Met5-enkephalin-Arg6-Gly7-Leu8 immunoreactivity in the human gut

Ferri, Gian-Luca; Morreale, Rosalba A.; Dockray, Graham J.

doi:10.1016/0196-9781(86)90087-2

Cited by 17 publications

(4 citation statements)

References 29 publications

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“…Gene expression of proenkephalin-A mRNA was documented using semi-nested RT-PCR. Hence, our results are in good agreement with some earlier studies which revealed the presence of proenkephalin-A-derived peptides in the gastrointestinal tract and pancreas of humans and other mammals [14][15][16][17][18][19][20] .…”

Section: Discussionsupporting

confidence: 82%

“…This may explain why we failed to detect proenkephalin-A mRNA expression in the gastrointestinal tract by means of Northern blot analysis. Although the presence of enkephalin peptide expression has been demonstrated in gut mucosal endocrine cells, especially of the stomach, it is believed that such peptides are of nerve origin [15,16] . Moreover, it has been concluded that the presence of different molecular forms of proenkephalin-A-derived peptides in the gut are generated by differential post-translational processing of proenkephalin-A propeptide [14] .…”

Section: Discussionmentioning

confidence: 99%

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Proenkephalin-A mRNA Is Widely Expressed in Tissues of the Human Gastrointestinal Tract

Monstein¹,

Grahn²,

Ohlsson

2006

Eur Surg Res

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Background: It has been shown that the non-opioid effects of Met-enkephalin, which is derived from proenkephalin-A, are mediated through a specific opioid growth factor (OGF) receptor which is assumed to be involved in the control of cell growth. The expression and tissue location of proenkephalin-A mRNA in the gastrointestinal tract remains largely unknown. Methods: In this study we have analyzed the expression of proenkephalin-A mRNA in the human esophagus, gastrointestinal tract and surrounding organs by means of reverse-transcriptase PCR (RT-PCR). Results: The present study demonstrates proenkephalin-A mRNA expression in the human esophagus, gastrointestinal tract, pancreas, and gallbladder. Conclusion: The present study demonstrates proenkephalin-A mRNA expression in regions of the human esophagus, gastrointestinal tract, pancreas, and gallbladder tissues which provides information for the future mapping of proenkephalin-A mRNA and protein expression/co-expression at the cellular level.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Proenkephalin-A mRNA Is Widely Expressed in Tissues of the Human Gastrointestinal Tract

Monstein¹,

Grahn²,

Ohlsson

2006

Eur Surg Res

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“…Intravenous infusion of naloxone, an opioid receptor antagonist, abolished the slowing effect of ileal fat, suggesting that an opioid pathway may be involved in the fat-induced ileal brake (2,19). Because intravenous naloxone may have accelerated gastrointestinal transit by acting on opioid receptors located either peripherally (gut) (10,31) or centrally (brain) (25), the location of this naloxoneblockable opioid pathway for the fat-induced ileal brake is unknown. Opioid receptors are found on ganglion cells of myenteric and submucosal plexuses of the small intestine as well as on intramural nerve fibers in dogs and humans (1,28).…”

mentioning

confidence: 99%

Slowing of intestinal transit by fat depends on naloxone-blockable efferent, opioid pathway

Zhao

Wang²,

Lin³

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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Slowing of transit through the proximal small intestine by fat in the distal gut is termed the ileal brake. Intravenous naloxone, an opioid receptor antagonist, abolished the fat-induced ileal brake, suggesting that an endogenous opioid pathway may be involved in this response. To test the hypothesis that slowing of intestinal transit by fat in the distal half of the gut depends on an opioid pathway located on the efferent limb of this response, we compared intestinal transit in dogs equipped with duodenal and midgut fistulas while naloxone was either compartmentalized with oleate to the distal half of the gut or with buffer to the proximal half of the gut. We found that intestinal transit depended on the perfusion conditions (P<0.00001). Specifically, compared with ileal brake (marker recovery of 35.7+/-7.4%), intestinal transit was accelerated when naloxone was delivered into the proximal half of the gut (76.2+/-5.2%) (P<0.005) but not the distal half of the gut (29.4+/-5.4%). We conclude that slowing of intestinal transit by fat in the distal half of the gut depends on an opioid pathway located on the efferent limb of the ileal brake.

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“…Expression of at least four enkephalin peptides (Leu-enk, Met-enk, Met-enk-Arg-Phe, and Met-enk-Arg-Gly-Leu) in the GIT has been confirmed ( Hughes et al, 1977 ; Linnoila et al, 1978 ; Tang et al, 1982 ; Giraud et al, 1984 ). Immunohistochemical studies demonstrate expression throughout the human GIT, with highest levels detected in the muscularis externa ( Polak et al, 1977 ; Ferri et al, 1986 , 1988 ). A similar expression pattern has been observed in rodents ( Keast et al, 1985 ).…”

Section: The Opioid System In the Gutmentioning

confidence: 99%

Biological redundancy of endogenous GPCR ligands in the gut and the potential for endogenous functional selectivity

Thompson¹,

Canals²,

Poole

2014

Front. Pharmacol.

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This review focuses on the existence and function of multiple endogenous agonists of the somatostatin and opioid receptors with an emphasis on their expression in the gastrointestinal tract. These agonists generally arise from the proteolytic cleavage of prepropeptides during peptide maturation or from degradation of peptides by extracellular or intracellular endopeptidases. In other examples, endogenous peptide agonists for the same G protein-coupled receptors can be products of distinct genes but contain high sequence homology. This apparent biological redundancy has recently been challenged by the realization that different ligands may engender distinct receptor conformations linked to different intracellular signaling profiles and, as such the existence of distinct ligands may underlie mechanisms to finely tune physiological responses. We propose that further characterization of signaling pathways activated by these endogenous ligands will provide invaluable insight into the mechanisms governing biased agonism. Moreover, these ligands may prove useful in the design of novel therapeutic tools to target distinct signaling pathways, thereby favoring desirable effects and limiting detrimental on-target effects. Finally we will discuss the limitations of this area of research and we will highlight the difficulties that need to be addressed when examining endogenous bias in tissues and in animals.

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Met5-enkephalin-Arg6-Gly7-Leu8 immunoreactivity in the human gut

Cited by 17 publications

References 29 publications

Proenkephalin-A mRNA Is Widely Expressed in Tissues of the Human Gastrointestinal Tract

Proenkephalin-A mRNA Is Widely Expressed in Tissues of the Human Gastrointestinal Tract

Slowing of intestinal transit by fat depends on naloxone-blockable efferent, opioid pathway

Biological redundancy of endogenous GPCR ligands in the gut and the potential for endogenous functional selectivity

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