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. 2012 Nov 27;91(21-22):1065-9.
doi: 10.1016/j.lfs.2012.04.028. Epub 2012 Apr 30.

Alterations in the Non-Neuronal Acetylcholine Synthesis and Release Machinery in Esophageal Epithelium

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Free PMC article

Alterations in the Non-Neuronal Acetylcholine Synthesis and Release Machinery in Esophageal Epithelium

Amanda S Wolf-Johnston et al. Life Sci. .
Free PMC article

Abstract

Aims: A non-neuronal cholinergic system has been described in epithelial cells including that of the urinary bladder (urothelium) and the upper gastrointestinal tract (esophagus). Epithelial dysfunction has been implicated in the pathophysiology of persistent pain conditions such as painful bladder syndrome as well as functional heartburn. For example, alterations in the ability to synthesize and release acetylcholine may contribute to changes in epithelial sensory and barrier function associated with a number of functional genitourinary and intestinal disorders.

Main methods: We examined using immunoblot, acetylcholine (ACh)-synthesis and release components in cat esophageal mucosa and whether elements of these components are altered in a naturally occurring model of chronic idiopathic cystitis termed feline interstitial cystitis (FIC).

Key findings: We identified proteins involved in ACh synthesis and release (high affinity choline transporter, CHT1; ACh synthesizing enzyme choline acetyltransferase ChAT and carnitine acetyltransferase CarAT; vesicular ACh transporter VAChT and the organic cation transporter isoforms 1-3 or OCT-1-3) in cat esophageal mucosa. Significant alterations in CHT, ChAT, VAChT and OCT-1 were detected in the esophageal mucosa from FIC cats. Changes in the vesicular nucleotide transporter (VNUT) and the junctional protein pan-cadherin were also noted.

Significance: Taken together, these findings suggest that changes in the non-neuronal cholinergic system may contribute to alterations in cell-cell contacts and possibly communication with underlying cells that may contribute to changes in sensory function and visceral hyperalgesia in functional esophageal pain.

Figures

Figure 1
Figure 1
Representative western blot analysis of components of the non-neuronal cholinergic system from normal and FIC esophageal mucosa tissue extracts. A, Expression of enzymes involved in acetylcholine synthesis (choline acetyltransferase, ChAT; carnitine acetyltransferase, CarNT) and degradation (acetylcholinesterase, AChE). B, Expression of molecular transporters including choline transporter (CHT), members of the organic cationic transporter family (OCT-1, OCT-2, OCT3), the vesicular acetylcholine transporter (VAChT) and VNUT, a transporter responsible for filling vesicles with ATP. C, Expression of pan-cadherin, an adhesion molecule, and muscarinic receptor type 2 (M2) and type 3 (M3). Shown in each panel is the loading control β-actin.

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