Corticotropin-releasing factor (CRF)-like immunoreactivity in the vertebrate endocrine pancreas.

Petrusz, Peter; Merchenthaler, Istvån; Maderdrut, Jerome L.; Vígh, S.; Schally, A. V.

doi:10.1073/pnas.80.6.1721

Cited by 87 publications

(38 citation statements)

References 36 publications

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“…Possible tissue sources for bombesin immunoreactivity in milk may be neural or extraneural tissue or both. For example, several known neuropeptides, thyrotropin-releasing hormone (56), somatostatin, corticotropin-releasing factor (57), and prolactin (58), are also found in the pancreas. Even GRP (59,60) and other bombesin-like peptides (60,61) are apparently associated with nerve tissue.…”

Section: Resultsmentioning

confidence: 99%

A bombesin immunoreactive peptide in milk.

Jahnke¹,

Lazarus²

1984

Proc. Natl. Acad. Sci. U.S.A.

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Immunoreactivity to the amphibian peptide bombesin was found in instant nonfat dry milk (ca. 0.7 ng/ml) and in the whey of whole or skim bovine milk (ca. 1.2 ng/ml) even after ultracentrifugation. The soluble immunoreactivity was associated with a peptide exhibiting the following characteristics: (i) parallel displacement in an immunoassay using an antiserum recognizing bombesin amino acid residues 5-8; (ii) separation from both gastrin-releasing peptide and amphibian bombesin by gel filtration-the approximate Mr was 3,200; (iii) denaturation in urea, reduction by dithiothreitol, and acetylation by iodoacetamide had no effect on its elution profile by gel-filtration chromatography and the aggregation of added bombesin to milk proteins or peptides was not observed; (iv) reversed-phase HPLC separated milk immunoreactivity from gastrin-releasing peptide and bombesin; (v) digestion by trypsin yielded a smaller immunoreactive peptide fragment, whereas nearly all immunoreactivity was lost by treatment with a-chymotrypsin; and (vi) the level of immunoreactivity was unaffected by boiling. These data show that milk is an exogenous source of bombesin-like immunoreactivity,, which may account for the increase of gastric acid and gastrointestinal hormone levels after the consumption of milk.Immunoreactivity to bombesin, an amphibian tetradecapeptide (1), is distributed throughout mammalian tissues (2-5). Bombesin administered through intraperitoneal or intracisternal injection or intravenous infusion elicits diverse physiological effects in a variety of animal species, including humans (6-12). These effects include hypertension (1, 6, 13, 14), satiety (for review, see ref. 15), change in sugar metabolism (16, 17), hypothermia (18), modulation of the level of many gastrointestinal-associated peptide hormones (6)(7)(8)(9)(10)(11)(12)(19)(20)(21)(22)(23)(24), and increase of gastric acid secretion (7,10,13,14,19,20). Bombesin also releases both gastrin and gastric acid from isolated fundic mucosa (25) and acts as a spasmogen in isolated smooth muscle preparations (1,6,13,14,26 MATERIALS AND METHODSMilk. Pasteurized skim and whole milk from several different local dairies were purchased 5-7 days before the expiration date. Instant nonfat dry milk was the product of several major companies and reconstituted according to the manu- [Tyr8]Bombesin and GRP were iodinated every 4-6 weeks as described (43). The production of the antiserum to bombesin has been described (44). Optimum RIA conditions, which were systematically determined, are as follows: 0.1 M sodium cacodylate, pH 5.6/bovine serum albumin (5 mg/ml)/125I-labeled [Tyr8]bombesin (or GRP) (2,500 cpm)/antiserum (final dilution, 1:4,000)/standard or test solution in a total vol of 100 ,ul. Nonionic (Triton X-100, Nonidet P-40) and ionic (sodium lauryl sulfate) detergents above 0.1% and chaotropic agents (urea, (Fig. 1). Other known peptides, such as physalaemin, neurotensin, and braAbbreviations: RIA, radioimmunoassay; GRP, gastrin-releasing peptide (bombesin-lik...

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Section: Resultsmentioning

confidence: 99%

A bombesin immunoreactive peptide in milk.

Jahnke¹,

Lazarus²

1984

Proc. Natl. Acad. Sci. U.S.A.

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“…Nevertheless, other lines of evidence suggest that CRF is expressed in organs outside the brain and might be released to act locally. CRF-IR was reported to be expressed in the digestive system (Petrusz et al, 1984;Suda et al, 1984;Wolter, 1984;Kawai et al, 1985;Kawahito et al, 1994), in endocrine organs (Petrusz et al, 1983;Suda et al, 1984), and by immune/inflammatory cells (Karalis et al, 1997).We found that CRF-IR neurons did not express IR for the CRF 1 receptor subtype, which is the functional receptor for CRF in the ENS (Liu et al, 2005). CRF 1 -IR was expressed in subgroups of neurons, which expressed chemical codes that were different from the codes for CRF-IR neurons.…”

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confidence: 99%

Distribution and chemical coding of corticotropin-releasing factor-immunoreactive neurons in the guinea pig enteric nervous system

