The subapical compartment and its role in intracellular trafficking and cell polarity

IJzendoorn, Sven C. D. van; Maier, Olaf; Wouden, Johanna M. van der; Hoekstra, Dick

doi:10.1002/1097-4652(200008)184:2<151::aid-jcp2>3.0.co;2-r

Cited by 50 publications

(32 citation statements)

References 89 publications

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“…In hepatocytes, the SAC, the equivalent of the common endosome in other epithelial cells (van IJzendoorn and Hoekstra, 1999b;van IJzendoorn et al, 2000) plays a crucial role in polarity development. In previous studies, we have demonstrated that polarity development in HepG2 cells requires the activation of a vesicular trafficking route exiting SAC and directed toward the developing BC, which can be monitored by the flow of the fluorescent probes C 6 -NBD-SM and C 6 -NBD-GalCer Hoekstra, 1999a,b, 2000).…”

Section: G 1 -S Phase Transition Pertubs Oncostatin M-regulated Polarmentioning

confidence: 77%

“…The activation of this membrane trafficking pathway has previously been demonstrated to play an important role in apical-basolateral polarity development in HepG2 cells (van IJzendoorn and Hoekstra, 1999a,b;van IJzendoorn et al, 2000;Hoekstra et al, 2004). OSM-stimulated membrane trafficking from SAC to the developing apical surface is dependent on intact microtubules (unpublished data).…”

Section: Discussionmentioning

confidence: 99%

“…Accurate estimation of the degree of HepG2 polarity was performed as described previously van IJzendoorn and Hoekstra, 2000). Briefly, the cells were fixed with Ϫ20°C ethanol for 10 s, rehydrated in Hank's balanced slat solution (HBSS), and subsequently incubated with a mixture of tetramethylrhodamine B isothiocyanate-labeled phalloidin (Molecular Probes, Eugene, OR) and 5 ng/ml the nuclear stain Hoechst 33528 (Sigma-Aldrich) at room temperature for 30 min.…”

Section: Determination Of Hepg2 Cell Polaritymentioning

confidence: 99%

“…As shown in Figure 2A, HepG2 cells acquire PM polarity in time, as evidenced by the ratio BC/100 cells, and reach optimal polarity 3 d after plating (Figure 2A; c.f. van IJzendoorn and Hoekstra, 2000). Treatment of the cells with dibutyryl (db) cAMP or the interleukin-6 family cytokine oncostatin M stimulates polarity development, i.e., apical PM biogenesis in HepG2 cells (Figure 2A, black bars and gray bars, respectively, c.f.…”

Section: Cell Polarity Development Is Positively Correlated With P27 mentioning

confidence: 99%

“…The SAC plays a prominent role in the polarized delivery of proteins and lipids, and thus in maintaining cell surface polarity (Ihrke et al, 1998; van IJzendoorn and Hoekstra, 1999a,b;Rahner et al, 2000; van IJzendoorn and Mostov, 2000). Moreover, polarized membrane traffic from SAC is also important for the de novo biogenesis of apical PM domains (van IJzendoorn and Hoekstra, 2000), triggered by extracellular stimuli, including OSM (van der Wouden et al, 2002) and those that elicit cAMP/PKA signaling cascades (Zegers and Hoekstra, 1997). Indeed, we have previously shown that OSM activates a vesicular membrane trafficking pathway from SAC to the apical PM, which is dependent on cAMP/PKA activity (van der Wouden et al, 2002).…”

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confidence: 99%

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Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

