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Introduction: Gallbladder carcinosarcoma (GBCS) is a rare neoplasm, and previous studies regarding to GBCS were case reports/case series, absence of large retrospective analyses, or systemic review. This review summarizes the current literature on accurate information of GBCS to assist clinicians to accurately diagnose and treat this malignancy. Areas covered: The authors retrieved relevant documents of GBCS from PubMed and Medline. This review elaborates on the knowledge of GBCS covering epidemiology, potential mechanism, clinical manifestation, diagnosis, treatment, and prognosis. Expert opinion: The majority of GBCS patients are easily misdiagnosed as GBC and usually treated as GBC. However, the biological behavior and outcome of GBCS is different from that of GBC. GBCS should be considered as a separate disease. [ABSTRACT FROM AUTHOR]

Exercise-induced gastrointestinal syndrome (EIGS) is a common characteristic of exercise. The causes appear to be multifactorial in origin, but stem primarily from splanchnic hypoperfusion and increased sympathetic drive. These primary causes can lead to secondary outcomes that include increased intestinal epithelial injury and gastrointestinal hyperpermeability, systemic endotoxemia, and responsive cytokinemia, and impaired gastrointestinal function (i.e. transit, digestion, and absorption). Impaired gastrointestinal integrity and functional responses may predispose individuals, engaged in strenuous exercise, to gastrointestinal symptoms (GIS), and health complications of clinical significance, both of which may have exercise performance implications. There is a growing body of evidence indicating heat exposure during exercise (i.e. exertional-heat stress) can substantially exacerbate these gastrointestinal perturbations, proportionally to the magnitude of exertional-heat stress, which is of major concern for athletes preparing for and competing in the upcoming 2020 Tokyo Olympic Games. To date, various hydration and nutritional strategies have been explored to prevent or ameliorate exertional-heat stress associated gastrointestinal perturbations. The aims of the current review are to comprehensively explore the impact of exertional-heat stress on markers of EIGS, examine the evidence for the prevention and (or) management of EIGS in relation to exertional-heat stress, and establish best-practice nutritional recommendations for counteracting EIGS and associated GIS in athletes preparing for and competing in Tokyo 2020. [ABSTRACT FROM AUTHOR]

Nanomaterials are a relatively new class of materials that acquire novel properties based on their reduced size. While these materials have widespread use in consumer products and industrial applications, the potential health risks associated with exposure to them remain to be fully characterized. Carbon nanotubes are among the most widely used nanomaterials and have high potential for human exposure by inhalation. These nanomaterials are known to penetrate the cell membrane and interact with intracellular molecules, resulting in a multitude of documented effects, including oxidative stress, genotoxicity, impaired metabolism, and apoptosis. While the capacity for carbon nanotubes to damage nuclear DNA has been established, the effect of exposure on mitochondrial DNA (mtDNA) is relatively unexplored. In this study, we investigated the potential of multi-walled carbon nanotubes (MWCNTs) to impair mitochondrial gene expression and function in human bronchial epithelial cells (BECs). Primary BECs were exposed to sub-cytotoxic doses (up to 3 μg/ml) of MWCNTs for 5 d and assessed for changes in expression of all mitochondrial protein-coding genes, heteroplasmies, and insertion/deletion mutations (indels). Exposed cells were also measured for cytotoxicity, metabolic function, mitochondrial abundance, and mitophagy. We found that MWCNTs upregulated mitochondrial gene expression, while significantly decreasing oxygen consumption rate and mitochondrial abundance. Confocal microscopy revealed induction of mitophagy by 2 hours of exposure. Mitochondrial DNA heteroplasmy and insertion/deletion mutations were not significantly affected by any treatment. We conclude that carbon nanotubes cause mitochondrial dysfunction that leads to mitophagy in exposed BECs via a mechanism unrelated to its reported genotoxicity. [ABSTRACT FROM AUTHOR]

