Endothelial progenitor cell trafficking in human immunodeficiency virus-infected persons

Teofili, Luciana; Iachininoto, Maria Grazia; Capodimonti, Sara; Ucciferri, Claudio; Nuzzolo, Eugenia Rosa; Martini, Maurizio; Torti, Lorenza; Falasca, Katia; Vecchiet, Jacopo; Leone, Giuseppe; Larocca, Luigi Maria

doi:10.1097/qad.0b013e32833ef79d

Cited by 33 publications

(29 citation statements)

References 29 publications

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“…Representative CFU-EC and E-CFC colonies and their RT-PCR characterization are shown in Figure 1. Capillary formation assay was performed as described 19,20 with the use of E-CFCs at passage 2. When appropriate, single E-CFC-derived colonies were expanded for 2 or 3 passages to obtain an amount of cells suitable for adhesion assays and for Western blot analysis.…”

Section: Cfu-ec and E-cfc Colony Assaymentioning

confidence: 99%

“…20 Briefly, for CFU-EC colonies, Ficoll density gradient-isolated mononuclear cells were suspended in EndoCult medium (EndoCult Liquid Medium Kit, Stem Cell Technologies) and plated on 6-well dishes coated with human fibronectin (Sigma-Aldrich). After 48 hours, nonadherent cells were recovered and replated in 24-well human fibronectin-coated dishes (SigmaAldrich) in the same culture medium, at 10 6 /mL cell concentration.…”

Section: Cfu-ec and E-cfc Colony Assaymentioning

confidence: 99%

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Endothelial progenitor cells are clonal and exhibit the JAK2V617F mutation in a subset of thrombotic patients with Ph-negative myeloproliferative neoplasms

Teofili¹,

Martini

Iachininoto³

et al. 2011

Blood

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In this study we investigated whether neoplastic transformation occurring in Philadelphia (Ph)-negative myeloproliferative neoplasms (MPNs) could involve also the endothelial cell compartment. We evaluated the level of endothelial colony-forming cells (E-CFCs) in 42 patients (15 with polycythemia vera, 12 with essential thrombocythemia, and 15 with primary myelofibrosis). All patients had 1 molecular abnormality (JAK2 V617F or MPL W515K mutations, SOCS gene hypermethylation, clonal pattern of growth) detectable in their granulocytes. The growth of colonies was obtained in 22 patients and, among them, patients with primary myelofibrosis exhibited the highest level of E-CFCs. We found that E-CFCs exhibited no molecular abnormalities in12 patients, had SOCS gene hypermethylation, were polyclonal at human androgen receptor analysis in 5 patients, and resulted in JAK2 V617F mutated and clonal in 5 additional patients, all experiencing thrombotic complications. On the whole, patients with altered E-CFCs required antiproliferative therapy more frequently than patients with normal E-CFCs. Moreover JAK2 V617F -positive E-CFCs showed signal transducer and activator of transcription 5 and 3 phosphorylation rates higher than E-CFCs isolated from healthy persons and patients with MPN without molecular abnormalities. Finally, JAK2 V617F -positive E-CFCs exhibited a high proficiency to adhere to normal mononuclear cells. This study highlights a novel mechanism underlying the thrombophilia observed in MPN. (Blood. 2011;117(9):2700-2707)

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Section: Cfu-ec and E-cfc Colony Assaymentioning

confidence: 99%

Section: Cfu-ec and E-cfc Colony Assaymentioning

confidence: 99%

Endothelial progenitor cells are clonal and exhibit the JAK2V617F mutation in a subset of thrombotic patients with Ph-negative myeloproliferative neoplasms

Teofili¹,

Martini

Iachininoto³

et al. 2011

Blood

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112

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“…Evidenza diretta di una relazione tra funzione endoteliale e misure più definitive di rigidità arteriosa è stata fornita da studi approfonditi in pazienti con malattia vascolare e vari fattori di rischio. D'altro canto, la relazione tra PWV, l'attuale misura "gold-standard" della rigidità arteriosa, e danni vascolari aterosclerosi precoci valutati con IMT non è ancora chiara e stabilita (20). È evidente che la diminuzione dell'elasticità o l'aumento della rigidità arteriosa nei soggetti normotensivi e pre-ipertesi aumenta il rischio per lo sviluppo di ipertensione arteriosa (21).…”

Section: Discussioneunclassified

Disfunzione vascolare nei pazienti con infezione da HIV.

