Gastric mucosal protection

From prostaglandins to gene-therapy

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents - prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide) - play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.

Original languageEnglish
Pages (from-to)203-215
Number of pages13
JournalCurrent Medicinal Chemistry
Volume12
Issue number2
Publication statusPublished - 2005

Fingerprint

Gene therapy
Genetic Therapy
Prostaglandins
Stomach
Nitric Oxide
Calcitonin Gene-Related Peptide
Neuropeptides
Vascular Endothelial Growth Factor A
Intercellular Signaling Peptides and Proteins
Ulcer
Microcirculation
Neurology
Neurons
Rats
Brain
Plasmids
Sodium
Tissue
Area Postrema
Stomach Diseases

Keywords

  • Central nervous system
  • Gastric mucosal protection
  • Ulcer healing
  • Vasoactive agents

ASJC Scopus subject areas

  • Organic Chemistry
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Pharmacology

Cite this

Gastric mucosal protection : From prostaglandins to gene-therapy. / Gyires, K.

In: Current Medicinal Chemistry, Vol. 12, No. 2, 2005, p. 203-215.

Research output: Contribution to journalArticle

@article{f1f4b41aa08a4833bd3ec8135d81711a,
title = "Gastric mucosal protection: From prostaglandins to gene-therapy",
abstract = "The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents - prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide) - play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.",
keywords = "Central nervous system, Gastric mucosal protection, Ulcer healing, Vasoactive agents",
author = "K. Gyires",
year = "2005",
language = "English",
volume = "12",
pages = "203--215",
journal = "Current Medicinal Chemistry",
issn = "0929-8673",
publisher = "Bentham Science Publishers B.V.",
number = "2",

}

TY - JOUR

T1 - Gastric mucosal protection

T2 - From prostaglandins to gene-therapy

AU - Gyires, K.

PY - 2005

Y1 - 2005

N2 - The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents - prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide) - play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.

AB - The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents - prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide) - play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.

KW - Central nervous system

KW - Gastric mucosal protection

KW - Ulcer healing

KW - Vasoactive agents

UR - http://www.scopus.com/inward/record.url?scp=11844261473&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=11844261473&partnerID=8YFLogxK

M3 - Article

VL - 12

SP - 203

EP - 215

JO - Current Medicinal Chemistry

JF - Current Medicinal Chemistry

SN - 0929-8673

IS - 2

ER -