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PubMed1977

Electron microscopic autoradiographic analysis of the uptake and intracellular transport of H3-leucine by the rat submandibular gland acinar cells in tissue slices.

Uptake of H3-leucine into secretory product and its subsequent intracellular transport was analyzed by electron microscopic autoradiographic techniques in the rat submandibular gland acinar cells in vitro. The route and kinetic timetable of intracellular transport was established for the acinar cell secretory product by calculating the present of silver grains and relative grain density associated with the various organelles on a time sequence basis. Radioactivity was first associated with the rough endoplasmic reticulum; then the convex surface of the Golgi apparatus; the concave surface of the Golgi apparatus; and finetics of intracellular transport in the rat submandibular gland acinar cell with other established systems revealed only a difference in the exit of radioactivity from the concave surface of the Golgi apparatus.

Animals↗
PubMed1998

Oncocytic lipoadenoma of the submandibular gland.

We report a case of oncocytic lipoadenoma of the submandibular gland, previously unrecognized benign tumor of the salivary gland. The patient was a 66-year-old Japanese woman with a left submandibular mass, measuring 11 x 7.5 x 5 cm. Microscopically, the mass was completely surrounded by a thin fibrous connective tissue capsule, and was composed of an intimate admixture of mature fat cells and oncocytes. There have been no English reports of such a neoplasm in the salivary gland with the exception of one recent case report of lipoadenoma of the parotid gland without oncocytic features. We propose the diagnostic term "oncocytic lipoadenoma" for this benign tumor.

Adenoma↗
PubMed1994

Effects of vasoactive intestinal peptide and its homologues on the substance P-mediated secretion of fluid and protein from the rat submandibular gland.

1. Vasoactive intestinal peptide (VIP) and secretin elicited slight secretion of saliva but peptide histidine isoleucine (PHI) and gastric inhibitory peptide (GIP) failed to elicit secretion of saliva from rat submandibular glands. 2. Substance P (SP)-mediated secretion of fluid and protein were enhanced by VIP and secretin but not by PHI or GIP. 3. These results suggest that the effects of VIP, PHI, secretin and GIP on the secretion of fluid from rat submandibular glands and the synergistic effects of VIP and its homologues on the SP-mediated secretion of fluid and protein do not correspond to the extent of the structural homology of each analogue to VIP.

Amino Acid Sequence↗
PubMed1989

Carbachol stimulation of inositol phosphate accumulation in rat submandibular gland fragments is not modified by VIP.

Formation of inositol phosphates in response to carbachol, phenylephrine and vasoactive intestinal polypeptide (VIP) was studied after labelling with [3H]myo-inositol in rat submandibular gland fragments. Carbachol enhanced the accumulation of inositol phosphates in a concentration-dependent manner. This effect was independent of calcium in the incubation medium and totally antagonized by atropine (IC50 = approx. I nM). Phenylephrine also induced an increase in inositol phosphate accumulation, which was totally antagonized by prazosin but not by atropine. Vasoactive intestinal polypeptide, isoproterenol and forskolin, compounds known to enhance the levels of cAMP in rat salivary gland, or addition of dibutyryl-cAMP (DB-cAMP) failed to alter basal or carbachol-evoked accumulation of inositol phosphates. It is concluded that the formation of inositol phosphates during muscarinic receptor stimulation with carbachol in rat submandibular gland fragments is not affected by adrenoceptor occupation or by cAMP. In particular, addition of VIP, which coexists with acetylcholine, did not alter the muscarinic inositol phosphate response.

Animals↗
PubMed1993

Immunoelectron microscopy of carbonic anhydrase isozyme VI in human submandibular gland: comparison with isozymes I and II.

