Esophageal smooth muscle reactivity is impaired in chronic reflux esophagitis by both receptor- and nonreceptor-mediated mechanisms

Tuğtepe, Halil; Tugay, Melih; Bozkurt, Süheyla; Yıldız, Fahrettin; Utkan, Tijen; Yeğen, Berrak Ç.; Dağlı, Tolga E.

doi:10.1016/j.jpedsurg.2006.12.048

Cited by 12 publications

(10 citation statements)

References 17 publications

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“…In other words, there were heightened immune responses within the duodenal mucosa in animals with SIBO. Recently, impaired esophageal smooth muscle reactivity was documented in a chronic reflux esophagitis rat model [28]. A mild chronic inflammatory state or immune response by SIBO might therefore maintain smooth muscle dysfunction in both the upper and lower gut in some predisposed individuals expressed as GERD and IBS symptoms.…”

Section: Discussionmentioning

confidence: 99%

Erosive esophagitis may be related to small intestinal bacterial overgrowth

Kim

Lee

et al. 2012

Scandinavian Journal of Gastroenterology

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Section: Discussionmentioning

confidence: 99%

Erosive esophagitis may be related to small intestinal bacterial overgrowth

Kim

Lee

et al. 2012

Scandinavian Journal of Gastroenterology

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“…It was reported that neurotransmitters regulating gastrointestinal motility, secretion, and sensation play an important role in the RE pathogenesis. Rats with esophageal reflux have decreased smooth muscle contractile responses to carbachol (receptor mediated) and KCl (non-receptor mediated), as well as decreased relaxation to 5-HT (receptor mediated) [9]. …”

Section: Discussionmentioning

confidence: 99%

The role of the 5-hydroxytryptamine pathway in reflux-induced esophageal mucosal injury in rats

et al. 2012

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BackgroundDysfunction of the 5-hydroxytryptamine (5-HT) signaling pathway can lead to gastrointestinal motility and secretion abnormalities and to visceral hypersensitivity. The aim of this study is to investigate the role of 5-HT in reflux-induced esophageal mucosal injury.MethodsFifty 8-week-old male Sprague-Dawley (SD) rats were randomly divided into a gastroesophageal reflux (GER) model group (30 rats) and a sham surgery control group (20 rats). Four weeks after surgery, the esophageal mucosa was collected for histological evaluation, 5-HT concentrations, and 5-HT selective reuptake transporter (SERT) mRNA and 5-HT4 receptor (5-HT4R) protein expressions.ResultsTwenty-seven rats in the GER model group survived, and three rats died. Histologically, in the GER model group, 20 rats had reflux esophagitis (RE group), and 7 rats had non-erosive reflux disease (NERD group). The 5-HT levels in the esophageal tissue from the RE group were significantly higher than those from the control and NERD groups. Both the RE and NERD groups showed significant increases in SERT mRNA expression of the esophageal mucosa than that of the controls, and the SERT mRNA level in the RE group was significantly higher than that in the NERD group. The 5-HT4R protein level of the esophageal mucosa in the RE group was significantly lower than that in the controls and the NERD group.ConclusionsWe conclude that a 5-HT signaling pathway disorder could be a major factor in the pathogenesis of GER and RE.

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“…The inflammatory factors affect esophageal motility through multiple ways. Except for inducing chemotaxis of leukocyte, they also directly impair the SMCs contractility 12,13. In addition, the inflammation factors also mediate the interaction between SMC and myenteric plexus neurons in esophagus by inducing glial cell line-derived neurotrophic factor (GDNF) and nerve growth factor (NGF) expression in SMCs 14.…”

Section: Introductionmentioning

confidence: 99%

Smooth Muscle Hgs Deficiency Leads to Impaired Esophageal Motility

Chen¹,

Hou²,

Zhang³

et al. 2015

Int. J. Biol. Sci.

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As a master component of endosomal sorting complex required for transport proteins, hepatocyte growth factor-regulated tyrosine kinase substrate (Hgs) participates multiple cellular behaviors. However, the physiological role of Hgs in smooth muscle cells (SMCs) is by far unknown. Here we explored the in vivo function of Hgs in SMCs by using a conditional gene knockout strategy. Hgs deficiency in SMCs uniquely led to a progressive dilatation of esophagus with a remarkable thinning muscle layer. Of note, the mutant esophagus showed a decreased contractile responsiveness to potassium chloride and acetylcholine stimulation. Furthermore, an increase in the inhibitory neurites along with an intense infiltration of T lymphocytes in the mucosa and muscle layer were observed. Consistently, Hgs deficiency in SMCs resulted in a disturbed expression of a set of genes involved in neurotrophin and inflammation, suggesting that defective SMC might be a novel source for excessive production of cytokines and chemokines which may trigger the neuronal dysplasia and ultimately contribute to the compromised esophageal motility. The data suggest potential implications in the pathogenesis of related diseases such as gastroesophageal reflux disease.

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Esophageal smooth muscle reactivity is impaired in chronic reflux esophagitis by both receptor- and nonreceptor-mediated mechanisms

Cited by 12 publications

References 17 publications

Erosive esophagitis may be related to small intestinal bacterial overgrowth

Erosive esophagitis may be related to small intestinal bacterial overgrowth

The role of the 5-hydroxytryptamine pathway in reflux-induced esophageal mucosal injury in rats

Smooth Muscle Hgs Deficiency Leads to Impaired Esophageal Motility

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