Th17 cells of the intestine and colon can produce several important cytokines during mucosal inflammation. However, few studies have focused on the role of IL-26 in intestinal inflammations. Colonic epithelial cells express receptors for IL-26, and this cytokine has been shown to induce the HT-29 colonic epithelial cell line to produce the chemokine CXCL8. However, epithelial cells would function in a cytokine network environment during mucosal inflammation and any effect of IL-26 on colonic epithelial cell chemokine responses could be affected by the presence of other potent pro-inflammatory cytokines like TNF-α and IL-1. Therefore, we investigated the effect of IL-26 with TNF-α or IL-1 on colonic epithelial cell line secretion of CXCL8. IL-26 alone had no effect on HT-29 or DLD1 cell line CXCL8 secretion. Yet, IL-26 was found to significantly enhance TNF-α-induced, but not IL-1-induced, CXCL8 secretion, but only at high levels of TNF-α. Similar results were seen with DLD1 cells. IL-26 did not enhance TNF-α-induced CXCL8 mRNA levels and did not affect TNF-α-induced IκBα phosphorylation or degradation. However, signaling through ERK and p38 MAPK were determined to be involved in the enhancing effect of IL-26 on the TNF-α-induced CXCL8 secretion, perhaps through known post-translational effects. These results suggest that the role of IL-26 in intestinal inflammation may be limited to enhancing CXCL8 secretion in the presence high levels of TNF-α, such as may occur in inflammatory bowel disease. Abbreviations: DMEM, Dulbecco's Modified Eagle's Medium; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; IBD, inflammatory bowel disease; IL, interleukin; ITS, insulin, transferrin, selenium; TBS, Tris buffered saline; TNF, tumor necrosis factor. [ABSTRACT FROM AUTHOR]

Epithelial cells expressing oncogenic Ras (RasV12) are detected by normal neighbors and are often extruded from tissues. We recently demonstrated that differential EphA2 signaling drives the segregation of mutant cells from normal monolayers via cell repulsion and increased RasV12 cell contractility. EphA2 signaling on RasV12 cells is triggered by ephrin-A ligands presented by normal cells. Here, we show that normal epithelial cells trigger the repulsion and enhanced contractility of Ras-transformed epithelial cells at the single cell level. We also reveal that ephrin-A ligands expressed on RasV12 cells are not required to drive RasV12 cell segregation following interaction with normal cells. Thus, normal-RasV12 cell-cell interaction triggers EphA2 forward signaling in RasV12 cells to drive repulsion and segregation of the transformed cells. [ABSTRACT FROM AUTHOR]

Conjunctival epithelial inclusion cysts are an infrequent complication in anophthalmic sockets. The ocular prosthesis may become difficult to retain or it may cause local discomfort. Treatment options described include surgical resection, marsupialisation, and the use of injected sclerosing agents. We present a case of a 27-year-old female who developed a conjunctival epithelial inclusion cyst two years after a left eye evisceration. This invariably caused the ocular prosthesis to become cosmetically unacceptable. Trichloroacetic acid 20% (TCA) was injected intracystically as a minor procedure at the slit lamp. Four months later there was no recurrence of the cyst and the prosthesis retained an excellent position in the socket. This case highlights the successful treatment of a conjunctival epithelial inclusion cyst with TCA (20%) without the need for a surgical procedure. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study is to establish the short tandem repeat (STR) profiles of several human cell lines commonly used in ocular surface research. Materials and Methods: Independently DNA was extracted from multiple passages of three human corneal epithelial cell lines, two human conjunctival epithelial cell lines and one meibomian gland cell line, from different laboratories actively involved in ocular surface research. The samples were then subjected to STR analysis on a fee-for-service basis in an academic setting and the data compared against that in available databases. Results: The STR profiles for the human corneal epithelial cells were different among the three cell lines studied and for each line the profiles were identical across the samples provided by three laboratories. Profiles for the human conjunctival epithelial cells were different among the two cell lines studied. Profiles for the meibomian gland cell line were identical across the samples provided by three laboratories. No samples were contaminated by elements of other cell lines such as HeLa. Conclusions: This comprehensive study provides verification of STR profiles for commonly used human ocular surface cell lines that can now be used as a reference by others in the field to authenticate the cell lines in use in their own laboratories. [ABSTRACT FROM AUTHOR]

This study examines dose effects of cadmium telluride quantum dots (CdTe-QDs) from two commercial sources on model macrophages (J774A.1) and colonic epithelial cells (HT29). Effects on cellular immune signalling responses were measured following sequential exposure to QDs and Pseudomonas aeruginosa strain PA01. At CdTe-QD concentrations between 10-2 and 10 µg/ml, cells exhibited changes in metabolism and morphology. Confocal imaging revealed QD internalisation and changes in cell-cell contacts, shapes and internal organisations. QD doses below 10-2 µg/ml caused no observed effects. When QD exposures at 10-7 to 10-3 µg/ml preceded PA01 (107 bacteria/ml) challenges, there were elevated cytotoxicity (5-22%, p < 0.05) and reduced levels (two- to fivefold, p < 0.001) of nitric oxide (NO), TNF-α, KC/CXC−1 and IL-8, compared with PA01 exposures alone. These results demonstrate that exposures to sub-toxic levels of CdTe-QDs can depress cell immune-defence functions, which if occurred in vivo would likely interfere with normal neutrophil recruitment for defence against bacteria. [ABSTRACT FROM AUTHOR]

