Effects mediated by the α7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells

Pernarella, M.; Piovesana, Roberta; Matera, Carlo; Faroni, Alessandro; Fiore, Mario; Dini, Luciana; Reid, Adam J.; Dallanoce, Clelia; Tata, Ada Maria

doi:10.4081/ejh.2020.3159

Cited by 6 publications

(8 citation statements)

References 54 publications

(102 reference statements)

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“…This compound, called ICH3 [(R)-(‒)-3-methoxy-1-oxa-2,7-diaza-7,10-ethanospiro [4.5] dec-2-ene sesquifumarate], has the ability of selectively binding with the α7 receptors. This ability was confirmed by the use of α7 antagonist α-BTX in different rodent cell types [ 80 , 81 ].…”

Section: α7 Nachr Neuropharmacologymentioning

confidence: 90%

Cholinergic Modulation of Neuroinflammation: Focus on α7 Nicotinic Receptor

Piovesana

Intriago

Dini

et al. 2021

IJMS

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All nervous system pathologies (e.g., neurodegenerative/demyelinating diseases and brain tumours) develop neuroinflammation, a beneficial process during pathological events, aimed at removing damaged cells, toxic agents, and/or pathogens. Unfortunately, excessive inflammation frequently occurs during nervous system disorders, becoming a detrimental event capable of enhancing neurons and myelinating glial cell impairment, rather than improving their survival and activity. Consequently, targeting the neuroinflammation could be relevant for reducing brain injury and rescuing neuronal and glial cell functions. Several studies have highlighted the role of acetylcholine and its receptors in the regulation of central and peripheral inflammation. In particular, α7 nicotinic receptor has been described as one of the main regulators of the “brain cholinergic anti-inflammatory pathway”. Its expression in astrocytes and microglial cells and the ability to modulate anti-inflammatory cytokines make this receptor a new interesting therapeutic target for neuroinflammation regulation. In this review, we summarize the distribution and physiological functions of the α7 nicotinic receptor in glial cells (astrocytes and microglia) and its role in the modulation of neuroinflammation. Moreover, we explore how its altered expression and function contribute to the development of different neurological pathologies and exacerbate neuroinflammatory processes.

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Section: α7 Nachr Neuropharmacologymentioning

confidence: 90%

Cholinergic Modulation of Neuroinflammation: Focus on α7 Nicotinic Receptor

Piovesana

Intriago

Dini

et al. 2021

IJMS

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“…nAChR [70]. Indeed, stimulation with ICH3, a selective α7 nAChR agonist, inhibits rat AD-MSCs proliferation.…”

Section: Adipose-derived Mscs (Ad-mscs)mentioning

confidence: 99%

“…Additionally, impaired chondrogenic differentiation of BM-MSCs in response to nicotine has been demonstrated to be mediated through α7 nAChR [69]. Interestingly, the α7 nAChR was shown to inhibit AD-MSCs proliferation however enhances migration [70]. In PDL-MSCs, the α7 nAChR mediates nicotine-induced apoptosis [71], and to an extent impaired these cells' ability to undergo osteogenic differentiation [72].…”

Section: Reaming Debris-derived Mscs (Rd-mscs)mentioning

confidence: 99%

Acetylcholine Receptors in Mesenchymal Stem Cells

Alqahtani

Butcher

Ramage

et al. 2023

Stem Cells and Development

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Mesenchymal stem cells (MSCs) are well known for their regenerative potential. Despite the fact that the ability of MSCs to proliferate and differentiate has been studied extensively, there still remains much to learn about the signalling mechanisms and pathways which control proliferation and influence differentiation phenotype. In recent years, there has been growing evidence for the utility of non-neuronal cholinergic signalling systems and that acetylcholine (ACh) plays an important, ubiquitous, role in cell-to-cell communication. Indeed, cholinergic signalling is hypothesised to occur in stem cells and ACh synthesis, as well as ACh receptor (AChR) expression, has been identified in several stem cell populations; including MSCs. Furthermore, AChRs have been found to influence MSC regenerative potential. In humans, there are two major classes of AChRs, muscarinic AChRs and nicotinic AChRs, with each class possessing several subtypes or subunits. In this review, the expression and function of AChRs in different types of MSC will be summarised with the aim of highlighting how AChRs play a pivotal role in regulating MSC regenerative function.

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“…The activation of nAChRs can induce an increase in the levels of intracellular calcium[ 14 ], which has been related to tumorigenesis in the lungs[ 15 ], liver[ 16 ], pancreas[ 17 ] and brain[ 18 ]. This increase in intracellular calcium can in turn activate kinase signaling pathways[ 19 , 20 ], which regulate different parameters of tumor biology such as proliferation, migration and invasion[ 21 - 23 ].…”

Section: Introductionmentioning

confidence: 99%

Nicotinic receptors modulate antitumor therapy response in triple negative breast cancer cells

Español¹,

Sanchez²,

Salem³

et al. 2022

WJCO

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BACKGROUND Triple negative breast cancer is more aggressive than other breast cancer subtypes and constitutes a public health problem worldwide since it has high morbidity and mortality due to the lack of defined therapeutic targets. Resistance to chemotherapy complicates the course of patients’ treatment. Several authors have highlighted the participation of nicotinic acetylcholine receptors (nAChR) in the modulation of conventional chemotherapy treatment in cancers of the airways. However, in breast cancer, less is known about the effect of nAChR activation by nicotine on chemotherapy treatment in smoking patients. AIM To investigate the effect of nicotine on paclitaxel treatment and the signaling pathways involved in human breast MDA-MB-231 tumor cells. METHODS Cells were treated with paclitaxel alone or in combination with nicotine, administered for one or three 48-h cycles. The effect of the addition of nicotine (at a concentration similar to that found in passive smokers’ blood) on the treatment with paclitaxel (at a therapeutic concentration) was determined using the 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The signaling mediators involved in this effect were determined using selective inhibitors. We also investigated nAChR expression, and ATP “binding cassette” G2 drug transporter (ABCG2) expression and its modulation by the different treatments with Western blot. The effect of the treatments on apoptosis induction was determined by flow cytometry using annexin-V and 7AAD markers. RESULTS Our results confirmed that treatment with paclitaxel reduced MDA-MB-231 cell viability in a concentration-dependent manner and that the presence of nicotine reversed the cytotoxic effect induced by paclitaxel by involving the expression of functional α7 and α9 nAChRs in these cells. The action of nicotine on paclitaxel treatment was linked to modulation of the protein kinase C, mitogen-activated protein kinase, extracellular signal-regulated kinase, and NF-κB signaling pathways, and to an up-regulation of ABCG2 protein expression. We also detected that nicotine significantly reduced the increase in cell apoptosis induced by paclitaxel treatment. Moreover, the presence of nicotine reduced the efficacy of paclitaxel treatment administered in three cycles to MDA-MB-231 tumor cells. CONCLUSION Our findings point to nAChRs as responsible for the decrease in the chemotherapeutic effect of paclitaxel in triple negative tumors. Thus, nAChRs should be considered as targets in smoking patients.

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Effects mediated by the α7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells

Cited by 6 publications

References 54 publications

Cholinergic Modulation of Neuroinflammation: Focus on α7 Nicotinic Receptor

Cholinergic Modulation of Neuroinflammation: Focus on α7 Nicotinic Receptor

Acetylcholine Receptors in Mesenchymal Stem Cells

Nicotinic receptors modulate antitumor therapy response in triple negative breast cancer cells

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