Human submucosal neurones regulate intestinal epithelial cell proliferation: evidence from a novel co‐culture model

Toumi, Férial; Neunlist, Michel; Cassagnau, Elizabeth; Parois, S.; Laboisse, Christian L.; Galmiche, Jean Paul; Jarry, Anne

doi:10.1046/j.1365-2982.2003.00409.x

Cited by 57 publications

(33 citation statements)

References 6 publications

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“…For example, maintaining postradiation microvascular integrity, such as in genetically modified mice where the endothelium is apoptosis resistant, is associated with decreased radiationinduced crypt cell death and less mucosal injury than in what is seen in wild-type littermate control mice (4). The enteric nervous system interacts directly with both microvascular endothelium (30,31) and intestinal epithelium (32,33). However, because enteric denervation is generally assumed to have a trophic effect on the epithelium (32), the observations in the present study can more easily be explained in terms of interactions with the microvasculature and/or cells of the immune system than by a primary epithelial effect.…”

Section: Discussionmentioning

confidence: 71%

Calcitonin Gene-Related Peptide and Substance P Regulate the Intestinal Radiation Response

Wang

Qiu

Kulkarni

et al. 2006

Clinical Cancer Research

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Purpose: Intestinal toxicity is important in the therapeutic use of radiation as well as in nontherapeutic radiation exposure scenarios. Enteric sensory nerves are critical for mucosal homeostasis and for an appropriate response to injury. This study assessed the role of the two major neuropeptides released by sensory nerves, calcitonin gene-related peptide (CGRP) and substance P, in the intestinal radiation response. Experimental Design: Male rats received full-length CGRP, CGRP antagonist (CGRP 8-37 ), a modified substance P peptide (GR73632), a small-molecule substance P receptor antagonist (neurokinin-1receptor antagonist, SR140333), or vehicle for 2 weeks after localized X irradiation of a 4-cm loop of small bowel. Structural, cellular, and molecular aspects of the intestinal radiation response were assessed. Results: Intestinal CGRP and substance P transcript levels increased after irradiation. Multivariate analysis showed that CGRP and SR140333 ameliorated and CGRP 8-37 and GR73632 exacerbated intestinal radiation injury. Univariate analysis revealed increased radiation injury score, bowel wall thickening, and collagen III deposition after treatment with CGRP 8-37 , whereas SR140333 ameliorated radiation injury score, loss of mucosal surface area, collagen III deposition, and mucosal inflammation. Conclusions: The two major neuropeptides released by sensory neurons, CGRP and substance P, are overexpressed after irradiation and have opposing effects during development of intestinal radiation injury. Systematic studies to assess CGRP agonists and/or neurokinin-1receptor blockers as protectors against intestinal toxicity during radiation therapy and after nontherapeutic radiation exposure are warranted.

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Section: Discussionmentioning

confidence: 71%

Calcitonin Gene-Related Peptide and Substance P Regulate the Intestinal Radiation Response

Wang

Qiu

Kulkarni

et al. 2006

Clinical Cancer Research

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“…The necessity for adaptation after birth suggests that development of new neuronal connection also occurs postnatally [30]. Several clinical and experimental observations suggest that homeostatic control of gut function in a changing environment might be achieved through adaptive changes occurring in the enteric ganglia [34]. Recent studies in infants and children [35] indicate that the density of ganglion cells in the myenteric plexus decreases significantly with age during the first 3-4 years of life and that the neurochemical differentiation in rat is accomplished during the first month of postnatal live [17].…”

Section: Discussionmentioning

confidence: 99%

Temporal and regional morphological differences as a consequence of FGF-2 deficiency are mirrored in the myenteric proteome

