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At least 109 records · Page 6Linked to original sources
PubMed1982

Vitamin D receptors in isolated rat parotid gland acinar cells.

Rat parotid gland was examined for the presence of 1 alpha, 25-dihydroxycholecalciferol receptors using sucrose density gradient ultracentrifugation techniques. [3H] DHCC bound specifically and with high affinity to a 3.2 S protein present in nuclear and cytosolic fractions of isolated parotid acinar cells. Values for the equilibrium dissociation constant and for the receptor concentration were determined to be approx. 0.1 nM, and 12 fmol/mg protein, respectively. In competitive inhibition experiments, the 3.2 S protein displayed 100-fold lower affinity for 25-hydroxycholecalciferol than for DHCC, and did not bind estradiol or methylprednisolone. These results suggest that rat parotid gland acinar cells contain classical DHCC receptors. A similar approach failed to provide evidence of DHCC receptors in isolated pancreas acinar cells, lacrimal gland or submandibular gland. It has been previously reported that vitamin D is essential for normal exocrine secretion from the rat parotid gland (Tenenhouse, A. and Afari, G. (1978) Biochim. Biophys. Acta 538, 631-634). The present findings suggest that this effect is the result of a direct action of DHCC on the parotid gland acinar cell. The absence of DHCC receptors in other exocrine cells suggests that tissue sensitivity to DHCC is not a general property of exocrine systems.

Animals↗
PubMed1977

Intra-vital staining as an aid to parotid gland surgery.

Successful parotid surgery depends on the careful identification and dissection of the facial nerve, and to prevent recurrence all tumours should be excised with a wide margin of normal tissue. These two requirements are facilitated by the technique of intra-vital staining of the parotid gland with 2.5% methylene blue solution.

Adenocarcinoma↗
PubMed1984

Subcellular location of stimulus-affected endogenous phosphoproteins in the rat parotid gland.

Rat parotid minces were labeled with [32P]Pi, stimulated with isoproterenol, homogenized in sucrose, and fractionated on continuous sucrose density gradients. We analyzed the resulting fractions by sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiograms were made from the gels. Comparison of fractions from control and isoproterenol-stimulated minces revealed seven phosphoproteins that were affected by isoproterenol. The subcellular location of these proteins was determined by comparing their distribution in the sucrose gradients with that of a number of enzymes that are characteristic of specific organelles. Isoproterenol decreased the phosphorylation of two cytoplasmic proteins (Mr 16,000 and 18,000) and increased the phosphorylation of a third (Mr 14,000). The phosphorylation of two endoplasmic reticulum proteins was increased by isoproterenol (Mr 20,500 and 22,500), as was an Mr 31,000 protein which was probably the S6 ribosomal protein. The phosphorylation of a secretory granule protein (Mr 24,000) was decreased by isoproterenol. We then developed a purification scheme for parotid secretory granules. By using this method, we demonstrated that the phosphorylation of the Mr 24,000 was also decreased by carbamylcholine. Granules purified by this method also contained a small number of other phosphoproteins whose phosphorylation was increased only by isoproterenol. Secretory granule-associated stimulus-affected phosphoproteins were found in the particulate fraction when the granules were hypotonically lysed, and were not extracted from the particulate fraction by washing with 0.6 M KCl.

5'-Nucleotidase↗
PubMed1977

Is calcium the final mediator of exocytosis in the rat parotid gland?

Rat parotid slices were partially depleted of cellular Ca by long (80-100 minute) incubations in media containing no added Ca and 5mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA). This treatment inhibited the secretory response (release of alpha-amylase) both to isoproterenol and to dibutyryl cyclic adenosine 3':5'-monophosphate. The isoproterenol-stimulated synthesis of cyclic adenosine 3':5'-monophosphate was inhibited by depletion of Ca but not to an extent sufficient to explain the effects of depletion of Ca on secretion. Isoproterenol did not affect influx of 45Ca but stimulated efflux of 45Ca suggesting release of Ca from intracellular stores. Isoproterenol caused vacuolation of the Golgi region and (in high concentration) enhanced the release of 86Rb, responses which are both believed to be mediated by an increase in cytoplasmic Ca concentration. The results of these experiments suggest that isoproterenol acts to increase the tissue level of cyclic adenosine 3':5'-monophosphate which in turn acts to release Ca from intracellular stores. The rise in intracellular Ca concentration is believed to mediate exocytosis.