Carbonic anhydrase VI (CA VI) was purified from human saliva by inhibitor-affinity chromatography, and its distribution was studied in human submandibular gland by the indirect immunoperoxidase technique with a rabbit polyclonal antibody raised against the isozyme. Polyclonal antibodies to human CA I and CA II purified from erythrocytes were also raised and used for immunostaining. SDS-polyacrylamide gel electrophoresis of the purified isozymes revealed a single protein band (CA VI, 42 KD; CA I and CA II, 30 KD). Antibody raised against CA VI did not crossreact with CA I or CA II either by Western or by dot-blotting. However, antibodies against CA I and CA II showed slight crossreaction with each other's antigen by dot-blotting. In a Western blot of purified submandibular gland CA, antibody to CA VI stained the 42 and 30 KD bands, and antibodies to CA I and CA II stained the 30 KD band. The 42 KD but not the 30 KD molecule was cleaved by endo-beta-N-acetylglucosaminidase F, indicating that the former contains N-linked oligosaccharides. Immunostaining for CA VI was seen in the secretory granules and cytosol of serous acinar cells and in the duct luminal contents. Staining specific for CA II was observed in the cytosol of serous acinar and duct epithelial cells. Antibody to CA I reacted only with the walls of small blood vessels. These results suggest that (a) serous acinar cells secrete 42 KD CA VI which functions in the oral cavity and that (b) serous acinar and duct epithelial cells possess cytosolic CA (30 KD CA VI and CA II) which functions in situ.

Blotting, Western↗
PubMed2002

Methacholine-induced cGMP production is regulated by nitric oxide generation in rabbit submandibular gland cells.

Guanosine 3',5'-monophosphate (cGMP) is an intracellular messenger in various kinds of cell. We investigated the regulation of cGMP production by nitric oxide (NO) in rabbit submandibular gland cells. Methacholine, a muscarinic cholinergic agonist, stimulated cGMP production in a dose- and time-dependent manner, but the alpha-agonist phenylephrine, substance P and the beta-agonist isoproterenol failed to evoke cGMP production. In fura-2-loaded cells, methacholine induced an increase in intracellular Ca2+ ([Ca2+]i) in a concentration-dependent manner, which was similar to that for cGMP production. When the external Ca2+ was chelated with EGTA, methacholine failed to induce cGMP production. Ca2+ ionophore A23187 and thapsigargin, which induce the increase in [Ca2+]i without activation of Ca2+-mobilizing receptors, mimicked the effect of methacholine. cGMP production induced by methacholine, A23187 and thapsigargin was clearly inhibited by NG-nitro-L-arginine methylester (L-NAME), a specific inhibitor of nitric oxide synthase (NOS). S-Nitroso-N-acetyl-DL-penicillamine (SNAP), a NO donor, induced cGMP formation. In the lysate of rabbit submandibular gland cells, Ca2+-regulated nitric oxide synthase activity was detected. These findings suggest that cGMP production induced by the activation of muscarinic cholinergic receptors is regulated by NO generation via the increase in [Ca2+]i.

Adrenergic alpha-Agonists↗
PubMed1997

Fine structure of tuft cells of the main excretory duct epithelium in the rat submandibular gland.

BACKGROUND: Tuft cells, which are characterized by long microvilli with prominent rootlets and by vesicular and tubular profiles, are present in the mucosal epithelium of a number of hollow organs, including the main excretory duct of the rat submandibular gland. Despite their widespread occurrence, little is known of their function. METHODS: Main excretory ducts of the submandibular gland were obtained from 20 male Wistar rats and prepared for electron microscopic examination. Specimens also were subjected to various histochemical procedures, including HRP (horseradish peroxidase) uptake, the demonstration of catalase in peroxisomes, glycoconjugate cytochemistry, and ruthenium red staining. RESULTS: The features of the tuft cells in the MED (main excretory duct) basically were similar to those described in other organs. However, for the first time it was observed that in the submicrovillus zone and intermicrovillus space, there were many membrane-bound electron-dense granules, which resemble the so-called glycocalyceal bodies found on the apical surface of normal and neoplastic intestinal-type epithelial cells. Hypolemmal nerve terminals were seen to be in contact with the basal portion of tuft cells. After injection of HRP, reaction products were observed on the luminal surface of the microvilli, but not within the vesicles. Vesicles and tubules in the supranuclear cytoplasm exhibited a positive cytochemical reaction for glycoconjugates. The surface coat of tuft cell microvilli was stained with ruthenium red, but the vesicles and tubules in the supranuclear cytoplasm remained unstained. CONCLUSIONS: Our observations suggest that the tuft cells may engage in secretory activity in addition to reception.