Abstract: Ovarian cancer is the most common cause of death among women with gynecologic malignancies. The standard management is maximal surgical cytoreduction followed by systemic chemotherapy. The aim of this retrospective study is to evaluate ovarian cancer cases presented at Alexandria Clinical Oncology Department (ACOD) during the years 2008–2010. Methods and materials: We reviewed the files of all patients presented at or referred to ACOD from January 2008 till December 2010 with the diagnosis of ovarian cancer, ovarian epithelial tumor, ovarian sex cord tumors, border line ovarian tumor and ovarian germ cell tumors. Results: The study included 116 patients, representing 1.4% of all cancer cases; the mean age for all patients was 47.9±13.9years. Only 13.7% of the patients had positive family history. Stages III and IV were seen in 79.2% of the cases. Epithelial ovarian cancer (EOC) constituted 75% of the cases, border line tumors 12.9%, granulosa cell tumor 6%, and germ cell tumors 4.3%. Among EOC, serous cystadenocarcinoma was seen in 58%. For EOC, surgery was the initial step in 80.4% of the cases. Paclitaxel-carboplatin was the most commonly used regimen as first line chemotherapy. Response rate to first line chemotherapy reached 87.3% (44.8% complete response). The mean follow up period was 15months. The progression free survival for EOC after first line chemotherapy was 10.8months. Conclusion: The age incidence of ovarian cancer in our patients is 10years younger than that seen in Western countries. EOC constitutes the majority among all ovarian cancer cases, followed by border line tumors. Papillary serous cystadenocarcinoma predominates other types of EOC. The response rate of EOC to first line chemotherapy was high but the progression free survival was lower than that seen in the literature. [Copyright &y& Elsevier]

The extracellular matrix (ECM) plays an essential role in organizing tissues, defining their shapes or in presenting growth factors. Their components have been well described in most species, but our understanding of the mechanisms that control ECM remodeling remains limited. Likewise, how the ECM contributes to cellular mechanical responses has been examined in few cases. Here, I review how studies performed in C. elegans have brought several significant advances on those topics. Focusing only on epithelial cells, I discuss basement membrane invasion by the anchor cell during vulva morphogenesis, a process that has greatly expanded our knowledge of ECM remodeling in vivo. I then discuss the ECM role in a novel mechanotransduction process, whereby muscle contractions stimulate the remodeling of hemidesmosome-like junctions in the epidermis, which highlights that these junctions are mechanosensitive. Finally, I discuss progress in defining the composition and potential roles of the apical ECM covering epidermal cells in embryos. [ABSTRACT FROM AUTHOR]

How cells sense and respond to mechanical forces is attracting considerable attention. We recently demonstrated that mechanical tension originating from one tissue strongly influences the differentiation and morphogenesis of another tissue during C. elegans embryogenesis (Nature 471: 99-103). Specifically, we found that the repeated contractions of muscle cells stimulate a signaling cascade involving the Rac GTPase within the epidermis. This pathway ultimately leads to strengthen hemidesmosome-like junctions and promote embryonic morphogenesis. Our work provides further evidence that mechanical inputs impact on development, much like inputs involving growth factors and morphogens. After briefly outlining the pioneering work that inspired us, I will present the mechanotransduction process underlying the response to tension and the key experiments supporting our conclusions. [ABSTRACT FROM AUTHOR]

The authors investigated the mechanisms by which hypoxia regulates glutathione (GSH) in lung epithelial cells, and specifically whether the mitogen-activated protein kinase (MAPK) system is involved in the response to hypoxia. Hypoxia decreased cellular GSH content and appeared to decrease the effect of N-acetylcysteine on repletion of GSH after hypoxia. Hypoxia decreased 2 key enzyme activities that regulate GSH synthesis, glutamate cysteine ligase (GCL) (E.C. 6.3.2.2) and glutathione synthase (GS) (E.C. 6.3.2.3). No hypoxia-dependent change occurred in GCL or GS protein expression on Western blots. When epithelial cells were transfected with an adenoviral vector that caused over expression of human catalase protein (Ad.Cat or Ad.mCat), GCL and GS activities did not decrease in hypoxia. Inhibition of p38MAPK (using SB203580) or extracellular signal-regulated kinase (ERK; PD98059) prevented the hypoxia-dependent decrease in GCL and GS activity. To seek in vivo correlation, the authors assayed total glutathione in lungs and livers from MK2−/− (homozygous knockout) mice. MK2−/− mice are presumably unable to phosphorylate heat shock protein 27 (Hsp27) normally, because of absent kinase (MK2) activity. Liver GSH content (expressed per mg protein) was 20% less in MK2−/− mice than in nontransgenic Black 6 controls. Down-regulation of lung GSH content in hypoxia depends on peroxide tone of the cell and the p38MAPK system. [ABSTRACT FROM AUTHOR]