Animals↗
PubMed1993

The B1-immunoreactive proteins of the perinatal submandibular gland: similarity to the major parotid gland protein, RPSP.

The B1-immunoreactive proteins of type III cells of the perinatal rat submandibular gland are immunologically cross-reactive with proteins of both the sublingual and parotid glands; in particular, protein SMG-A appears similar to a major parotid protein. We isolated SMG-A and the parotid protein (known as M1 or leucine-rich protein), prepared polyclonal antibodies to them, and compared their biochemical properties and immunological reactivities. They were identical in their molecular weight on SDS-PAGE (23.5 kDa), tenacious binding to Affi-gel Blue, isoelectric point (pH 4.53), and proteolysis to a 14 kDa peptide: Antibodies to SMG-A showed reactivity with protein SMG-C, a product of the neonatal type I cells, as well as with proteins SMG-B1 and SMG-B2, contrasted with the absence of reactivity of anti-M1 IgG with these proteins. Anti-M1 reacted with the "parotid secretory protein" (PSP) of the mouse, and M1 appears to be the homologue, in the rat, of mouse PSP.

Animals↗
PubMed1993

Mycobacterial infection of the parotid gland: an unusual cause of parotid swelling.

Six cases of mycobacterial infection of the parotid gland are reviewed. All six cases presented solely with a slowly enlarging parotid swelling clinically indistinguishable from a parotid tumour. All of the swellings required surgical removal, superficial parotidectomy in four cases, and enucleation in two cases to obtain a definitive diagnosis.

Adult↗
PubMed1994

Characterization of an SH2 containing protein tyrosine phosphatase in rat parotid gland acinar cells.

Rat parotid glands were shown to possess protein phosphatase activity capable of catalyzing the dephosphorylation of several model phosphatase substrates, including p-nitrophenyl phosphate, tyrosine phosphorylated myelin basic protein and serine phosphorylated casein. A portion of this activity closely resembled dephosphorylation patterns of known protein tyrosine phosphatases. The reaction showed sensitivity to sodium orthovanadate, proceeded efficiently in the presence of metal chelators and favored acidic pH for optimum activity. Cell lysates from EGF- or isoproterenol-stimulated parotid glands, when immuno-precipitated with anti-Syp antibody, showed the induction of protein tyrosine phosphatase activity significantly higher than the unstimulated controls. The protein of M(r) = 65kDa also had elevated levels of tyrosine phosphorylation following isolation from cells treated to undergo proliferation. Thus parotid gland acinar cells possess protein tyrosine phosphatase activity of the PTPase 1D class associated with inducible cell growth, in addition to other phosphatases.

Animals↗
PubMed1992

The NK-1 receptor and a calcium-phospholipid pathway: inositol trisphosphate production and calcium movements induced by selective agonists of neurokinin receptors in rat parotid glands.

In the rat parotid gland, substance P has been shown to induce a phosphatidylinositol bisphosphate breakdown resulting in an inositol trisphosphate production. These data suggested that substance P activated a phospholipase C and thus mediated its effects through the calcium-phospholipid pathway. To determine which neurokinin (NK) receptor was involved in the substance P response, we have used selective agonists of the different NK receptors and examined their effects on both inositol trisphosphate production and calcium movements. A selective NK-1 receptor agonist, [Sar9Met(O2)11]-substance P, evoked an [3H]inositol trisphosphate production and a rapid and transient 45Ca2+ efflux. On the other hand, selective NK-2 and NK-3 receptor agonists, [beta-Ala8]-NKA(4-10) and [MePhe7]-NKB, respectively, were without effect. We conclude that, in the rat parotid glands, only the NK-1 receptors are coupled to the calcium-phospholipid pathway. The C-terminal part of substance P appeared to be sufficient to stimulate this route because the C-terminal octapeptide, substance P(4-11), mimicked substance P effects on both inositol trisphosphate production and calcium movements. The NK-2 and NK-3 receptors, if present in the rat parotid glands, are not associated with the calcium-phospholipid pathway.

