<i>Retracted</i>: Tumor necrosis factor enhances SN38‐mediated apoptosis in mesothelioma cells

Russo, Patrizia; Catassi, Alessia; Malacarne, Davide; Margaritora, Stefano; Cesario, Alfredo; Festi, Luigi; Mulè, Antonino; Ferri, Luigi; Granone, Pierluigi

doi:10.1002/cncr.20924

Cited by 16 publications

(10 citation statements)

References 33 publications

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“…Pleural effusion occurs in many diseases, including parapneumonic effusions, tuberculosis, and malignant pleural mesothelioma (49). Nucleotide-stimulated ENaC channels in human mesothelial cells may govern pleural fluid transport in the pleural cavity in normalcy, inflammatory disorders, and in pleural malignancy, and thereby contribute to homeostatic control of pleural fluid or the pathogenesis of pleural effusions.…”

Section: Discussionmentioning

confidence: 99%

Expression and Regulation of Epithelial Na⁺ Channels by Nucleotides in Pleural Mesothelial Cells

Nie

Tucker²,

et al. 2009

Am J Respir Cell Mol Biol

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Pleural effusions are commonly clinical disorders, resulting from the imbalance between pleural fluid turnover and reabsorption. The mechanisms underlying pleural fluid clearance across the mesothelium remain to be elucidated. We hypothesized that epithelial Na 1 channel (ENaC) is expressed and forms the molecular basis of the amiloride-sensitive resistance in human mesothelial cells. Our RT-PCR results showed that three ENaC subunits, namely, a, b, g, and two d ENaC subunits, are expressed in human primary pleural mesothelial cells, a human mesothelioma cell line (M9K), and mouse pleural tissue. In addition, Western blotting and immunofluorescence microscopy studies revealed that a, b, g, and d ENaC subunits are expressed in primary human mesothelial cells and M9K cells at the protein level. An amiloride-inhibitable short-circuit current was detected in M9K monolayers and mouse pleural tissues when mounted in Ussing chambers. Whole-cell patch clamp recordings showed an ENaC-like channel with an amiloride concentration producing 50% inhibition of 12 mM in M9K cells. This cation channel has a high affinity for extracellular Na 1 ions (K m : 53 mM). The ion selectivity of this channel to cations follows the same order as ENaC: Li 1 . Na 1 . K 1 . The unitary Li 1 conductance was 15 pS in on-cell patches. Four ENaC subunits form a functional Na 1 channel when coinjected into Xenopus oocytes. Furthermore, we found that both forskolin and cGMP increased the short-circuit currents in mouse pleural tissues. Taken together, our data demonstrate that the ENaC channels are biochemically and functionally expressed in human pleural mesothelial cells, and can be up-regulated by cyclic AMP and cyclic GMP.

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Section: Discussionmentioning

confidence: 99%

Expression and Regulation of Epithelial Na⁺ Channels by Nucleotides in Pleural Mesothelial Cells

Nie

Tucker²,

et al. 2009

Am J Respir Cell Mol Biol

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“…Apoptosis was detected using different methods: (1 ) internucleosomal DNA fragmentation; (2 ) annexin V-PI staining; and (3 ) cellular DNA fragmentation ELISA assay, as described previously (21,22).…”

Section: Apoptosismentioning

confidence: 99%

“…DNA damage was evaluated by the alkaline filter elution assay under deproteinizing conditions, as described previously (21).…”

Section: Dna Damagementioning

confidence: 99%

Molecular Mechanisms of Hexavalent Chromium–Induced Apoptosis in Human Bronchoalveolar Cells

Russo

Catassi

Cesario

et al. 2005

Am J Respir Cell Mol Biol

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Hexavalent chromium (Cr[VI]) is classified by the International Agency for Research on Cancer as a group I carcinogen. Although the U.S. Occupational Safety and Health Administration was obliged to reduce the permissible exposure limit (PEL), it was reported that U.S. workers continue to be exposed to dangerously high Cr(VI) levels. In this study, we examined the role of p53 and target genes in a bronchoalveolar carcinoma isogenic cell line system and in primary human bronchial epithelial cells. p53-Negative parental H358 cell line, the same line in which the wild-type p53 expression vector (pC53-SN3) was introduced, and cells obtained from biopsies of human bronchus were exposed to chromate. Induction of DNA strand breaks were evaluated by alkaline elution assay, and apoptosis was analyzed by gel ladder, annexin V-PI staining, and ELISA, whereas p53 and target genes were evaluated by Western blots. Although Cr(VI) induced DNA strand breaks in both H358 cell clones, apoptosis was present only in the p53-transfected cells (H358p53(+/+)). In these cells, Cr(VI)-induced apoptosis is mediated by p53 upregulation of p53-upregulated modulator of apoptosis (PUMA), BAX translocation to mitochondria, cytochrome c release, and caspase-3 activation. In primary human bronchial epithelial cells expressing functional p53, Cr(VI) induced expression of PUMA and Noxa, which promote apoptosis through BAX. This result establishes p53 as the "necessary" player in Cr(VI)-induced apoptosis. To the best of our knowledge, this is the first report indicating strict correlation of Cr(VI) apoptosis to PUMA induction on primary human bronchoalveolar cells in short-term cultures.

