عرض بسيط للتسجيلة

المؤلفSafiedeen, Zainab
المؤلفRodríguez-Gómez, Isabel
المؤلفVergori, Luisa
المؤلفSoleti, Raffaella
المؤلفVaithilingam, Dayannath
المؤلفDouma, Imene
المؤلفAgouni, Abdelali
المؤلفLeiber, Denis
المؤلفDubois, Séverine
المؤلفSimard, Gilles
المؤلفZibara, Kazem
المؤلفAndriantsitohaina, Ramaroson
المؤلفMartínez, M. Carmen
تاريخ الإتاحة2017-04-16T08:05:24Z
تاريخ النشر2017-01-01
اسم المنشورAntioxidants & Redox Signaling
المعرّفhttp://dx.doi.org/10.1089/ars.2016.6771
الاقتباس"Temporal Cross Talk Between Endoplasmic Reticulum and Mitochondria Regulates Oxidative Stress and Mediates Microparticle-Induced Endothelial Dysfunction" Safiedeen Zainab, Rodríguez-Gómez Isabel, Vergori Luisa, Soleti Raffaella, Vaithilingam Dayannath, Douma Imene, Agouni Abdelali, Leiber Denis, Dubois Séverine, Simard Gilles, Zibara Kazem, Andriantsitohaina Ramaroson, and Martínez M. Carmen. Antioxidants & Redox Signaling. January 2017, 26(1): 15-27
الرقم المعياري الدولي للكتاب1523-0864
معرّف المصادر الموحدhttp://hdl.handle.net/10576/5462
الملخصAims: Circulating microparticles (MPs) from metabolic syndrome patients and those generated from apoptotic T-cells induce endothelial dysfunction; however, the molecular and cellular mechanism(s) underlying in the effects of MPs remain to be elucidated. Results: Here, we show that both types of MPs increased expression of endoplasmic reticulum (ER) stress markers XBP-1, p-eIF2alpha and CHOP and nuclear translocation of ATF6 on human aortic endothelial cells. MPs decreased in vitro nitric oxide release by human aortic endothelial cells, whereas in vivo MP injection into mice impaired the endothelium-dependent relaxation induced by acetylcholine. These effects were prevented when ER stress was inhibited suggesting that ER stress is implicated in the endothelial effects induced by MPs. MPs affected mitochondrial function and evoked sequential increase of cytosolic and mitochondrial reactive oxygen species (ROS). Pharmacological inhibition of ER stress and silencing of neutral sphingomyelinase with siRNA abrogated all MP-mediated effects. Neutralization of Fas-Ligand carried by MPs abolished effects induced by both MP types, whereas neutralization of low density lipoprotein-receptor on endothelial cells prevented T-lymphocyte MP-mediated effects. Innovation and Conclusion: Collectively, endothelial dysfunction triggered by MPs involves temporal cross-talk between ER and mitochondria with respect to spatial regulation of ROS via the neutral sphingomyelinase and interaction of MPs with Fas and/or low density lipoprotein-receptor. These results provide a novel molecular insight into the manner MPs mediate vascular dysfunction and allow identification of potential therapeutic targets to treat vascular complications associated with metabolic syndrome.
راعي المشروعInstitut National de la Santé et de la Recherche Médicale, Université dʼAngers and Centre Hospitalo-Universitaire dʼAngers.
اللغةen
الناشرMary Ann Liebert, Inc.
الموضوعER stress
Microparticles
Endothelial dysfunction
العنوانTemporal cross talk between endoplasmic reticulum and mitochondria regulates oxidative stress and mediates microparticle-induced endothelial dysfunction
النوعArticle
الصفحات15-27
رقم العدد1
رقم المجلد26
ESSN1557-7716
dc.accessType Open Access


الملفات في هذه التسجيلة

Thumbnail

هذه التسجيلة تظهر في المجموعات التالية

عرض بسيط للتسجيلة