Imbalance between endothelial progenitors cells and microparticles in HIV-infected patients naive for antiretroviral therapy

Silva, Erika Ferrari Rafael da; Fonseca, Francisco A.H.; França, Carolina Nunes; Ferreira, Paulo Roberto Abrão; Izar, Maria C.O.; Salomão, Reinaldo; Camargo, Lázaro Manoel de; Tenore, Simone de Barros; Lewi, David Salomão

doi:10.1097/qad.0b013e32834980f4

Cited by 50 publications

(35 citation statements)

References 46 publications

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“…HIV/AIDS is the leading individual cause of infectious disease-related mortality, and HIV, too, has been shown to change circulating MV levels. Patients with HIV-1 had increased circulating endothelial-derived [64] and platelet-derived MVs, which decreased with antiretroviral therapy [65]. HIV may utilize vesiculation pathways to enhance immune suppression and viral spread [66,67].…”

Section: Microvesicles and Redox Biologymentioning

confidence: 99%

Circulating membrane-derived microvesicles in redox biology

Larson

Hillery

Hogg

2014

Free Radical Biology and Medicine

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Microparticles or microvesicles (MV) are sub-cellular membrane blebs shed from all cells in response to various stimuli. MVs carry a battery of signaling molecules, many of them related to redox-regulated processes. The role of MVs, either as a cause or result of cellular redox signaling has been increasingly recognized over the past decade. This is in part due to advances in flow cytometry and its detection of MVs. Notably, recent studies have shown circulating MVs from platelets and endothelial cells drive reactive species-dependent angiogenesis; circulating MVs in cancer alter the microenvironment and enhance invasion through horizontal transfer of mutated proteins and nucleic acids, and harbor redox-regulated matrix metalloproteinases and pro-coagulative surface molecules; and circulating MVs from RBCs and other cells modulate cell-cell interactions through scavenging or production of nitric oxide and other free radicals. While our recognition of MVs in redox-related processes is growing, especially in the vascular biology field, much remains unknown regarding the various biologic and pathologic functions of MVs. Like reactive oxygen and nitrogen species, MVs were originally believed to have a solely a pathological role in biology. And like our understanding of reactive species, it is now clear that MVs also play an important role in normal growth, development, and homeostasis. We are just beginning to understand how MVs are involved in various biological processes—developmental, homeostatic and pathological—and the role of MVs in redox signaling is an rich and exciting area of investigation.

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Section: Microvesicles and Redox Biologymentioning

confidence: 99%

Circulating membrane-derived microvesicles in redox biology

Larson

Hillery

Hogg

2014

Free Radical Biology and Medicine

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“…At this stage, the pro-apoptotic gene C/EBP homologous protein (CHOP)/GADD153 is upregulated triggering cell death. Intriguingly, endothelial apoptosis has been implicated as a characteristic feature of BBB breach in patients with HAND compared with non-demented infected individuals or HIV-negative controls [13]. …”

Section: Introductionmentioning

confidence: 99%

HIV Tat-Mediated Induction of Human Brain Microvascular Endothelial Cell Apoptosis Involves Endoplasmic Reticulum Stress and Mitochondrial Dysfunction

Lü

Niu

et al. 2014

Mol Neurobiol

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Endoplasmic reticulum (ER) stress triggered under hyperglycemic, hypoxic, and oxidative conditions has been implicated in cellular dysfunction through activation of the unfolded protein response (UPR). Recent clinical studies have documented that the release of soluble cellular and host factors following HIV infection in the central nervous system (CNS) results in induction of the ER stress response. Herein, we demonstrate that exposure of human brain microvascular endothelial cells (HBMECs) to HIV transactivator protein Tat101 resulted in early induction of several major ER stress regulators including ER chaperones Bip/GRP78 and ER stress sensors ATF6, p-PERK, and downstream mediators p-eIF2α and ATF4. Upregulation of the ER stress mediators was accompanied by decreased cell viability and increased apoptosis as evidenced by MTT and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assays, respectively. Pretreatment of HBMECs with either ER inhibitor or knockdown of the effector C/EBP homologous protein (CHOP) resulted in increased cell viability and abrogation of apoptosis following Tat exposure. Notably, Tat-mediated activation of the UPR response involved reactive oxygen species. Furthermore, treatment of Tat also resulted in mitochondrial dysfunction, evidenced by decrease in Bcl2/Bax ratio, dysfunction of mitochondrial membrane potential, and release of cytochrome c, all of which could be partially reversed by the ER stress inhibitor. The current study demonstrates that exposure of HBMECs to Tat induces multiple stress responses, including ER stress and mitochondrial dysfunction which in turn lead to apoptosis.

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“…Endothelial dysfunction has been associated with decreased circulating endothelial progenitor cells (1,2) and increased circulating endothelial microparticles (3,4). Both conditions are influenced by classic risk factors (4-6) and inflammatory status (7,8).…”

Section: Introductionmentioning

confidence: 99%

Effects of simvastatin/ezetimibe on microparticles, endothelial progenitor cells and platelet aggregation in subjects with coronary heart disease under antiplatelet therapy

Camargo

França

Izar

et al. 2014

Braz J Med Biol Res

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It is not known whether the addition of ezetimibe to statins adds cardiovascular protection beyond the expected changes in lipid levels. Subjects with coronary heart disease were treated with four consecutive 1-week courses of therapy (T) and evaluations. The courses were: T1, 100 mg aspirin alone; T2, 100 mg aspirin and 40 mg simvastatin/10 mg ezetimibe; T3, 40 mg simvastatin/10 mg ezetimibe, and 75 mg clopidogrel (300 mg initial loading dose); T4, 75 mg clopidogrel alone. Platelet aggregation was examined in whole blood. Endothelial microparticles (CD51), platelet microparticles (CD42/CD31), and endothelial progenitor cells (CD34/CD133; CDKDR/CD133, or CD34/KDR) were quantified by flow cytometry. Endothelial function was examined by flow-mediated dilation. Comparisons between therapies revealed differences in lipids (T2 and T3T1 and T4, P=0.001). Decreased platelet aggregation was observed after aspirin (arachidonic acid, T1

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Imbalance between endothelial progenitors cells and microparticles in HIV-infected patients naive for antiretroviral therapy

Abstract: Our findings suggest an imbalance between endothelial progenitor cells mobilization and endothelial apoptosis. The alteration in the turnover of endothelial cells may contribute to cardiovascular events in HIV-infected patients.

Cited by 50 publications

References 46 publications

Circulating membrane-derived microvesicles in redox biology

Circulating membrane-derived microvesicles in redox biology

HIV Tat-Mediated Induction of Human Brain Microvascular Endothelial Cell Apoptosis Involves Endoplasmic Reticulum Stress and Mitochondrial Dysfunction

Effects of simvastatin/ezetimibe on microparticles, endothelial progenitor cells and platelet aggregation in subjects with coronary heart disease under antiplatelet therapy

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