IJzendoorn

Théard

Wouden

et al. 2004

MBoC

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Oncostatin M regulates membrane traffic and stimulates apicalization of the cell surface in hepatoma cells in a protein kinase A-dependent manner. Here, we show that oncostatin M enhances the expression of the cyclin-dependent kinase (cdk)2 inhibitor p27 Kip1 , which inhibits G 1 -S phase progression. Forced G 1 -S-phase transition effectively renders presynchronized cells insensitive to the apicalization-stimulating effect of oncostatin M. G 1 -S-phase transition prevents oncostatin M-mediated recruitment of protein kinase A to the centrosomal region and precludes the oncostatin M-mediated activation of a protein kinase A-dependent transport route to the apical surface, which exits the subapical compartment (SAC). This transport route has previously been shown to be crucial for apical plasma membrane biogenesis. Together, our data indicate that oncostatin M-stimulated apicalization of the cell surface is critically dependent on the ability of oncostatin M to control p27 Kip1 /cdk2-mediated G 1 -S-phase progression and suggest that the regulation of apical plasma membrane-directed traffic from SAC is coupled to centrosome-associated signaling pathways. INTRODUCTIONThe establishment and maintenance of apical and basolateral plasma membrane (PM) domains in epithelia require a careful orchestration of extra-and intracellular signals, triggering crucial cytoskeleton-, organelle-, and membrane traffic-linked machineries, as partly elucidated in systems as diverse as yeast, Drosophila, and mammalian cells (Lecuit and Pilot, 2003;Mostov et al., 2003;Baas et al., 2004). Impairment of these events may cause a loss of apical-basolateral asymmetry and may lead to deranged cell growth (Bilder et al., 2000;Vermeer et al., 2003;Baas et al., 2004) or spindle misorientation . Recent studies have reported an evolutionary conserved genetic program that may link the process of polarity development and proliferation (Bilder et al., 2000;Humbert et al., 2003;Rolls et al., 2003;Klezovitch et al., 2004). However, many aspects of such a link remain unclear, e.g., the extent to which cell proliferation can directly affect epithelial cell organization or vice versa. Indeed, epithelial cell proliferation and apical-basolateral polarity may be controlled by different signaling pathways (Liu et al., 2004).Signaling cascades stimulated by interleukin-6 family cytokines, including oncostatin M (OSM), elicit multiple responses in the cell. Originally, as its name indicates, oncostatin M was primarily recognized to inhibit the proliferation of tumor cells (Tanaka and Miyajima, 2003), presumably by modulating cell cycle regulatory proteins, including the cyclin-dependent kinase (cdk)2-inhibitor p27 Kip1 (Kortylewski et al., 1999;Klausen et al., 2000;Li et al., 2001). Disruption of the regulatory system that controls G 1 -phase progression is a common event in human hepatocarcinogenesis (Hui et al., 1998), and p27 Kip1 has been associated with differentiation, invasiveness, and metastasis of hepatocellular carcinoma tumors (Zhou et al., 2003). ...

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Section: G 1 -S Phase Transition Pertubs Oncostatin M-regulated Polarmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Determination Of Hepg2 Cell Polaritymentioning

confidence: 99%

Section: Cell Polarity Development Is Positively Correlated With P27 mentioning

confidence: 99%

mentioning

confidence: 99%

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Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

IJzendoorn

Théard

Wouden

et al. 2004

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The maintenance and generation of membrane polarity in hepatocytes

Wang

Boyer

2004

Hepatology

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H epatocytes, the major epithelial cells in the liver, are highly polarized. Their plasma membranes are separated by tight junctions into sinusoidalbasolateral and canalicular-apical domains, which contain distinct sets of proteins and lipids. A normal membrane polarity is vital for hepatocytes to perform many diverse functions, such as canalicular bile secretion and simultaneous sinusoidal secretion of large quantities of serum proteins into blood. Hepatocyte polarity is lost in many diseases like cholestasis. A complete understanding of the molecular mechanisms involved in hepatocyte polarity therefore is of considerable significance to both liver cell biology and the pathogenesis of liver diseases.To maintain the distinct distribution of proteins and lipids in the canalicular and sinusoidal membranes, hepatocytes have developed complex polarized trafficking and retention mechanisms. The establishment of membrane polarity in hepatocytes begins during liver embryogenesis. During hepatocyte differentiation, specific routes and mechanisms are defined for the delivery of plasma membrane proteins. How this polarity is maintained in adult hepatocytes and is generated during development are two major unanswered questions in this field.In this review, we first give an overview of the current knowledge about how membrane polarity is maintained in hepatocytes with the focus on recent developments in polarized protein trafficking. We then present a hypothetical model about how membrane polarity may be generated during liver development, and finally, we present an example of how membrane polarity is altered in cholestasis. Readers are directed to recent reviews for discussion of lipid trafficking in hepatocytes. 1,2

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Ocsyn, a Novel Syntaxin-Interacting Protein Enriched in the Subapical Region of Inner Hair Cells

Safieddine

Wang

et al. 2002

Molecular and Cellular Neuroscience

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The subapical compartment and its role in intracellular trafficking and cell polarity

Cited by 50 publications

References 89 publications

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

The maintenance and generation of membrane polarity in hepatocytes

Ocsyn, a Novel Syntaxin-Interacting Protein Enriched in the Subapical Region of Inner Hair Cells

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The subapical compartment and its role in intracellular trafficking and cell polarity

Cited by 50 publications

References 89 publications

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27Kip1-Regulated Cell Cycle Dynamics

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27Kip1-Regulated Cell Cycle Dynamics

The maintenance and generation of membrane polarity in hepatocytes

Ocsyn, a Novel Syntaxin-Interacting Protein Enriched in the Subapical Region of Inner Hair Cells

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Product

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Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics

Oncostatin M-stimulated Apical Plasma Membrane Biogenesis Requires p27^Kip1-Regulated Cell Cycle Dynamics