RETRACTED ARTICLE: Modulation of the TGF-β1-induced epithelial to mesenchymal transition (EMT) mediated by P1 and P2 purine receptors in MDCK cells

Zuccarini, Mariachiara; Giuliani, Patricia; Buccella, Silvana; Liberto, Valentina Di; Mudò, Giuseppa; Belluardo, Natale; Carluccio, Marzia; Rossini, Margherita; Condorelli, D. F.; Rathbone, Michel P.; Caciagli, Francesco; Ciccarelli, Renata; Iorio, Patrizia Di

doi:10.1007/s11302-017-9571-6

Cited by 23 publications

(18 citation statements)

References 65 publications

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“…Conversely, when cAMP levels remained low, it seems to mediate the opposite effects, promoting a slight decrease in epithelial markers and an increase in the mesenchymal markers. This controversial nature of the cAMP analogue on the EMT process is in accordance with the recent data reported by Zuccarini et al (2017) .…”

Section: Resultssupporting

confidence: 92%

“…In this respect, we could speculate that the increase in the cAMP, mediated by A 2B AR activation, could counteract the cytokine-mediated effects on EMT. This is in accordance with the ability of other G s coupled receptors (i.e., A 2A AR) or cAMP inducers (i.e., forskolin, 8-Br-cAMP) to prevent TGF-β1-mediated EMT ( Zhang et al, 2006a , b ; Zuccarini et al, 2017 ). It should also be considered that cAMP/PKA has a negative effect on TGF-β induced pERK 1/2, but only when the cytokine downstream pathways are highly expressed ( Weng et al, 2015 ).…”

Section: Discussionsupporting

confidence: 84%

“… Zhang et al (2016) have demonstrated that norepinephrine, which activates G s protein, induces the epithelial-mesenchymal transition in A549 cells; similarly, the P2X7 stimulation, which activates the PI3K/Akt and ERK1/2 signaling pathways, promotes the mesenchymal phenotype in epithelial renal cells ( Zuccarini et al, 2017 ). A 2A ARs have been reported to modify the epithelial/mesenchymal phenotype in renal cells by downregulating TGF-β1-induced EMT ( Zuccarini et al, 2017 ) in accordance with the effects elicited by A 2B AR activation in our cellular model when the cytokine was present. TGF-β1 activates both Smad signaling and non-Smad signaling including the ERK pathway, critically regulating EMT ( Xie et al, 2004 ).…”

Section: Discussionmentioning

confidence: 99%

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The A2B Adenosine Receptor Modulates the Epithelial– Mesenchymal Transition through the Balance of cAMP/PKA and MAPK/ERK Pathway Activation in Human Epithelial Lung Cells

et al. 2018

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The epithelial-mesenchymal transition (EMT) is a complex process in which cell phenotype switches from the epithelial to mesenchymal one. The deregulations of this process have been related with the occurrence of different diseases such as lung cancer and fibrosis. In the last decade, several efforts have been devoted in understanding the mechanisms that trigger and sustain this transition process. Adenosine is a purinergic signaling molecule that has been involved in the onset and progression of chronic lung diseases and cancer through the A2B adenosine receptor subtype activation, too. However, the relationship between A2BAR and EMT has not been investigated, yet. Herein, the A2BAR characterization was carried out in human epithelial lung cells. Moreover, the effects of receptor activation on EMT were investigated in the absence and presence of transforming growth factor-beta (TGF-β1), which has been known to promote the transition. The A2BAR activation alone decreased and increased the expression of epithelial markers (E-cadherin) and the mesenchymal one (Vimentin, N-cadherin), respectively, nevertheless a complete EMT was not observed. Surprisingly, the receptor activation counteracted the EMT induced by TGF-β1. Several intracellular pathways regulate the EMT: high levels of cAMP and ERK1/2 phosphorylation has been demonstrated to counteract and promote the transition, respectively. The A2BAR stimulation was able to modulated these two pathways, cAMP/PKA and MAPK/ERK, shifting the fine balance toward activation or inhibition of EMT. In fact, using a selective PKA inhibitor, which blocks the cAMP pathway, the A2BAR-mediated EMT promotion were exacerbated, and conversely the selective inhibition of MAPK/ERK counteracted the receptor-induced transition. These results highlighted the A2BAR as one of the receptors involved in the modulation of EMT process. Nevertheless, its activation is not enough to trigger a complete transition, its ability to affect different intracellular pathways could represent a mechanism at the basis of EMT maintenance/inhibition based on the extracellular microenvironment. Despite further investigations are needed, herein for the first time the A2BAR has been related to the EMT process, and therefore to the different EMT-related pathologies.