Animals↗
PubMed1976

Stimulus-secretion coupling: role of cyclic AMP, cyclic GMP and calcium in mediating enzyme (kallikrein) secretion in the submandibular gland.

1. The role of adenosine 3':5'-phosphate (cyclic AMP) and guanosine 3':5'-phosphate (cyclic GMP) as second messengers for the enzyme secretory response evoked by the autonomic neurotransmitters, noradrenaline and acetylcholine, is examined in this in vitro study on the guinea-pig submandibular gland. 2. Noradrenaline increased enzyme (kallikrein) secretion. The initial stimulation of enzyme release appeared to be dose-dependent. The time course of cumulative kallikrein secretion revealed a complex pattern. Isoprenaline and phenylephrine were almost as potent as noradrenaline in releasing kallikrein. Both propranolol and phentolamine were required to fully inhibit the noradrenaline-stimulated enzyme secretion. 3. The cumulative secretion of kallikrein evoked by acetylcholine was dose-dependent. The onset of secretion showed a significantly greater time-lag than that observed with noradrenaline. Atropine effectively blocked the release of kallikrein by acetylcholine. 4. Dibutyryl cyclic AMP stimulated enzyme secretion. Dibutyryl cyclic GMP caused an initial increase which was not maintained. 5. The cyclic nucleotide phosphodiesterase inhibitors, theophylline and papaverine, increased basal kallikrein secretion. The action of the cyclic phosphodiesterase inhibitors on the secretory response to noradrenaline, acetylcholine, dibutyryl cyclic AMP and dibutyryl cyclic GMP was complex. In general, the increase in enzyme release produced by the secretagogues was additively enhanced by both inhibitors. 6. Omission of calcium inhibited both acetylcholine and dibutyryl cyclic GMP stimulated kallikrein release, but to a lesser degree than that of noradrenaline and dibutyryl cyclic AMP. High concentrations of extracellular calcium (10 mM) appeared to enhance the action of acetylcholine. 7. Noradrenaline produced a rise in the intracellular level of cyclic AMP. The increase preceded the stimulated secretion of kallikrein. Of the various adrenergic agonists, noradrenaline and isoprenaline were the most potent, whereas phenylephrine was significantly less effective in raising basal cyclic AMP values. Acetylcholine was without effect, even in the presence of a cyclic phosphodiesterase inhibitor. 8. Acetylcholine and noradrenaline raised intracellular levels of cyclic GMP only when the tissue incubations were performed in the presence of a cyclic phosphodiesterase inhibitor. The increase in cyclic GMP produced by acetylcholine preceded enzyme secretion. 9. Morphological data substantiated the finding that the in vitro release of kallikrein evoked by the secretagogues was associated with the depletion of secretory granules and vacuolations in acinar cells of the gland slices. 10. The molecular mechanisms which control enzyme secretion in the exocrine submandibular gland are discussed. Models are presented for the role of transmitter-specific cyclic nucleotides and calcium in stimulus-secretion coupling.

Acetylcholine↗
PubMed2004

Rat submandibular gland during the maturation process: changes in enzyme activities, protein and lectin-binding profiles.

The total protein glycosylation profile and specific activity of lysosomal enzymes were investigated in rat submandibular glands isolated from very young (1-month), young (1.5-months) and adult rats (3-months) rats. The specific activity of lysosomal hydrolases (i.e. acid phosphatase, arylsulfatases A and B, beta-N-acetyl-D-glucosaminidase, beta-galactosidase and beta-glucuronidase) decreased in parallel to increasing age of the animals. Furthermore, the thermal stability of acid phosphatase and beta-N-acetyl-D-glucosaminidase was influenced by the age of rats. Age-related changes in protein profile regarding the intensity of particular bands as well as the appearance of certain proteins limited to special age groups were also demonstrated as revealed by Coomassie and lectin staining. Moreover, the marked age-related increase in structures Man (alpha1-2, alpha1-3, alpha1-6) Man, Fuc (alpha1-6) GlcNAc as well as Gal (beta1-3) GlcNAc was observed, whereas staining with terminal NeuAc and GlcNAc showed an inverse correlation. The reaction with (beta1-6) branched N-glycans and Gal (beta1-3) Gal structures was limited to 1-month-old rats. No significant changes in a specific reaction with NeuAc (alpha2-3) Gal were observed. We speculate that the observed differences with respect to protein and glycosylation profiles between 1-month-old rats and older ones could be caused by a modification of the diet composition as well as by the functional and morphological maturation of the rat submandibular gland.