Falasca¹,

Ucciferri²,

Pontolillo³

et al. 2017

JHA

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RiassuntoLa malattia cardiovascolare aterosclerotica è un crescente problema per il paziente con infezione da virus dell'immunodeficienza umana (HIV). Abbiamo arruolato 80 pazienti HIV+, 68 dei quali trattati con terapia antiretrovirale combinata (cART) e 12 naïve, abbinati per età, pressione sanguigna sistolica e diastolica a 82 soggetti sani. Abbiamo studiato lo spessore intima-media carotide (IMT), la dilatazione mediata dal flusso (FMD), la velocità dell'onda dell'impulso (PWV) e l'indice di aumento (AIx), come indici di aterosclerosi subclinica, nei pazienti HIV+ rispetto ai controlli non infetti e comparato parametri viroimmunologici, marcatori infiammatori, microalbuminuria e altri parametri biochimici. Rispetto a soggetti non infetti, i soggetti HIV+ avevano valori più elevati di IMT, PWV e AIx (tutti p=0,0001); e FMD inferiore (p=0,001). Nel gruppo HIV +, i pazienti naïve avevano livelli statisticamente più bassi di IMT (p=0,02) e AIx (p=0,042) e FMD più elevati (p=0,032) rispetto ai pazienti trattati con cART. Nel gruppo HIV+, i valori IMT erano significativamente correlati al numero di cellule CD4 + (r=-0,31, p=0,008) e CD8+ (r=0,261, p=0,025), interleuchina-6 (r=0,284, p=0,015) e endotelina-1 (r=0,302, p=0,009). La disfunzione vascolare è più prevalente nei pazienti con infezione da HIV che nei soggetti sani. Inoltre, i pazienti trattati con cART hanno presentato valori di IMT e AIx più alti e valori inferiori rispetto ai pazienti naïve. I nostri dati supportano l'ipotesi che sia l'infezione da HIV che il trattamento cART siano fattori di rischio per l'arteriosclerosi accelerata. P=0.008) and CD8+ cells (r=0.261, P=0.025), P=0.009 Abstract Atherosclerotic cardiovascular disease is an increasing concern for patient with human immunodeficiency virus (HIV) infection. We enrolled 80 HIV infected patients, 68 of whom treated with combined antiretroviral therapy (cART) and 12 therapy-naïve, matched for age, systolic and diastolic blood pressure with 82 healthy subjects. We investigated carotid intima-media thickness (IMT), flow-mediated dilation (FMD), pulse wave velocity (PWV) and the augmentation index (AIx), as indices of subclinical atherosclerosis, in HIV-infected patients compared with control, uninfected subjects, along with viro-immunological parameters, inflammatory markers, microalbuminuria and other biochemical parameters. Compared with uninfected subjects, HIV-infected subjects had higher IMT, PWV and AIx values (all P=0.0001); and lower FMD (P=0.001). In the HIV+ group, naïve patients had statistically lower levels of IMT (P=0.02), and AIx (P=0.042) and higher FMD (P=0.032) compared with cART-treated patients. In the HIV+ group, IMT values was significantly related to the number of IntroduzioneLa malattia cardiovascolare aterosclerotica, causa di morbilità e mortalità nella popolazione generale, è un problema emergente anche nei pazienti HIV+. È stato riportato un aumento di eventi cardiovascolari (CVD) in pazienti HIV+ prima della disponibilità della terapia antiretrovirale (cART) (1, 2), ...

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“…Direct cells' death occurs not only through apoptosis or necrosis but also by the effects on lipid and glucose metabolism and by the decrease of endothelial progenitor cells the circulating colony forming unit-endothelial cells (CFU-EC), which are necessary for the endothelial damage repair [4,6]. Not to mention that some of the HIV proteins have an influence on the endothelium in many various manners.…”

Section: Endothelial Dysfunction and Hiv Infectionmentioning

confidence: 99%

Endothelial dysfunction—An important factor in the progression of atherosclerosis in HIV-infected persons

Skowyra¹,

Zdziechowicz²,

Mikuła

et al. 2012

HIV & AIDS Review

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a b s t r a c tThe antiretroviral therapy has remarkably modified the process of HIV disease, enhancing higher quality of life and longer survival, however it has contemporaneously lead to the occurrence of earlier unrecognized complications, such as endothelial dysfunction and cardiovascular events. The endothelial dysfunction is directly caused by HIV-induced endothelial cell death (effects on metabolism, increase level of proinflammatory cytokines and adhesion molecules). Endothelial dysfunction accelerates the process of atherosclerosis and causes an increase of cardiovascular risk. In addition, HIV-infected patients who are coinfected with HCV have higher cardiovascular risk as a result of the increase of serum levels of VCAM-1 and ICAM-1, and production of inflammatory cytokines and lipids. Despite the treatment effects of antiretroviral therapy on HIV-positive patients, some drugs cause endothelial damage and increased risk of heart disease. This review attempts to summarize the HIV infection mechanism and other factors associated with infection and treatment that affect the endothelium resulting in cardiovascular events.

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Endothelial progenitor cell trafficking in human immunodeficiency virus-infected persons

Abstract: Although HIV does not affect the 'true endothelial progenitor' compartment, it infects and strongly depletes circulating endothelial progenitors with hematopoietic signature. We unravel a novel pathogenetic mechanism by which HIV infection might cause vascular diseases.

Cited by 33 publications

References 29 publications

Endothelial progenitor cells are clonal and exhibit the JAK2V617F mutation in a subset of thrombotic patients with Ph-negative myeloproliferative neoplasms

Endothelial progenitor cells are clonal and exhibit the JAK2V617F mutation in a subset of thrombotic patients with Ph-negative myeloproliferative neoplasms

Disfunzione vascolare nei pazienti con infezione da HIV.

Endothelial dysfunction—An important factor in the progression of atherosclerosis in HIV-infected persons

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