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“…The pathogenesis of these diseases may involve increased transmesothelial membrane filtration, reduced fluid reabsorptive transport, pulmonary capillary pressure, decreased negative intrapleural or oncotic pressure, or obstructed lymphatic flow which is a most common complication in mesothelioma, bacterial infection, and tuberculosis [58]. For example, most patients with earlier stage mesothelioma present with pleural effusions [59]. Ion transport systems in mesothelial cells, such as voltage-gated Na + channels [24], not only regulate the balance of fluid turnover and absorption, but also relate to cell proliferation.…”

Section: Physiological and Clinical Relevancementioning

confidence: 99%

Electrolyte and Fluid Transport in Mesothelial Cells

Ji¹,

Nie²

2008

JEBP

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Mesothelial cells are specialized epithelial cells, which line the pleural, pericardial, and peritoneal cavities. Accumulating evidence suggests that the monolayer of mesothelial cells is permeable to electrolyte and fluid, and thereby govern both fluid secretion and re-absorption in the serosal cavities. Disorders in these salt and fluid transport systems may be fundamental in the pathogenesis of pleural effusion, pericardial effusion, and ascites. In this review, we discuss the location, physiological function, and regulation of active transport (Na + -K + -ATPase) systems, cation and anion channels (Na + , K + , Cl − , and Ca 2+ channels), antiport (exchangers) systems, and symport (co-transporters) systems, and water channels (aquaporins). These secretive and absorptive pathways across mesothelial monolayer cells for electrolytes and fluid may provide pivotal therapeutical targets for novel clinical intervention in edematous diseases of serous cavities. Keywords mesothelioma; ion channel; permeability; effusion; filtration; ENaC Mesothelial cells are specialized epithelial cells that line the serous cavities, including the pleural, pericardial, and peritoneal cavities in addition to internal organs [1]. While the mesothelium was first described more than a century ago, one of its critical essential functions, namely, its active roles in transerosal transport, in particular, cavity fluid secretion and reabsorption, was long overlooked. Only in last two decades compelling evidence accumulated that mesothelial cells actively transport electrolytes and fluid and, in turn, regulate liquid volume within the cavities. The mesothelium, on the basis of recent increasing experimental evidence, both in vitro and in vivo, is less permeable to electrolytes than was previously assumed, with ion permeability characteristics similar to those in epithelia [2,3]. Herein this article we will review the expression and biophysical features of salt and fluid transport systems, both active and passive, that have been identified in mesothelial cells (Fig. 1, Tables 1 and 2). I. ION CHANNELS AND ATPASE I-1. Amiloride-Inhibitable Cation ChannelsThe epithelial sodium channel (ENaC), as a major pathway which participates in sodium movement across the apical membrane of polarized epithelial cells, has been cloned and characterized [4][5][6] ENaC subunits have been cloned to date, namely α-, β-, γ-, δ-, and ε-ENaC [7]. The biophysical properties of various ENaC channels depend on their subunit compositions. When expressed in oocytes one of "conductive" subunits (α, δ, and ε-ENaC) can form a channel sharing identical biophysical properties to three-subunit channels composed of both a "conductive" subunit and two "non-conductive" subunits, namely, β-and γ-ENaCs. When α-, β-, and γ-ENaC subunits are assembled together, the result is a 4-to 6-pS channel that is highly selective for Na + over K + . In contrast, two-subunit α β-and α γ-ENaC channels display diverse amiloride sensitivity, conductance, and Na + permeability [8]. ENaC is...

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Retracted: Tumor necrosis factor enhances SN38‐mediated apoptosis in mesothelioma cells

Cited by 16 publications

References 33 publications

Expression and Regulation of Epithelial Na⁺ Channels by Nucleotides in Pleural Mesothelial Cells

Expression and Regulation of Epithelial Na⁺ Channels by Nucleotides in Pleural Mesothelial Cells

Molecular Mechanisms of Hexavalent Chromium–Induced Apoptosis in Human Bronchoalveolar Cells

Electrolyte and Fluid Transport in Mesothelial Cells

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Retracted: Tumor necrosis factor enhances SN38‐mediated apoptosis in mesothelioma cells

Cited by 16 publications

References 33 publications

Expression and Regulation of Epithelial Na+ Channels by Nucleotides in Pleural Mesothelial Cells

Expression and Regulation of Epithelial Na+ Channels by Nucleotides in Pleural Mesothelial Cells

Molecular Mechanisms of Hexavalent Chromium–Induced Apoptosis in Human Bronchoalveolar Cells

Electrolyte and Fluid Transport in Mesothelial Cells

Contact Info

Product

Resources

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Expression and Regulation of Epithelial Na⁺ Channels by Nucleotides in Pleural Mesothelial Cells

Expression and Regulation of Epithelial Na⁺ Channels by Nucleotides in Pleural Mesothelial Cells