Related Experiment Videos

Myenteric denervation downregulates galectin-1 and -3 expression in gastric carcinogenesis

Cássia F Estofolete1, Sérgio Zucoloto, Sonia M Oliani

  • 1Department of Anatomy, São José do Rio Preto School of Medicine, FAMERP, Avenida Brigadeiro Faria Lima 5416, São José do Rio Preto, 15090-000 São Paulo, Brazil. cassia.estofolete@hotmail.com

Digestive Diseases and Sciences
|December 29, 2010
PubMed
Abstract

Insights

Myenteric denervation downregulates galectin-1 and -3 expression in rat stomachs, potentially inhibiting gastric tumor development in this N-methyl-N'-nitro-N-nitrosoguanidine model.

Area of Science:

  • Gastroenterology
  • Oncology
  • Immunology

Background:

  • Investigated galectin-1 and -3 expression in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis.
  • Utilized benzalkonium chloride to induce lesions in denervated rat stomachs.

Purpose of the Study:

  • To evaluate the role of galectin-1 and -3 in gastric carcinogenesis.
  • To determine the effect of myenteric denervation on galectin expression during MNNG-induced carcinogenesis.

Main Methods:

  • Compared nondenervated and denervated rat stomachs with and without MNNG-induced lesions.
  • Employed histopathological and immunohistochemical analyses using anti-Gal-1 and anti-Gal-3 antibodies.

Main Results:

  • MNNG induced benign and malignant epithelial lesions, more severe in nondenervated stomachs.
  • Galectin-1 and -3 were expressed in epithelial cells, blood vessels, muscle, and myenteric plexus.
  • Denervation significantly decreased Gal-1 and -3 expression in epithelial cells, mast cells, and neutrophils compared to nondenervated lesions.

Conclusions:

  • Myenteric denervation downregulates endogenous galectin-1 and -3 expression.
  • This downregulation may play a role in inhibiting tumor development in this experimental gastric carcinogenesis model.

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Esophageal Achalasia01:27

Esophageal Achalasia

Esophageal achalasia is a chronic neurogenic disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and absent or ineffective peristalsis in the distal esophagus. This leads to a functional obstruction without a physical blockage, despite significant disruption of esophageal motility.EtiologyAchalasia is caused by degeneration of the myenteric (Auerbach's) plexus, specifically the loss of inhibitory ganglion cells that produce vasoactive intestinal peptide (VIP)...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...