Two novel cholesterol-based cytofectins containing primary amino head groups, glycylcholesteryl formylhydrazide (MS10) and β-alanylcholesterylformylhydrazide (MS11), have been prepared and incorporated into unilamellar cationic liposomes in equimolar amounts with dioleoylphosphatidylethanolamine (DOPE) as colipid. Stable lipoplexes were formed with pGL3 DNA which afforded protection to the DNA from serum nuclease digestion. Packing of the DNA was shown by ethidium displacement to be more effective in MS11 lipoplexes. High transfection levels in three human transformed epithelial cell lines HeLa (cervical), SNO (esophageal), HepG2 (hepatocyte-derived), and the murine fibroblast line NIH-3T3 were achieved by both lipoplexes at liposome:DNA ratios of 6:1 and 7:1 (w/w) corresponding to +/- charge ratios of 1.6:1 and 1.9:1. MS11 lipoplexes, in particular, afforded high transfection activities in the presence of fetal bovine serum. [ABSTRACT FROM AUTHOR]

Purpose: The first reports that ionizing radiation (IR) induces rapid and persistent activation of transforming growth factor β1 (TGFβ) were nearly two decades ago. Subsequent studies have shown that TGFβ is a major mediator of cellular and tissue responses to IR and have revealed novel facets of its complex biology. Results: We and others have recently shown that inhibition of production or signaling of TGFβ in epithelial cells modulates radiosensitivity and impedes activation of the DNA damage response program. The primary transducer of cellular response to DNA damage caused by ionizing radiation is the nuclear protein kinase ataxia telangiectasia mutated, whose activity is severely compromised when TGFβ is inhibited. Thus, in conjunction, with its well-recognized contribution to normal tissue fibrosis, the role of TGFβ in the genotoxic stress program provides a previously unsuspected avenue to modulate radiotherapy. Conclusions: We hypothesize that identification of the circumstances and tumors in which TGFβ manipulation enhances tumor cell radiosensitivity, while protecting normal tissues, could significantly increase therapeutic index. [ABSTRACT FROM AUTHOR]

Autocrine production of growth factors can have significant effects on cell activity. We report for the first time that autocrine production of insulin-like growth factor-I (IGF-I) alters paracellular transport across bovine mammary epithelial cells in vitro. Paracellular transport was assessed by measuring phenol red transport across mammary alveolar cells-large T antigen (MAC-T cells) derived from parental mammary epithelial cells, cultured on porous membranes and compared with two different transfected MAC-T cell lines that constitutively secrete IGF-I. Phenol red transport was essentially blocked in parental cell culture after six days, while IGF-I secreting cells provided essentially no barrier. Surprisingly, neither co-culture studies between parental and IGF-I-secreting cells nor addition of exogenous IGF-I or IGF-binding protein-3 reversed the phenol red transport properties. IGF-I-secreting cells did however express lower levels of the junction components occludin and E-cadherin than parental cells, suggesting that localized autocrine IGF-I activity might lead to increased permeability via changes in both the tight and adherens junction protein levels. [ABSTRACT FROM AUTHOR]

Mammary epithelial side population cells have been suggested as candidate mammary stem cells. To date, for technical reasons, these cells have been poorly defined and cross-comparison of data between different laboratories has been difficult. Here, we set out to define mammary side population cells in a way that improves the ability to carry out such comparisons. Mouse mammary epithelial cells were stained with Hoechst 33342. Light scatter, PI staining and clonogenicity of different regions of the Hoechst profile were examined. Time–course analyzes of Hoechst 33342 loading were carried out. Detailed examination of the light scatter and PI staining of Hoechst 33342-stained mammary cells enabled single live side population and non-side population cells to be defined with greater accuracy. Comparison of ABC pump inhibitors identified potential discrepancies in results obtained using these inhibitors. Time–course analyzes enabled side populations cells to be identified as a dynamic cell population that could be defined accurately by using the relationship between Hoechst 33342-staining profiles of consecutive time points. Defining the side population of solid tissues as a ‘stabilized side population percentage’ will enable a more rigorous study of the side population phenomenon and improve evaluation of results from different laboratories. [ABSTRACT FROM AUTHOR]