Age Factors↗
PubMed1981

[Juxtaglomerular cells after removal of the submandibular glands in male mice: quantitative electron microscopy (author's transl)].

The juxtaglomerular cells in the kidney were studied qualitatively and quantitatively on the 7th and 49th day after removal of the bilateral submandibular glands at 60 days of age in male mice. In normal mice, the juxtaglomerular cells contained numerous specific granules. The Golgi apparatus was not well developed and the rough endoplasmic reticulum was generally flat and short in profile. At 7 days after extirpation of the submandibular glands, the specific granules were sparsely distributed, the Golgi apparatus was relatively prominent, and the rough endoplasmic reticulum was dilated and increased in amount. At 49 days after operation, the specific granules were increased in number, and the Golgi apparatus and rough endoplasmic reticulum were as prominent as at 7 days. The volume ratios of the nucleus, specific granules, Golgi apparatus, rough endoplasmic reticulum and mitochondria were examined by quantitative electron microscopy. After operation, the volume ratio of specific granules was significantly decreased at 7 days, but was increased at 49 days. The volume ratios of Golgi apparatus and rough endoplasmic reticulum were significantly increased at both 7 and 49 days after operation. The volume ratios of nucleus and mitochondria showed no significant difference from those in normal and sham-operated mice. The volumes of adrenal cortex and medulla at 49 days after operation were also examined by quantitative microscopy. They were not significantly different from those in normal mice.

Animals↗
PubMed1998

Interaction between substance P and beta-adrenergic agonists in the modulation of the secretion of fluid and protein by the rat submandibular gland.

The interactions between substance P and beta-adrenergic agonists such as isoprenaline, dobutamine and terbutaline in the control of the secretion of fluid and protein from the rat submandibular gland have been examined. Substance P elicited large volumes of saliva whereas isoprenaline, dobutamine and terbutaline elicited small volumes only. The secretion of fluid in response to substance P was markedly enhanced when substance P was administered in combination with isoprenaline or dobutamine but not when it was administered in combination with terbutaline. Isoprenaline elicited large amounts of protein, whereas substance P elicited small amounts. The secretion of protein in response to isoprenaline did not change when isoprenaline was administered in combination with substance P. The secretion of fluid and protein induced by substance P in combination with isoprenaline was antagonized by metoprolol and by spantide, but it was unaffected by pretreatment with ICI118551. These results suggest that in the rat submandibular gland stimulation of beta1-adrenoceptors but not of beta2-adrenoceptors potentiates the secretion of fluid that is induced by stimulation of tachykinin receptors, whereas stimulation of tachykinin receptors does not enhance the secretion of protein that is induced by stimulation of beta1-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1976

Chemical analysis of a sulphated macromolecule isolated from rabbit submandibular gland.

Chemical analysis of a sulphated macromolecule isolated from the rabbit submandibular gland showed that about 70 per cent of the dry weight could be accounted for in terms of amino acids of which the acidic amino acids, proline and alanine were the most abundant. Total carbohydrate was 11%. Galactose was the main neutral sugar but galactosamine, glucosamine, neuraminic acid, glucose and mannose could also be demonstrated. Sulphate accounted for 1,4%. No uronic acid was found. The data indicate that the sulphated macromolecule from the rabbit gland is in fact a sulphated glycoprotein.

Amino Acids↗
PubMed1991

Location of glandular kallikrein mRNAs in mouse submandibular gland at the cellular and ultrastructural level by hybridization histochemistry using 32P- and 3H-labeled oligodeoxyribonucleotide probes.

