0054-y.

Title:
Proteasome inhibitor bortezomib promotes a rupture-prone plaque phenotype in ApoE-deficient mice | Basic Research in Cardiology
Description:
The ubiquitin–proteasome system is involved in the development and progression of atherosclerosis. The aim of this study was to investigate whether plaque composition is affected by proteasome function. In vitro, the potent and selective proteasome inhibitor bortezomib induced apoptosis in both cultured smooth muscle cells (SMCs) and activated macrophages. This effect was associated with increased expression of C/EBP homologous protein and cleavage of caspase-12, indicative of endoplasmic reticulum stress. The sensitivity to the proapoptotic effects of proteasome inhibition correlated with the protein synthesis rate. Proteasome inhibition in explanted atherosclerotic plaques of ApoE-deficient mice resulted in a significant decrease in SMCs and macrophages, indicating that both cell types in the atherosclerotic plaque were susceptible to the proapoptotic effects of proteasome inhibition. In vivo proteasome inhibition in ApoE-deficient mice did not affect plaque size or composition of early atherosclerotic plaques, but resulted in a significant decrease in collagen content as well as a significant enlargement of the necrotic core in advanced atherosclerotic plaques. In conclusion, our results indicate that an impaired proteasome function promotes features of a more rupture-prone plaque phenotype.
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Keywords {🔍}

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Topics {✒️}

endoplasmic reticulum stress month download article/chapter monocyte-derived dcs induced rupture-prone plaque phenotype systemic nuclear factor-{{kappa}} apolipoprotein e-deficient mice collar-induced intimal thickening apoe-deficient mice resulted ubiquitin–proteasome proteolytic pathway article basic research proteasome inhibitor ps-341 bortezomib induces apoptosis jozef van herck van der pluijm full article pdf protein synthesis rate nuclear factor-kappab apoe-deficient mice proteasome inhibitors bortezomib privacy choices/manage cookies apolipoprotein e-deficient /ebp homologous protein caspase-3-dependent apoptosis squamous cell carcinoma ubiquitin–proteasome pathway multiple myeloma cells de meyer gry beta-catenin signaling nonadherent cells cultured affect plaque size ubiquitin–proteasome system human carotid atherosclerosis cell-matrix contacts protein quality disease proteasome inhibitors induce van put djm van de ruit van berkel tj holmes dr jr harrington wj jr protein synthesis proteasome inhibition correlated european economic area effective antitumor agents sala-newby gb integrin-linked kinase myelin figure formation bochaton-piallat m complete drug reference epstein-barr virus

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         description:The ubiquitin–proteasome system is involved in the development and progression of atherosclerosis. The aim of this study was to investigate whether plaque composition is affected by proteasome function. In vitro, the potent and selective proteasome inhibitor bortezomib induced apoptosis in both cultured smooth muscle cells (SMCs) and activated macrophages. This effect was associated with increased expression of C/EBP homologous protein and cleavage of caspase-12, indicative of endoplasmic reticulum stress. The sensitivity to the proapoptotic effects of proteasome inhibition correlated with the protein synthesis rate. Proteasome inhibition in explanted atherosclerotic plaques of ApoE-deficient mice resulted in a significant decrease in SMCs and macrophages, indicating that both cell types in the atherosclerotic plaque were susceptible to the proapoptotic effects of proteasome inhibition. In vivo proteasome inhibition in ApoE-deficient mice did not affect plaque size or composition of early atherosclerotic plaques, but resulted in a significant decrease in collagen content as well as a significant enlargement of the necrotic core in advanced atherosclerotic plaques. In conclusion, our results indicate that an impaired proteasome function promotes features of a more rupture-prone plaque phenotype.
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