Purpose. To investigate the in Vitro and in vivo proliferative capacity of human conjunctival epithelial cells cultured in serum-free media, and to compare this with current methods that utilize serum-containing media and 3T3 feeder layers. Methods. Human conjunctival epithelial cells were cultivated in serum-free media alone, serum-free media with a 3T3 feeder layer. and serum-containing media with a 3T3 feeder layer. The areas of outgrowth, colony-forming efficiencies and number of population doublings were compared. The in vivo proliferative potential was assessed by analyzing the number of cells generated by the implantation of cultured cells into athymic mice. Cultured cells were evaluated for the expression of cytokeratins K3, K4, K12, K19, as well as the get-forming goblet cell mucin. MUC5AC. Results. Cells cultivated in serum-free media, serum-free media and feeder cells, and serum-containing media and feeder cells achieved colony-forming efficiencies of 14.5 ± 4.1%. 10.1 ± 3.1%. and 20.4 ± 6.7%. respectively, and number of population doublings of 24.8 ± 4.3. 14.8 ± 3.6, and 30.0 ± 5.0, respectively. Nine-day old athymic mice conjunctival cysts derived from serum-free cultures comprised 1.29 × 106 ± 0.46 × 106 cells, while cysts derived from serum-containing cultures comprised 1.30 × 106 ± 0.53 × 106 cells. The degree of epithelial stratification was similar in both conditions. Serum-free cultivated conjunctival cells retained their in vivo characteristics and expressed K4, K19 and MUC5AC. The presence of MUC5AC rnRNA in these cells was confirmed by RT-PCR. Conclusions. Conjunctival epithelial cells propagated in serum-free media demonstrated a similar in vivo proliferative capability, as compared to serum-containing media with 3T3 feeder cells. This has important clinical implications, as the serum-free ex vivo expansion of cells for clinical transplantation overcomes the problems associated with the use of animal serum and cells. [ABSTRACT FROM AUTHOR]

A case of cerebellopontine angle epithelial cyst is described. Lesions in this region usually present with hearing loss, tinnitus, dysequilibrium, headaches, facial numbness and occasionally trigeminal neuralgia. Our patient presented with the unusual phenomenon of episodic facial palsy. The literature reporting this lesion as well as this mode of presentation has been reviewed. [ABSTRACT FROM AUTHOR]

The nasal epithelium protects the underlying tissue from damage. Epithelial cell growth is controlled by epidermal growth factor (EGF) and is possibly affected by toxic proteins, e.g. eosinophil cationic protein (ECP). The aims of this study were to examine nasal fluid epithelial cell counts and their relations to EGF, eosinophils and ECP in 23 patients with seasonal allergic rhinitis and 20 healthy controls. Nasal fluid epithelial cell counts were lower in patients than in controls. EGF levels did not differ between patients and controls, and correlated with epithelial cell counts in controls but not in patients. Eosinophils and ECP were higher in patients than in controls, but did not correlate with epithelial cell counts. The role of growth factors, such as EGF, in regulating epithelial cells merits further study. [ABSTRACT FROM AUTHOR]

Basal cells exist as a separate layer of cells covering most of the airway basal lamina. In this central position, they can interact with columnar epithelium, neurons, basement membrane, and the underlying mesenchymal cells. In addition, they interact with inflammatory cells, lymphocytes and dendritic cells. These interactions take place in the lateral intercellular space between basal cells. In this central position basal cells become a very important part of the epithelial-mesenchymal trophic unit of larger airways. In this review it is shown that basal cells may function as progenitor cells of airway epithelium and have a role in attachment of columnar epithelium with the basement membrane. They also have the potential to function in regulation of neurogenic inflammation, the inflammatory response, transepithelial water movement, oxidant defense of the tissue and formation of the lateral intercellular space. Other characteristics of basal cells were not clearly associated with a particular function. The functions for basal cells listed attempt to explain the presence of recently identified molecules in basal cells of airway epithelium. It should be pointed out that specific studies have not been carried out which test the relationship between the molecular functions we describe in this review and the basal cell in airway epithelium. [ABSTRACT FROM AUTHOR]

