The Nicotinic Acetylcholine Receptor: Structure and Autoimmune Pathology

Conti‐Tronconi, Bianca M.; McLane, Kathryn E.; Raftery, Michael A.; Grando, Sergei A.; Protti, Maria Pia

doi:10.3109/10409239409086798

Cited by 145 publications

(105 citation statements)

References 361 publications

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“…The anti--BT-binding site titre in serum against rAChR was below detection level (data not shown). Since the structural homology between the -BT-binding site of rAChR and tAChR is very high [28,29], we measured the inhibition of 125 I--BT binding to the -BT-binding site of tAChR using purified IgG derived from serum of young and aged rats. Total IgG antibody levels against tAChR were about four times higher in females, regardless of age.…”

Section: Anti-achr Antibody Fine Specificitymentioning

confidence: 99%

Age- and sex-related resistance to chronic experimental autoimmune myasthenia gravis (EAMG) in Brown Norway rats

Hoedemaekers¹,

Graus²,

Vriesman³

et al. 1997

Clinical and Experimental Immunology

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SUMMARYThe influence of age and sex on the induction of chronic EAMG was analysed. Aged male rats, immunized with Torpedo acetylcholine receptor (tAChR), showed no clinical signs of disease or AChR loss. Immunization of young male Brown Norway (BN) rats resulted in both clinical signs of disease and 65% AChR loss. In contrast, both young and aged female BN rats showed comparable AChR loss (58% and 50%, respectively), although aged female rats did not develop clinical signs of disease. Differences in antibody titres, isotype distribution, fine specificity or complement activation could not account for the observed resistance. These results suggest that resistance against EAMG in aged rats is due to resistance of the AChR against antibody-mediated degradation, or to mechanisms able to compensate for AChR loss.

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Section: Anti-achr Antibody Fine Specificitymentioning

confidence: 99%

Age- and sex-related resistance to chronic experimental autoimmune myasthenia gravis (EAMG) in Brown Norway rats

Hoedemaekers¹,

Graus²,

Vriesman³

et al. 1997

Clinical and Experimental Immunology

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“…Recent evidence indicates that nAChRα7 (as well as other subtypes) are also expressed by numerous non-neuronal cell types including distinct populations of astrocytes, epithelial cells, adipocytes, lymphocytes, macrophages and keratinocytes (Conti-Tronconi et al, 1994;Gahring and Rogers, 2005;Kurzen et al, 2007;Misery, 2004). In this context, nAChRα7, in addition to its role in depolarization, exhibits remarkably high calcium permeability that is sufficient to impact on intracellular signaling pathways including those using ERK and CREB (Brunzell et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Neuronal nicotinic alpha7 receptors modulate inflammatory cytokine production in the skin following ultraviolet radiation

Osborne-Hereford

Rogers

Gahring

2008

Journal of Neuroimmunology

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The anti-inflammatory effects of the neuronal nicotinic receptor alpha7 (nAChRα7) are proposed to require acetylcholine release from vagal efferents. The necessity for vagal innervation in this antiinflammatory pathway was tested in the skin, which lacks parasympathetic innervation, using ultraviolet radiation (UVB) to induce a local pro-inflammatory response. Cytokine responses to UV in mice administered chronic oral nicotine, a nAChR agonist, were reduced. Conversely, nAChRα7 knock-out mice exposed to UVB elicit an enhanced pro-inflammatory cytokine response in the skin. Altered pro-inflammatory responses correlated with changes in SOCS3 protein. These results demonstrate that nAChRα7 can participate in modulating a local pro-inflammatory response in the absence of parasympathetic innervation.

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“…Exposure of Het-1A or BEP2D cells to either NNK or NNN in both cases increased their proliferative potential which could be abolished in the presence of the nAChR antagonist α-bungarotoxin that worked most effectively against NNK or mecamylamine that was most efficient against NNN. α-Bungarotoxin is a specific inhibitor of the "central" subtype of the neuronal nAChRs, such as α7; and mecamylamine is a preferential blocker of the "ganglionic" nAChR subtypes, such as α3-or α4-made nAChRs (14). Treatment of Het-1A or BEP2D cells with either NNK or NNN facilitated the anchorage-independent growth, which could be inhibited by antagonists.…”

Section: Introductionmentioning

confidence: 99%

Basic and Clinical Aspects of Non-neuronal Acetylcholine: Biological and Clinical Significance of Non-canonical Ligands of Epithelial Nicotinic Acetylcholine Receptors

Grando

2008

J Pharmacol Sci

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Abstract. Mucocutaneous keratinocytes and bronchial epithelial cells express nicotinic acetylcholine receptors (nAChRs). Emerging evidence indicates that nAChRs can be stimulated also by the tobacco-derived nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) that can induce tumors in laboratory animals. Nitrosamines may disturb the delicate balance between cell proliferation, growth arrest, and apoptosis. A novel paradigm of cell regulation via nAChR has been discovered in studies of SLURP (secreted mammalian Ly-6/ urokinase plasminogen activator receptor-related protein)-1 and -2. Experimental results suggest that SLURP-1 and -2 regulate keratinocyte proliferation, apoptosis, and differentiation. Most importantly, SLURPs and professional nicotinic antagonists can abolish, in part, the abilities of NNK and NNN to cause tumorigenic transformation of immortalized keratinocytes. Learning the pharmacology of the nitrosamine vs. SLURP action on epithelial cells may help develop an effective anti-cancer treatment and prevention programs wherein hazardous effects of tobacco products are anticipated, or even abolished, by a pharmacologic ligand of the specific nicotinic receptor acting as an antidote.

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The Nicotinic Acetylcholine Receptor: Structure and Autoimmune Pathology

Cited by 145 publications

References 361 publications

Age- and sex-related resistance to chronic experimental autoimmune myasthenia gravis (EAMG) in Brown Norway rats

Age- and sex-related resistance to chronic experimental autoimmune myasthenia gravis (EAMG) in Brown Norway rats

Neuronal nicotinic alpha7 receptors modulate inflammatory cytokine production in the skin following ultraviolet radiation

Basic and Clinical Aspects of Non-neuronal Acetylcholine: Biological and Clinical Significance of Non-canonical Ligands of Epithelial Nicotinic Acetylcholine Receptors

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