Salivary Mucin Secretion

Quissell, David O.; Tabak, Lawrence A.

doi:10.1002/cphy.cp060305

Cited by 8 publications

(4 citation statements)

References 123 publications

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“…Because kallikreins are produced by ductal cells (Schachter, 1980) and cystatins are products of acinar cells of submandibular glands (Cohen et al, 1990), these observations suggest that there may be a differential control of secretion of proteins synthesized by ductal and acinar cells. The secretion of many ductal proteins such as epidermal growth factor, nerve growth factor, renin-like enzymes, and kallikrein appears to be initiated by a-adrenergic receptors (Orstavik and Gautvik, 1977;Wallace and Partlow, 1976;Hirata and Orth, 1980), whereas the synthesis and secretion of acinar cell products is regulated by ,-adrenergic receptors (Johnson and Cortez, 1988;Quissell and Tabak, 1989). The significance of these differences and the mechanisms that control the differential regulation of these proteins is not clear at this time and further studies are needed.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Adrenergic Agonists and Antagonists on the Expression of Proteins in Rat Submandibular and Parotid Glands

Bedi

1993

Critical Reviews in Oral Biology & Medicine

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The present investigation was undertaken to study the effect of adrenoreceptor modulators on the expression of salivary proteins. Sprague-Dawley rats were treated for 10 consecutive days with adrenergic agonists isoproterenol, dobutamine, terbutaline, salbutamol, methoxyphenamine, or methoxamine. Antiserum to selected salivary proteins was used to compare the concentration of these proteins in the submandibular and parotid glands of treated animals. Chronic treatments of rats (50 lmol/ kg body weight for 10 d) with either isoproterenol or dobutamine induced synthesis of a cysteine-proteinase inhibitor (cystatin) in the submandibular glands. When isoproterenol was injected concomitantly with the mixed p-antagonist propranolol or the V,-adrenergic antagonists metaprolol, proctocol, or atenolol, the induction of cystatin was totally suppressed. However, the 32-antagonist, ICI-1 18551, produced only partial reduction in cystatin induction elicited by isoproterenol. On the contrary, rats treated with either isoproterenol or 5,-agonists demonstrated a significantly reduced concentration of serine-proteinase kallikrein in submandibular glands. The decrease observed in submandibular kallikrein of rats treated with isoproterenol was prevented by concomitant treatment with 0,-antagonists but not with P2-antagonists. Because kallikreins are produced by ductal cells and cystatins are produced by acinar cells of submandibular glands, these observations suggest that there may be differential control of expression of proteins synthesized by ductal and acinar cells. Chronic treatment of rats with nonselective ,B-agonist isoproterenol or p1-selective agonists increased markedly the proline-rich proteins (PRP) in parotid glands, but the parotid amylase concentration was not significantly affected by P-adrenergic agonists. Coinjection of ,1-antagonists along with isoproterenol blocked the induction of PRP in the parotid glands. These findings suggest that there may be a differential control of expression of proteins by different cell populations of salivary glands.

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Section: Discussionmentioning

confidence: 99%

The Effect of Adrenergic Agonists and Antagonists on the Expression of Proteins in Rat Submandibular and Parotid Glands

Bedi

1993

Critical Reviews in Oral Biology & Medicine

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“…This process is continuous in most cells (`constitutive' exocytosis), but it can be greatly accelerated following an appropriate cellular signal such as neural stimulation (`regulatory' exocytosis). In the three major salivary glands, parotid, submandibular and sublingual, exocytotic protein secretion is primarily controlled by the autonomic nervous system; sympathetic stimulation elicits protein release from parotid and submandibular gland acini, and parasympathetic stimulation elicits protein release from sublingual gland acini as well as some release from parotid acini (Quissell and Tabak, 1989; Spearman and Butcher, 1989). We will focus here on amylase secretion from rat parotid acinar cells as recent studies on this system are promoting a better understanding of the cellular events involved in salivary gland exocytosis.…”

Section: Salivary Protein Secretionmentioning

confidence: 99%

Understanding salivary fluid and protein secretion

2002

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“…Mucin in salivary secretion is accompanied by epidermal growth factor (EGF), prosta glandins and various other nonmucin proteins [19][20][21][22][23][24][25][26], Secretion o f water and electrolytes, including buffers, by salivary glands is mediated by parasympathetic branches o f the autonomic nervous system, whereas secre tion o f organic components (salivary mucin, EGF. prosta glandins) is modulated by the adrenergic pathway [27], predominantly P-adrenergic [28]. Since the rate o f sali vary secretion and its composition is also greatly in fluenced by esophageal intraluminal mechanical (stroking o f the mucosa and stretching the wall by distention) and chemical stimuli (pH), its role in combating GER cannot be overestimated.…”

Section: Evolving Role Of Saliva In Esophageal Mucosal Protectionmentioning

confidence: 99%

Do Salivary Organic Components Play a Protective Role in Health and Disease of the Esophageal Mucosa?

Sarosiek¹,

McCallum²

1995

Digestion

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Aggressive factors operating within the esophageal lumen during gastroesophageal reflux are balanced by adequately mobilized protective mechanisms. Esophageal mucosal protection operates at three different although complementary dimensions: (1) preepithelial, (2) epithelial and (3) postepithelial. Since aggressive factors predominantly operate within the esophageal lumen, preepithelial defense is pivotal in mucosal protection. The preepithelial barrier is significantly enhanced by the quantity and the quality of salivary organic components such as salivary mucin, nonmucin protein, salivary epidermal growth factor (EGF) and salivary prostaglandin E₂. The rate of secretion of salivary mucin, nonmucin protein and EGF under the impact of intraesophageal mechanical (bolus) and chemical (HCl/pepsin) stimulation, mimicking the natural gastroesophageal reflux scenario, is significantly impaired in patients with RE, whereas the rate of salivary PGE₂ output remains essentially unchanged. Salivary secretory response to esophageal mechanical and chemical stimuli in terms of organic components, mediated by the esophagosalivary reflex pathway, exhibits a significant impairment in patients with reflux esophagitis.

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Salivary Mucin Secretion

Cited by 8 publications

References 123 publications

The Effect of Adrenergic Agonists and Antagonists on the Expression of Proteins in Rat Submandibular and Parotid Glands

The Effect of Adrenergic Agonists and Antagonists on the Expression of Proteins in Rat Submandibular and Parotid Glands

Understanding salivary fluid and protein secretion

Do Salivary Organic Components Play a Protective Role in Health and Disease of the Esophageal Mucosa?

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