et al. 2007

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The enteric nervous system with its intricate network of neurons and glia shows a high plasticity, which not only changes during pre- and postnatal development, but also with disease or changing dietary habits. FGF as a potent neurotrophic factor in the central nervous system might also play a specific role for the ENS development, FGF-2 knockout and corresponding wild-type mice were histologically and functionally analyzed. FGF-2 knockout mice are viable and thrive normally and do apparently not display any obvious neurological deficit. Morphological differences were studied on whole mount preparations of muscle and submucous layer using either cuprolinic blue or immunohistochemical stainings for the neuronal marker PGP 9.5. Ussing-chamber and isometric muscle contraction experiments were performed on isolated gut wall, respectively muscle preparations. Intravital microscopy with GFP-transfected E. coli bacteria was used to investigate influences upon bacterial translocation. In additional experiments the protein pattern of the isolated myenteric plexus of knockout and wild-type mice were compared using 2D-DIGE technology. The morphometric analysis of the myenteric plexus revealed significant differences between FGF-2 knockout and wild-type animals, resulting in larger neurons in the knock out animals, embedded in less densely packed enteric ganglia. While muscle contractility appeared not to be affected, there was a significant difference in bacterial translocation as well as differences in basal chloride secretion to be seen. The observed morphological differences were reflected in the varying protein patterns, which were revealed by 2D-DIGE. A large number of differentially expressed proteins were found in both colonic and duodenal samples. FGF obviously influences the development of well established gastrointestinal functions by various means, thus leading to minor but significant deficiencies. Whether the revealed deficits in the mucous barrier are indebted to the morphological alterations in the ENS cannot yet be proved, but is very likely.

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“…The ENS has been shown to exert an important role in the regulation of several intestinal mucosal functions, including mucosal blood flow, regulation of epithelial permeability, organization and cell proliferation. [9] All of these functions contribute to the maintenance of the intestinal barrier. [9] Visceral hypersensitivity is a key mechanism underlying abdominal pain, one of the main The CNS is also essential in the perception of events occurring within the gut.…”

Section: Irritable Bowel Syndrome (Ibs) Is Defined As 'A Functional Bmentioning

confidence: 99%

“…[9] All of these functions contribute to the maintenance of the intestinal barrier. [9] Visceral hypersensitivity is a key mechanism underlying abdominal pain, one of the main The CNS is also essential in the perception of events occurring within the gut. Alteration at any level can lead to altered sensation, dysmotility, or psychological distress.…”

Section: Irritable Bowel Syndrome (Ibs) Is Defined As 'A Functional Bmentioning

confidence: 99%

UNDERSTANDING GRAHANI THROUGH GUT AND BRAIN RELATION & IT’S MANAGEMENT “GRAHANI AND BRAIN”

Bams¹

2017

WJPPS

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Irritable Bowel Syndrome (IBS) is one of several highly prevalent, multi-symptom gastrointestinal motility disorders that have a wide clinical spectrum and is one of the most common conditions encountered in clinical practice but one of the least well understood.Grahani is an organ situated between āmāshaya (stomach) and pakvāshaya (colon) which is the main seat of digestive glands comprising of digestive juices and where proper digestion of the food takes place. It is also responsible for retention of food for sufficient time for proper digestion and assimilation of the nutrient from the digested food. Dysfunction of Grahani is termed as Grahani Dosha. This condition may lead to formation of Ama which is the cause of many other diseases [1] (Charaka Chikitsa 15/45-49). It has rightly been said by Vagbhata that all ailments in the body, specially diseases of alimentary tract arise due to the malformation of AGNI. IBS is also one among such diseases which occurs due to the mandagni. And psychological factors like krodha, shoka, bhaya, kama etc. which results in Agnidushti leading to Grahanidosha [2] (c,chi 15/71). IBS has strong Psyho-somatic base. No cure has been found out to the disease. But only symptomatic treatment & assurance is given to the patient by the modern medical science. As world is looking forward for Ayurveda for safe treatment modalities, it is essential to find out the effective therapeutic procedures from our science. In this paper an effort will be made to explore the utility of drugs that relieves stress (manasika bhavas) in grahani roga.

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Human submucosal neurones regulate intestinal epithelial cell proliferation: evidence from a novel co‐culture model

Cited by 57 publications

References 6 publications

Calcitonin Gene-Related Peptide and Substance P Regulate the Intestinal Radiation Response

Calcitonin Gene-Related Peptide and Substance P Regulate the Intestinal Radiation Response

Temporal and regional morphological differences as a consequence of FGF-2 deficiency are mirrored in the myenteric proteome

UNDERSTANDING GRAHANI THROUGH GUT AND BRAIN RELATION & IT’S MANAGEMENT “GRAHANI AND BRAIN”

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