Animals↗
PubMed1997

[Primary salivary gland tumors in lymph nodes of the parotid gland. Report of 3 cases and review of the literature].

Multiple intra- and paraglandular lymph nodes develop in the parotid gland, including salivary gland tissue with acinar and ductal formations. In the same way heterotopic salivary gland tissue can be localized in cervical lymph nodes. Except for the frequently occurring Warthin tumours, primary salivary gland tumours, which develop in the lymph nodes of the parotid gland or the cervical lymph nodes, are rare. Examples of these are adenomas (pleomorphic adenoma, basal cell adenoma) and carcinomas (acinic cell carcinoma, mucoepidermoid carcinoma, sebaceous gland carcinoma). Three of our own observations (sebaceous lymphadenoma, acinic cell carcinoma, mucoepidermoid carcinoma) are analysed. The condition for the diagnosis of primary salivary gland tumour within a lymph node is reliable evidence that the salivary gland tissue is tumour-free and that no other occult carcinoma is present.

Adenoma↗
PubMed1976

Ultrasound of the parotid gland.

Five cases of parotid gland masses were studied by ultrasound. Only retention cysts and true cysts of the parotid gland appear sonolucent at low and high gain settings. Benign and malignant tumor present as solid masses except for the Warthin's tumor which is sonolucent at lower gain settings but has a lattice of internal echoes at higher gain settings.

Adenolymphoma↗
PubMed1997

[Parotid tumors of non-glandular origin: local and distant metastases in the parotid gland].

BACKGROUND: Secondary involvement of the parotid gland by nonsalivary gland malignancies is relatively common. Especially if the primary site is unknown, distinguishing a primary neoplasm from a metastasis can be difficult. PATIENTS: This text reviews 10 metastatic lesions to the parotid gland from 252 consecutive parotid tumors. Moreover we present the metastasis of an oat cell carcinoma as initial presentation of a lung tumor. RESULTS: The percentage of metastatic tumors of the parotid gland in our study group was 4%, representing 32% of all malignancies. The majority (80%) originate from primary tumors in the head and neck region with skin cancer being the most important primary site (70%). In 40% the parotid gland metastasis was the first manifestation of a malignancy. CONCLUSIONS: The distinction between primary salivary gland tumor and metastasis is of particular importance for therapy and prognosis. The possibility of a metastatic tumor should always be considered when primary salivary gland tumors have histologic features similar to those of tumors occurring in other regions of the body (squamous carcinoma, melanoma, adenocarcinoma, clear cell, oat cell, and undifferentiated carcinoma). The skin of the head and neck is of primary interest during clinical examination, followed by the mucosa of the upper respiratory and digestive tract. Histologic and especially immunohistochemical characteristics can be helpful in identifying the primary tumor. If metastases to the parotid gland are the only manifestation and if they only spread to regional lymph nodes, more aggressive surgical treatment may be beneficial.

Adult↗
PubMed1998

Carbachol-induced oxygen consumption in slices from developing rat submandibular and parotid glands.

