Differentiation Restricted Endocytosis of Cell Penetrating Peptides in MDCK Cells Corresponds with Activities of Rho-GTPases

Foerg, Christina; Ziegler, Urs; Fernández‐Carneado, Jimena; Giralt, Ernest; Merkle, Hans P.

doi:10.1007/s11095-006-9212-1

Cited by 52 publications

(42 citation statements)

References 79 publications

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“…Consistent with this result, we find in MDCK cells that caveolin-1 knockdown also blunts the responses to cytokines. However, although endocytosis is demonstrably an important component of the response to cytokines (Foerg et al, 2007), another role for caveolin is the organization of lipid-dependent signaling domains (Wei et al, 1999).We speculate that extra occludin in MDCK cells could be acting to enhance association with, and therefore the response to, these signaling molecules; occludin KD could have the opposite effect. This hypothesis is supported not only by the occludin-dependent change in caveolin localization demonstrated in this study, but also by published studies demonstrating that occludin can immunoprecipitate caveolin (Nusrat et al, 2000;Lynch et al, 2007).…”

Section: Discussionmentioning

confidence: 91%

Occludin is required for cytokine-induced regulation of tight junction barriers

Itallie

Fanning

Holmes

et al. 2010

Journal of Cell Science

179

173

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SummaryThe function of occludin remains elusive. Proposed roles include maintenance of tight junction barriers, signaling and junction remodeling. To investigate a potential role in mediating cytokine-induced changes in barrier properties, we measured barrier responses to interferon- plus TNF in control, occludin-overexpressing and occludin knockdown MDCK II monolayers. MDCK cells show a complex response to cytokines characterized by a simultaneous increase in the transepithelial electrical resistance and a decrease in the barrier for large solutes. We observed that overexpression of occludin increased and occludin knockdown decreased sensitivity to cytokines as assessed by both these parameters. It is known that caveolin-1 interacts with occludin and is implicated in several models of cytokine-dependent barrier disruption; we found that occludin knockdown altered the subcellular distribution of caveolin-1 and that partitioning of caveolin into detergent-insoluble lipid rafts was influenced by changing occludin levels. Knockdown of caveolin decreased the cytokine-induced flux increase, whereas the increase in the electrical barrier was unaltered; the effect of double knockdown of occludin and caveolin was similar to that of occludin single knockdown, consistent with the possibility that they function in the same pathway. These results demonstrate that occludin is required for cells to transduce cytokine-mediated signals that either increase the electrical barrier or decrease the large solute barrier, possibly by coordinating the functions of caveolin-1.

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Section: Discussionmentioning

confidence: 91%

Occludin is required for cytokine-induced regulation of tight junction barriers

Itallie

Fanning

Holmes

et al. 2010

Journal of Cell Science

179

173

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“…Endocytosis and vesicular transport is known to be regulated from external signals via Rho-GTPases and downstream effector Rhoassociated kinase (Rock) modulation of the actin cytoskeleton (Foerg et al, 2007;Nelson, 2009;Chi et al, 2013). We examined the localisation of RhoA and actin in NPD and Emb-LPD blastocysts following FITC-dextran incubation to quantify endocytosis.…”

Section: Induction and Regulation Of Blastocyst Te Response To Maternmentioning

confidence: 99%

Mouse early extra-embryonic lineages activate compensatory endocytosis in response to poor maternal nutrition

et al. 2014

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Mammalian extra-embryonic lineages perform the crucial role of nutrient provision during gestation to support embryonic and fetal growth. These lineages derive from outer trophectoderm (TE) and internal primitive endoderm (PE) in the blastocyst and subsequently give rise to chorio-allantoic and visceral yolk sac placentae, respectively. We have shown maternal low protein diet exclusively during mouse preimplantation development (Emb-LPD) is sufficient to cause a compensatory increase in fetal and perinatal growth that correlates positively with increased adult-onset cardiovascular, metabolic and behavioural disease. Here, to investigate early mechanisms of compensatory nutrient provision, we assessed the influence of maternal Emb-LPD on endocytosis within extraembryonic lineages using quantitative imaging and expression of markers and proteins involved. Blastocysts collected from Emb-LPD mothers within standard culture medium displayed enhanced TE endocytosis compared with embryos from control mothers with respect to the number and collective volume per cell of vesicles with endocytosed ligand and fluid and lysosomes, plus protein expression of megalin (Lrp2) LDL-family receptor. Endocytosis was also stimulated using similar criteria in the outer PE-like lineage of embryoid bodies formed from embryonic stem cell lines generated from Emb-LPD blastocysts. Using an in vitro model replicating the depleted amino acid (AA) composition found within the Emb-LPD uterine luminal fluid, we show TE endocytosis response is activated through reduced branched-chain AAs (leucine, isoleucine, valine). Moreover, activation appears mediated through RhoA GTPase signalling. Our data indicate early embryos regulate and stabilise endocytosis as a mechanism to compensate for poor maternal nutrient provision.

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“…It has also been shown that the efficiency of recycling can be modulated by cell density. As described by Foerg et al (2007), massive, compound-unspecific slow-down of endocytosis occurs in confluent MDCK cells. Interestingly, treatment of dense cells with IFN-γ/TNF-α results in restoration of the density-restricted endocytosis possibly by a cytokineinduced redistribution of lipid rafts.…”

Section: Endocytosis Of Cell Surface Receptorsmentioning

confidence: 85%

Modulation of cell surface density of carbonic anhydrase IX by shedding of the ectodomain and endocytosis

Zaťovičová¹,

Pastoreková²

2013

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Summary. -Carbonic anhydrase IX (CA IX) is a cell surface protein frequently present in human tumors but not in the corresponding normal tissues. Expression of CA IX is primarily determined by the strong transcriptional activation of the gene encoding CA IX by hypoxia via the hypoxia-inducible transcription factor HIF-1. However, the ultimate abundance of the CA IX protein on the cell surface can be affected by additional mechanisms, including ectodomain shedding and endocytosis. In this paper, we summarize the basic knowledge on how these processes modulate CA IX expression at the post-translational level. We propose that the regulation of the CA IX protein residence in the plasma membrane can influence its biological function as well as its clinical exploitation.Keywords: carbonic anhydrase IX; ADAM17; ectodomain shedding; proteolysis; endocytosis; monoclonal antibody; hypoxia; cancer * Corresponding author. E-mail: virusipa@savba.sk; phone: +421-2-59302404. Abbreviations: ADAM = a disintegrin and metalloproteinase; ADCC = antibody-dependent cell-mediated cytotoxicity; AE2 = anion exchanger 2; CA IX = carbonic anhydrase IX; CCV = clathrin-coated vesicles; ECD = ectodomain; EGF = epidermal growth factor; HIF = hypoxia-inducible factor; MAb(s) = monoclonal antibody(ies); NBCe1 = sodium bicarbonate cotransporter 1; PRNC = perinuclear compartment; TACE = TNF alpha-converting enzyme

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Differentiation Restricted Endocytosis of Cell Penetrating Peptides in MDCK Cells Corresponds with Activities of Rho-GTPases

Abstract: Our findings emphasize the significance of differentiated cell models in the study of CPP internalization and point towards inflammatory epithelial pathologies as potential niche for the application of CPPs for cellular delivery.

Cited by 52 publications

References 79 publications

Occludin is required for cytokine-induced regulation of tight junction barriers

Occludin is required for cytokine-induced regulation of tight junction barriers

Mouse early extra-embryonic lineages activate compensatory endocytosis in response to poor maternal nutrition

Modulation of cell surface density of carbonic anhydrase IX by shedding of the ectodomain and endocytosis

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