Liu

Gao

et al. 2005

J. Comp. Neurol.

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Immunofluorescence was used to study immunoreactivity (IR) for corticotropin releasing factor (CRF) in the guinea-pig enteric nervous system. CRF-IR was expressed in both the myenteric and submucosal plexuses of all regions of the large and small intestine and the myenteric plexus of the stomach. CRF-IR-nerve fibers were present in the myenteric and submucosal plexuses, in the circular muscle coat and surrounding submucosal arterioles. Most of the CRF-IR fibers persisted in the myenteric and submucosal plexuses after 7 days in organotypic culture. CRF-IR was not coexpressed with tyrosine hydroxylase-IR or calcitonin gene-related peptide-IR fibers. The proportions of CRF-IR cell bodies in the myenteric plexus increased progressively from the stomach (0.6%) to the distal colon (2.8%). Most of the CRF-IR myenteric neurons (95%) had uniaxonal morphology; the remainder had Dogiel type II multipolar morphology. CRF-IR cell bodies in the myenteric plexus of the ileum expressed IR for choline acetyltransferase (56.9%), substance P (55.0%), and nitric oxide synthase (37.9%). CRF-IR never co-localized with IR for calbindin, calretinin, neuropeptide Y, serotonin or somatostatin in the myenteric plexus. CRF-IR cell bodies were more abundant in the submucosal plexus (29.9-38.0%) than in the myenteric plexus. All CRF-IR neurons in submucosal ganglia expressed vasoactive intestinal peptide-IR and were likely to be secretomotor/vasodilator neurons. CRF-IR neurons did not express IR for the CRF 1 receptor. CRF 1 -IR was expressed in neuronal neighbors of those with CRF-IR. Collective evidence suggests that VIPergic secretomotor neurons might provide synaptic input to neighboring cholinergic neurons. Keywordsgastrointestinal tract; myenteric plexus; submucosal plexus; stress Clinical and experimental evidence suggests that stress is associated with the onset, symptom exacerbation and reactivation of gastrointestinal disorders, which include the irritable bowel syndrome, ulcerative colitis, Crohn's disease, gastroesophageal reflux disease and gastric ulcer (Duffy et al., 1991;Greene et al., 1994;Levenstein et al., 1994;Mayer, 2000;Peck and Wood, 2000;Wood et al., 2000;Wood, 2002;Drossman, 2004). Exposure of animals to stress causes erosions and ulceration in the gastric mucosa and inhibits gastric emptying coincident with stimulation of colonic motility, colonic transit, fecal pellet expulsion, mucosal electrolyte secretion and opening of the mucosal barrier to antigenic molecules (Fone et al., 1990; Taché, 1999;2001;Maillot et al., 2000 al., 20002;Million et al., 2002; Saunders et al., 2002a,b). Moreover, environmental stress factors initiate ulcerative colitis-like disease that is associated with colon cancer in primates Wood et al., 2000). The mechanistic details of these stressinduced gastrointestinal functional abnormalities are poorly understood. Nevertheless, the available evidence points to corticotropin releasing factor (CRF) signaling pathways in the brain and the gut as significant factors in the stress-evoked ...

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“…This strongly suggested an alternative, non-hypothalamic origin of irCRF-41 present in the systemic circulation. Multiple sources of peripheral irCRF-41 may be Postulated on the basis of immunohistochemical or content studies (18)(19)(20)(21)(22)(23)(24). Of particular interest were the adrenal glands, which contain and secrete CRF-like immunoreactivity (23,24).…”

Section: Discussionmentioning

confidence: 99%

“…During pregnancy, peripheral irCRF-41 appears to be derived from the placenta (18)(19)(20). The source of peripheral irCRF-41 in non-pregnant animals is unknown and it has been postulated that it may reflect, at least in part, hypothalamic irCRF-41 secretion (13,14,16,17); other sources include the gastrointestinal tract (21), the pancreas (22) and the adrenal gland (23,24). In the present study, the relationship between peripheral and hypophysial-portal plasma concentration profiles of irCRF-41 was evaluated by direct measurements in both circulatory compartments under a variety of experimental conditions.…”

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confidence: 99%

Lack of Correlation Between Immunoreactive Corticotropin‐Releasing Factor Concentration Profiles in Hypophysial‐Portal and Peripheral Plasma

Plotsky¹,

Otto²,

Toyama³

et al. 1990

J Neuroendocrinology

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Corticotropin-releasing factor (CRF-41) is the primary mediator of adrenocorticotropin secretion from the adenohypophysis. This 41-amino-acid peptide is synthesized in perikarya of the paraventricular nuclei, transported to nerve terminals in the external zone of the median eminence and released into the hypophysial-portal circulation. It is also synthesized in multiple extrahypothalamic and peripheral sites. In addition, immunoreactive (ir) CRF-41 is present in the systemic circulation, raising the possibility that systemic measurements might provide a useful index of hypothalamic irCRF-41 secretion. This hypothesis was tested in several rat models. Neither bilateral destruction of hypothalamic irCRF-41 producing perikarya, nor infundibular stalk transection altered peripheral plasma irCRF-41 concentration. Furthermore, central administration of norepinephrine, an agent previously shown to evoke irCRF-41 secretion into the portal circulation, was without effect on peripheral irCRF-41 concentration. Finally, while increased irCRF-41 levels in both the hypophysial-portal and the peripheral circulation were associated with nitroprusside-induced hypotension, bilateral paraventricular nuclei lesions blocked irCRF-41 secretion into the hypophysial-portal circulation without blunting the rise observed in the peripheral circulation. The source of peripheral irCRF-41 remains undetermined; however, the adrenals may be excluded as bilateral adrenalectomy failed to alter circulating irCRF-41 levels. Therefore, our observations do not support the concept that peripheral irCRF-41 levels provide a useful index of hypothalamic secretion of this peptide into the hypophysial-portal circulation under the conditions tested.

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Corticotropin-releasing factor (CRF)-like immunoreactivity in the vertebrate endocrine pancreas.

Cited by 87 publications

References 36 publications

A bombesin immunoreactive peptide in milk.

A bombesin immunoreactive peptide in milk.

Distribution and chemical coding of corticotropin-releasing factor-immunoreactive neurons in the guinea pig enteric nervous system

Lack of Correlation Between Immunoreactive Corticotropin‐Releasing Factor Concentration Profiles in Hypophysial‐Portal and Peripheral Plasma

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