In contrast to the submandibular gland, the developing rat parotid gland shows refractoriness to cholinergic secretagogues until 2 wks of age. To assess the underlining mechanism of this refractoriness, I investigated changes in oxygen consumption as a function of animal age in slices from rat submandibular and parotid glands, measuring both basal and carbachol-stimulated levels. The oxygen consumption was determined by a direct manometric method in the Warburg apparatus. Carbachol-induced oxygen uptake in submandibular gland slices was observed by 1 day of age and reached the adult level of stimulation by 3 wks of age. In the parotid gland, carbachol failed to stimulate oxygen uptake in the early post-natal period, and the first response was detected at 2 wks of age, reaching the adult level at 4 wks of age. Para-fluorohexahydro-sila-diphenidol (pFHHSiD), a selective M3 antagonist, inhibited carbachol-induced oxygen uptake in both glands, while pirenzepine, a selective M1 antagonist, had no effect, suggesting that the M3 muscarinic receptors are involved in this process. The respiratory effect of carbachol, in both glands, was inhibitable by ouabain and, to a lesser extent, by furosemide, indicating that carbachol-enhanced oxygen uptake is due to Na,K-ATPase and that the furosemide-sensitive co-transport of Na+ entry is underdeveloped in immature cells. The ouabain-sensitive Na,K-ATPase activity in the parotid gland increased from birth until 28 days of age. At the time of parotid gland refractoriness to carbachol, Ca2+ ionophore A23187 caused an increase of oxygen uptake only in the presence of extracellular Ca2+. In the presence of carbachol, the effect of ionophore was significantly higher than that of ionophore alone. These results raise the possibility that the refractoriness of the parotid gland to carbachol is due to the inability of carbachol to increase Ca2+ uptake rather than to the lack of distal limb, which resides on the pathway from receptor stimulation to Na,K-ATPase activation.

Age Factors↗
PubMed1983

Bilateral parotid gland aplasia.

Bilateral parotid gland aplasia is a cause of xerostomia. A case is presented in which the clinical diagnosis was confirmed with the use of 99mTcO-4 salivary gland scintiscanning and computerised tomography. The literature of this rare condition is reviewed and significance to the patient discussed.

Humans↗
PubMed2006

Repeated androgen and thyroid hormone injection modulates the morphology of hormone-responsive duct cells in the mouse parotid gland.

When the parotid glands of normal male and female ICR mice (12 weeks of age) were examined under a light microscope, no granular cells were seen in the duct system. However, transmission electron microscopy revealed that, in both sexes, many striated duct cells contained a few electron-dense secretory granules in their subluminal cytoplasm and had formed so-called granular striated tubules (GSTs) in some of the striated duct segments. These secretory granules were not large enough to be visible with a light microscope. Fully fledged granular cells, containing large secretory granules visible with a light microscope, could be induced in the GST segments of the glands of males by injection with 5alpha-dihydrotestosterone (DHT), triiodothyronine (T(3)), and dexamethasone (Dex), given alone or in combination every other day for 2 weeks. Dex alone showed no effect on the GSTs in this study. Both DHT and T(3), either individually or with Dex, were moderately effective, inducing a few scattered fully fledged granular cells. A stronger effect was detected after concomitant injection of DHT and T(3), with or without Dex, with more abundant fully developed granular cells appearing in the GST segments. Electron microscopy revealed that these granular cells had abundant large secretory granules in their apical two-thirds, a basal nucleus, and modest basal infoldings. By contrast, the effect of the same hormones was very weak in the glands of females, and even the concomitant injection of DHT and T(3), with or without Dex, rarely induced fully fledged granular cells. These results indicate a close similarity between the ductal systems of the major salivary glands of the mouse, in terms of some of the striated duct segments containing secretory granules, being under the same multihormonal regulation, and being sexually dimorphic.

Animals↗
PubMed1980

Effects of carbachol on extracellular Na-dependent AIB uptake in rat parotid gland.

In rat parotid glands the uptake of 2-[1-14C]aminoisobutyric acid (AIB), in vitro, depends on a Na concentration gradient between the intra- and extracellular medium. Ouabain (1 mM) which inhibits the Na+-K+-ATPase and a Na+ ionophore, monensin (which dissipates the Na+ gradient), both suppress this amino acid uptake. Carbachol (5 microM) (through muscarinic receptors) evokes a decrease in AIB uptake, and in the presence of 0.1 mM ouabain the cholinergic effect is enhanced. Ouabain alone (0.1 mM) very slightly depresses the [14C]AIB uptake. Neither 1 microM isoproterenol, nor 1 microM Ca2+ ionophore A23187, which affect the membrane potential in rat parotid acinar cells, modifies the AIB uptake. When the Ca is removed from the incubation medium, carbachol still evokes a small decreasing effect on AIB uptake. From these data we can suggest that the reduced AIB uptake (induced by the cholinergic agonist) appears to be related to a process dependent on variation of intracellular Na concentration that may be triggered by the cholinergic agonist.

Absorption↗