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Section: Resultssupporting

confidence: 92%

Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

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The A2B Adenosine Receptor Modulates the Epithelial– Mesenchymal Transition through the Balance of cAMP/PKA and MAPK/ERK Pathway Activation in Human Epithelial Lung Cells

et al. 2018

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“…Upregulated GS indicated the activation of SGCs. Enhanced P2X7 receptor was co‐expressed with GS (Zuccarini et al, ). Retrograde tracing test showed the sprouting of calcitonin gene‐related peptide (CGRP) or substance P (SP) sensory nerves (the markers of sensory afferent fibers) from dorsal root ganglia (DRG) to SCG neurons.…”

Section: Upregulated P2x Receptors Mediate the Abnormal Interaction Bmentioning

confidence: 99%

P2X receptors mediated abnormal interaction between satellite glial cells and neurons in visceral pathological changes

Wang

Yang

et al. 2019

Cell Biology International

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The adenosine triphosphate (ATP)-gated P2X receptor cation channel family consists of permeable ligand-gated ion channels that expand on the binding of extracellular adenosine 5'-ATP. ATP-gated P2X receptors are trimer ion channels that assemble homo or isomer from seven cloned subunits. P2X receptors are discovered mostly in mammalian and are being found in an increasing number of non-vertebrates, such as zebrafish, bullfrog, and ameba. P2X receptors are involved in many physiological processes, including regulation of heart rhythm and contractility, and regulation of pain, especially chronic pain and glia integration. This review summarizes the current studies on the regulation of P2X receptors in abnormal neuronal-glial interaction and the pathological changes in viscera, especially in myocardial ischemia.

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“…Previous studies showed that imbalance of PAI-1 and t-PA in pleural spaces may lead to fibrin deposition and pleural inflammation [10,11]. Another cytokine, transforming growth factor -beta (TGF-β), a superfamily regulates tissue regeneration can also induce epithelial-mesenchymal transition (EMT) [12,13]. TGF-β might increase the levels of PAI-1 [14,15].…”

Section: Introductionmentioning

confidence: 99%

Predictive Risk Factors of Pleural Tuberculoma Occurrence on Patients with Pleural Tuberculosis

Dong¹,

Zhang²,

Wu³

et al. 2019

Preprint

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Background: Pleural tuberculoma (PTM) had been observed more and more frequently on patients with pleural tuberculosis (PT). The occurrence of PTM is not favorable for the treatment outcome of PT. However, its predictive risk factors had not been clarified. This study was to explore the predictive risk factors of PTM occurrence on the patients with PT. Methods: From January 2017 to June 2018, patients diagnosed as PT were enrolled prospectively into the study. All clinical characteristics and pleural changes during the chemotherapy were recorded and adenosine aminase (ADA)、 lactate dehydrogenase (LDH)、glucose and protein of pleural fluid were quantified. Interferon-gamma (IFN- γ)、 transforming growth factor -beta (TGF-β), plasminogen activator inhibitor type-1 (PAI-1) and tissue plasminogen activator (t-PA) of pleural fluid were tested before chemotherapy by enzyme-linked immunosorbent assay (ELISA). Results: A total of 162 patients with PT were enrolled. 82 patients (51.3%, 82/162) developed PTM during chemotherapy. We found the probability of PT to develop PTM reached 99.5% when the patients with pleural thickness, packaged plural effusion, LDH>461.5 IU/L , ADA>62.9 IU/L , GLU<4.75 mmol/L and age>32.5 years old. The probability to develop PTM was as low as 1.4% when these 6 indices were in the opposite trend to the conditions list above. Using tested cytokines in pleural fluid from 76 cases, the probability of PTM if patients satisfied 3 indexes including increased TGF-β(>15.235 μ g/L) , increased PAI-1(>180.720 μ g/L) and decreased t-PA(<2.875 μ g/L ) was 78%, and the probability to develop PTM was only as low as 2.7% when these 3 cytokines were in the opposite trend. Conclusions: Age, pleural thickness, packaged pleural fluid, increased ADA, LDH, TGF-β, PAI-1 and decreased glucose and t-PA might be predictive risk factors of developing PTM for patients with PT, clinicians should take deep consideration if patients had above factors.

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RETRACTED ARTICLE: Modulation of the TGF-β1-induced epithelial to mesenchymal transition (EMT) mediated by P1 and P2 purine receptors in MDCK cells

Cited by 23 publications

References 65 publications

The A2B Adenosine Receptor Modulates the Epithelial– Mesenchymal Transition through the Balance of cAMP/PKA and MAPK/ERK Pathway Activation in Human Epithelial Lung Cells

The A2B Adenosine Receptor Modulates the Epithelial– Mesenchymal Transition through the Balance of cAMP/PKA and MAPK/ERK Pathway Activation in Human Epithelial Lung Cells

P2X receptors mediated abnormal interaction between satellite glial cells and neurons in visceral pathological changes

Predictive Risk Factors of Pleural Tuberculoma Occurrence on Patients with Pleural Tuberculosis

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