Specific Changes in the Posttranslational Regulation of Nucleolin in Lymphocytes from Patients Infected with Human Immunodeficiency Virus

Galati, Domenico; Paiardini, Mirko; Cervasi, Barbara; Albrecht, Helmut; Bocchino, Marialuisa; Costantini, Andrea; Montroni, M; Magnani, Mauro; Piedimonte, Giuseppe; Silvestri, Guido

doi:10.1086/379249

Cited by 24 publications

(36 citation statements)

References 28 publications

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“…by measuring to what extent fragments of nucleolin (C23), which is the prominent structural protein of the nucleus [58][59][60], are degraded and passively diffuse towards the cytoplasm as a consequence of the nuclear membrane evanescence [30]. Our idea is that a consistent aliquot of circulating T lymphocytes is 'adapted' to hypoxia, dying by necrosis and destined to hemocatheresis.…”

Section: Physiologically Energy Production Ensures Main Housekeepingmentioning

confidence: 99%

Lymph Node Involution, T-Cell Adaptation and T-Cell Death in HIV Infection

et al. 2010

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Fibrotic tissue involution occurs in a large variety of chronic diseases. As the final phase of follicular atrophy and depletion, a diffuse fibrosis is the more severe consequence of the chronic process of lymph node involution that characterizes HIV infection. This review focuses on the comparison between HIV-induced lymph node fibrosis and other chronic fibroproliferative diseases, in terms of cell types participating in the process and signaling intermediates that together cause the deposition of collagen and remodel normal tissue architecture. Given that the histological quantification of this type of fibrosis cannot be easily introduced as a routine method in clinical pathology, we will discuss the possibility of exploiting some functional modifications, which express the adaptation of T cells to the fibrotic/hypoxic environment, as biochemical markers of the evolution of lymph node damage.

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Section: Physiologically Energy Production Ensures Main Housekeepingmentioning

confidence: 99%

Lymph Node Involution, T-Cell Adaptation and T-Cell Death in HIV Infection

et al. 2010

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“…The HIV-associated immune activation is thought to contribute to the AIDS-associated T-cell depletion (12,21,22,25,30,41), and high levels of circulating activated T cells are a strong predictor of disease progression in humans (16,17,24,28,44). A biological link between chronic immune activation and increased T-cell apoptosis during HIV infection was suggested by the presence of specific perturbations of cell cycle control in T lymphocytes isolated from HIV-infected patients (4,15,33,38). Lymphocytes isolated from chronically HIVinfected patients with active viral replication manifest two main perturbations of cell cycle control: (i) increased activation of the G 2 /M phase-associated cyclin B/p34-cdc2 complex, and (ii) the presence of multiple and enlarged argyrophilic nucleolar organizing regions with deregulation of nucleolin turnover (4,15,35,38).…”

Section: While the Majority Of Human Immunodeficiency Virus (Hiv)-infmentioning

confidence: 99%

“…A biological link between chronic immune activation and increased T-cell apoptosis during HIV infection was suggested by the presence of specific perturbations of cell cycle control in T lymphocytes isolated from HIV-infected patients (4,15,33,38). Lymphocytes isolated from chronically HIVinfected patients with active viral replication manifest two main perturbations of cell cycle control: (i) increased activation of the G 2 /M phase-associated cyclin B/p34-cdc2 complex, and (ii) the presence of multiple and enlarged argyrophilic nucleolar organizing regions with deregulation of nucleolin turnover (4,15,35,38). It should be noted that unscheduled p34-cdc2 activation may induce cell death by a mechanism called mitotic catastrophe (5)(6)(7)37).…”

Section: While the Majority Of Human Immunodeficiency Virus (Hiv)-infmentioning

confidence: 99%

Perturbations of Cell Cycle Control in T Cells Contribute to the Different Outcomes of Simian Immunodeficiency Virus Infection in Rhesus Macaques and Sooty Mangabeys

Paiardini

Cervasi

Sumpter

et al. 2006

J Virol

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In contrast to human immunodeficiency virus (HIV) infection of humans and experimental simian immunodeficiency virus (SIV) infection of rhesus macaques (RMs), SIV infection of sooty mangabeys (SMs), a natural host African monkey species, is typically nonpathogenic and associated with preservation of CD4+ T-cell counts despite chronic high levels of viral replication. In previous studies, we have shown that the lack of SIV disease progression in SMs is related to lower levels of immune activation and bystander T-cell apoptosis compared to those of pathogenic HIV/SIV infection (G. Silvestri, D. Sodora, R. Koup, M. Paiardini, S. O’Neil, H. M. McClure, S. I. Staprans, and M. B. Feinberg, Immunity 18:441-452, 2003; G. Silvestri, A. Fedanov, S. Germon, N. Kozyr, W. J. Kaiser, D. A. Garber, H. M. McClure, M. B. Feinberg, and S. I. Staprans, J. Virol. 79:4043-4054, 2005). In HIV-infected patients, increased T-cell susceptibility to apoptosis is associated with a complex cell cycle dysregulation (CCD) that involves increased activation of the cyclin B/p34-cdc2 complex and abnormal nucleolar structure with dysregulation of nucleolin turnover. Here we report that CCD is also present during pathogenic SIV infection of RMs, and its extent correlates with the level of immune activation and T-cell apoptosis. In marked contrast, naturally SIV-infected SMs show normal regulation of cell cycle control (i.e., normal intracellular levels of cyclin B and preserved nucleolin turnover) and a low propensity to apoptosis in both peripheral blood- and lymph node-derived T cells. The absence of significant CCD in the AIDS-free, non-immune-activated SMs despite high levels of viral replication indicates that CCD is a marker of disease progression during lentiviral infection and supports the hypothesis that the preservation of cell cycle control may help to confer the disease-resistant phenotype of SIV-infected SMs.

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“…Cytokines, in contrast, prevented both the apoptotic phenotype and the cell death by preserving mitochondrial membrane potential staining for the argyrophilic Nucleolar Organizing Regions (AgNOR) and the subcellular localization of nucleolin in confocal microscopy. [122][123][124][125][126][127] Importantly, the HIV-associated cell cycle dysregulation is exacerbated by in vitro treatment with mitogens and appears to be correlated with induction of T-cell apoptosis; 122,123,126 however, these cell cycle perturbations and apoptosis are reduced after exogenous administration of IL-2 in vitro. 122 In mitogen-activated lymphocytes from HIV-infected patients, the inappropriate activation of the cyclin B1/p34 cdc2 kinase complex is temporally associated with increased threonine phosphorylation, augmented fragmentation, and prominent extranuclear and cell surface localization of nucleolin.…”

Section: Cell Cycle Dysregulationmentioning

confidence: 99%

“…122 In mitogen-activated lymphocytes from HIV-infected patients, the inappropriate activation of the cyclin B1/p34 cdc2 kinase complex is temporally associated with increased threonine phosphorylation, augmented fragmentation, and prominent extranuclear and cell surface localization of nucleolin. 127 It is of note that increased lymphocyte apoptosis is observed at the time of cell surface localization of nucleolin. Interestingly, a recent comparative study of cell cycle dysregulation in two models of pathogenic (i.e.…”

Section: Cell Cycle Dysregulationmentioning

confidence: 99%