Intracellular Trafficking of a Fiber-modified Adenovirus Using Lipid Raft/Caveolae Endocytosis

Rogée, Sophie; Grellier, Elodie; Bernard, C.; Loyens, Anne; Beauvillain, Jean-Claudé; D'Halluin, Jean-Claude; Colin, Morvane

doi:10.1038/sj.mt.6300283

Cited by 27 publications

(31 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is believed that the molecular events leading to the induction of immunoregulatory genes are triggered due to virus-cell interaction (Tibbles et al, 2002). Ad serotypes that utilize distinct cellular receptors differ in their intracellular trafficking and localization (Leopold and Crystal, 2007; Rogee et al, 2007). For instance, CD46-utilizing Ads tend to accumulate in lysosomes unlike subgroup C Ads that traffic rapidly to the nuclear envelope (Iacobelli-Martinez and Nemerow, 2007).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of innate immunity and vector toxicity following inoculation of bovine, porcine or human adenoviral vectors in a mouse model

et al. 2010

View full text Add to dashboard Cite

Nonhuman adenovirus (Ad) vectors derived from bovine Ad serotype 3 (BAd3) or porcine Ad serotype 3 (PAd3) can circumvent pre-existing immunity against human Ad (HAd). We have previously reported differential transduction of human and nonhuman cells by these Ad vectors, and their distinct receptor usage and biodistribution. To compare the induction of innate immunity, vector toxicity and vector uptake by Kupffer cells (KCs) following intravenous administration of PAd3, BAd3, or HAd5 vectors in mice, we determined mRNA expression levels of proinflammatory chemokines and cytokines, and Toll-like receptors (TLRs) in the liver and spleen. Tissue toxicity of these vectors was assessed by comparing serum levels of liver-specific enzymes, histopathology and Kupffer cell (KC) depletion. Compared to the HAd5 vector, PAd3 and BAd3 vectors were more potent stimulators of innate immune responses as indicated by enhanced mRNA expression of TLRs and proinflammatory chemokines and cytokine genes. Histopathological changes in the liver were most pronounced in HAd5-inoculated mice while BAd3-or PAd3-inoculated mice revealed mild histologic changes that were confined to early time points. Inoculation with HAd5 or PAd3 vectors resulted in a significant (P <0.05) decline of the number of KCs in the liver. Together, these results extend our previous observations regarding distinct in vivo biology of nonhuman and human Ad vectors.

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of innate immunity and vector toxicity following inoculation of bovine, porcine or human adenoviral vectors in a mouse model

et al. 2010

View full text Add to dashboard Cite

show abstract

“…Adenovirus Growth and Labeling-HAdV-5-hTau44Wt (wild-type Tau isoform 2-3-10-) and HAdV-5-hTau44-NLS were constructed using the gateway system (Invitrogen), and they were amplified and purified in our laboratory as described previously (13). HAdV-5-hTau44-NLS was obtained by insertion of a nuclear localization signal (NLS) 2 from the Epstein-Barr virus mRNA export factor EB2 (14) to the Nterminal part of human Tau.…”

Section: Methodsmentioning

confidence: 99%

Nuclear Tau, a Key Player in Neuronal DNA Protection

Sultan

Nesslany

Violet

et al. 2011

Journal of Biological Chemistry

Self Cite

351

366

View full text Add to dashboard Cite

Tau, a neuronal protein involved in neurodegenerative disorders such as Alzheimer disease, which is primarily described as a microtubule-associated protein, has also been observed in the nuclei of neuronal and non-neuronal cells. However, the function of the nuclear form of Tau in neurons has not yet been elucidated. In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wildtype and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. These results highlight a novel role for nuclear Tau as a key player in early stress response.

show abstract

“…Caveolae is a specialized invaginated structure, located in or near the cell plasma membrane. They are flask-shaped or like Greek letter Ω. Caveolins are the principal structural proteins in caveolae, which are named, respectively, as caveolin-1, caveolin-2, and caveolin-3 in mammals (Rogee et al 2007;Silva et al 2007). Studies demonstrated VEGF could combine with caveolae to form transmembrane channels allowed large molecule substances pass through and expression of caveolin-1 enhanced (Nag et al 2007;Cogger et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Vascular Endothelial Growth Factor Increases Permeability of the Blood–Tumor Barrier via Caveolae-Mediated Transcellular Pathway

et al. 2010

View full text Add to dashboard Cite

The first goal of this study was to determine the effect of vascular endothelial growth factor (VEGF) on permeability of the blood-tumor barrier (BTB). The second goal was to determine possible cellular mechanisms by which VEGF increases permeability of the BTB. In the rat C6 glioma model, the permeability of the BTB was significantly increased after VEGF injection at dose of 0.05 ng/g and reached its peak at 45 min. Meanwhile, we observed that the density of pinocytotic vesicles of brain microvascular endothelial cells (BMECs) in the BTB increased dramatically by transmission electron microscopy. The immunohistochemistry and western blot analysis revealed that the expression level of caveolae structure proteins caveolin-1 and caveolin-2 in BMECs was increased after VEGF injection, peaked at 45 min, and then decreased to the untreated level. The time peak of expression level of caveolin-1 and caveolin-2 was identical with the peak time of permeability of the BTB and the density of pinocytotic vesicles. All of these results strongly indicated that VEGF increased permeability of the BTB caused by enhancement of the density of pinocytotic vesicles, and the molecular mechanism might be associated with upregulated expression of caveolin-1 and caveolin-2.

show abstract

Intracellular Trafficking of a Fiber-modified Adenovirus Using Lipid Raft/Caveolae Endocytosis

Cited by 27 publications

References 48 publications

Evaluation of innate immunity and vector toxicity following inoculation of bovine, porcine or human adenoviral vectors in a mouse model

Evaluation of innate immunity and vector toxicity following inoculation of bovine, porcine or human adenoviral vectors in a mouse model

Nuclear Tau, a Key Player in Neuronal DNA Protection

Vascular Endothelial Growth Factor Increases Permeability of the Blood–Tumor Barrier via Caveolae-Mediated Transcellular Pathway

Contact Info

Product

Resources

About