Type 2 pneumocytes are progenitor cells of alveolar epithelium and important for re-epithelialization following lung injury. This study examined the role of persistent versus transient mitogen-activated protein (MAP) kinase (extracellular signal-regulated kinase; ERK) in type 2 cell proliferation. Three different types of agents; epidermal growth factor (EGF), 12-O-tetradecanoylphorbol-13-acetate (TPA), and fetal bovine serum (FBS) induced different patterns of ERK activation. FBS induced a strong and persistent MAP kinase response, whereas the effect of EGF was transient with a strong activation at 5 minutes and only a slight stimulation at 4 hours. The TPA response was more prolonged than the EGF response, but not by far as strong and persistent as the FBS response. Activation by EGF and TPA and the early response induced by FBS were strongly reduced by the MEK inhibitor PD98059. The sustained FBS-induced ERK activation was inhibited by 50%. The total number of cells, the percentage of cells in S and G[sub 2]/Mphase of the cell cycle and the incorporation of [sup 3]H-thymidine into DNA were strongly increased in response to FBS, whereas EGF and TPA were without effect. The proliferation was reduced by 50% after pretreatment with PD98059. The results indicate that a persistent ERK activation of a critical size leads to type 2 cell proliferation, and that the proliferative response may also depend on a MEK-independent ERK activation. [ABSTRACT FROM AUTHOR]

We examined whether transalveolar fluid transport is modulated by aldosterone in adult rats. Because colocalization of mineralocorticoid receptors (MR) with 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) is important for aldosterone specific action, we first determined the immunohistochemical distribution of MR and 11βHSD2 in the lung. We found that alveolar epithelial cells express both MR and 11βHSD2. Reverse transcriptase polymerase chain reaction (RT-PCR) demonstrated that rat alveolar type II epithelial cells express both MR and 11βHSD2. We then measured alveolar fluid clearance in rats treated with chronic low-sodium diet. A low-sodium diet (0.1% NaCl for 12 to 14 days) caused hyperaldosteronism accompanied by hypokalemia, whereas serum corticosterone and adrenaline levels remained normal. We found that hyperaldosteronism was associated with significantly higher alveolar fluid clearance and that this increase was related to the amiloride-sensitive component. In addition, the increase in alveolar fluid clearance was inhibited by spironolactone. Our results show that aldosterone is able to stimulate Na[sup +] channels of alveolar epithelial cells. We conclude that alveolar epithelium is a physiological target tissue for aldosterone and transalveolar fluid absorption could in part be modulated by endogenous aldosterone acting via MR. [ABSTRACT FROM AUTHOR]

The influence of cell differentiation and proliferation on cationic vector mediated gene transfer into the explant-outgrowth cell culture from nasal polyps was investigated. Respiratory cells were categorized into two groups based on the expression of cytokeratin filaments (CKs), which were used as differentiation markers. Outgrowths grown for 2 weeks expressed similar levels of CKs 14, 13 and 18 showing a de-differentiated phenotype, while outgrowths cultured for 4 weeks presented very high levels of CK 13, high CK 14 and low CK 18 expression and were squamous differentiated. De-differentiated cells presented higher proliferation indexes than squamous cells. Gene transfer levels, as evaluated using a quantitative reporter gene (firefly luciferase), were significantly higher in the 2- than in the 4-week-old outgrowths. Cationic vector transfected respiratory cells were located both proximally and distally to the explant, as shown by enzymatic staining of β-galactosidase-positive cells. Respiratory cell outgrowths from nasal polyps can be considered a suitable model to study gene transfer protocols in vitro. [ABSTRACT FROM AUTHOR]

The cytoskeleton is crucially important for the assembly of cell-cell junctions and the homeostatic regulation of their functions. Junctional proteins act, in turn, as anchors for cytoskeletal filaments, and as regulators of cytoskeletal dynamics and signalling proteins. The cross-talk between junctions and the cytoskeleton is critical for the morphogenesis and physiology of epithelial and other tissues, but is not completely understood. Microtubules are implicated in the delivery of junctional proteins to cell-cell contact sites, in the differentiation and spatial organization of the cytoplasm, and in the stabilization of the barrier and adhesive functions of junctions. Here we focus on the relationships between microtubules and junctions of vertebrate epithelial cells. We highlight recent discoveries on the molecular underpinnings of microtubule-junction interactions, and report new data about the interaction of cingulin and paracingulin with microtubules. We also propose a possible new role of junctions as "molecular sinks" for microtubule-associated signalling proteins. [ABSTRACT FROM AUTHOR]