We investigated the location of expression of mouse glandular kallikrein genes in the submandibular gland of adult male mice at the ultrastructural level by hybridization histochemistry, using 32P- and 3H-labeled oligodeoxyribonucleotide probes. Vibratome slices were hybridized, flat-embedded, sectioned, and autoradiographs prepared. The 32P-labeled probe, which was specific for a region common to all mouse glandular kallikrein mRNAs, provided resolution at the cellular and subcellular level, demonstrating mRNA transcripts encoded by the majority of the 12 mouse glandular kallikrein genes in the perinuclear area of granular convoluted tubule cells (GCT) associated with rough endoplasmic reticulum (RER). The 3H-labeled probe was specific for mRNA transcripts of mGK-6, the renal kallikrein gene, which is also expressed in salivary glands. Occasional morphologically distinct granulated cells within GCTs, as well as striated duct cells, were found to express this gene. Resolution obtained with this 3H-labeled probe showed mGK-6 mRNA in striated duct cells to be located on RER and in the nucleus and perinuclear area of the cell. There was also an apparent mitochondrial association with regions of RER that labeled with this probe. The location of hybrids was confirmed by simultaneous assessment of sites of silver grains in serial sections. There are therefore at least two types of mGK-6-expressing cells in ducts of the submandibular gland, which are distinct from those expressing other kallikrein genes. In striated duct cells, there is evidence of a close mitochondrial association with RER that contains labeled mGK-6 transcripts, which is unexplained.

Animals↗
PubMed2001

Expression of volume-sensitive Cl(-) channels and ClC-3 in acinar cells isolated from the rat lacrimal gland and submandibular salivary gland.

1. The expression of ClC-3 was examined in rat lacrimal gland and submandibular salivary gland cells using RT-PCR and Western analysis. Whole-cell patch clamp methods were used to investigate the expression of volume-sensitive anion channels in acinar cells isolated from these tissues. 2. Expression of mRNA encoding ClC-3, and ClC-3 protein, was found in rat submandibular gland by RT-PCR and Western analysis. Rat lacrimal gland cells, however, did not appear to express mRNA encoding for ClC-3, nor the ClC-3 protein. 3. Volume-sensitive anion conductances were observed in both rat lacrimal gland and submandibular salivary gland acinar cells. The conductance was of a similar size in the two cell types, but was much slower to activate in the lacrimal cells. 4. The properties of the conductances in lacrimal and submandibular cells were similar, e.g. halide selectivity sequence (P(I) > P(Cl) > P(aspartate)) and inhibition by 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid, 5-nitro-2-(3-phenylpropylamino)-benzoate and tamoxifen. 5. The data suggest that the expression of ClC-3 is not an absolute requirement for the activity of volume-sensitive anion channels in rat lacrimal gland acinar cells.

Animals↗
PubMed1999

Sex-related expression of sialic acid acceptor sugars in the mouse submandibular gland. Simultaneous visualization by confocal laser scanning microscopy.

The novel combination of sialidase digestion with simultaneous PNA and DBA binding yielded marked differences on sialoglycoconjugate occurrence and distribution in the mouse submandibular gland acinar cells of the two sexes. Striking differences in the structure of terminal disaccharides within stored secretory sialoglycoconjugates were also found. High content of sialic acid, characterized by the terminal sequence sialic acid-alpha-N-acetylgalactosamine, was established to only occur in the male acini where secretory cells appeared to be differently stained; indeed, some cells exhibited codistribution of sialic acid-alpha-N-acetylgalactosamine and sialic acid-beta-galactose terminal disaccharides, whereas other ones exclusively contained one of the two kinds of terminal sequences. In the female acinar cells, the secretory products were found to be almost exclusively composed by glycoconjugates having sialic acid subtended to beta-galactose without appreciable differences between acinar cells. Our finding of such extensive differences in the acinar cells of male and female mice adds new insights into the submandibular gland sexual dimorphism, commonly attributed to the androgen responsiveness of the granular convoluted tubule portion of the gland.

Acetylgalactosamine↗
PubMed1981

[The sublingual and submandibular glands after preganglionic parasympathetic blockade. A histological, electron optical, autoradiographic and scintigraphic study on the guinea pig].

After preganglionic parasympathetic block three histological and histochemical phases could be determined in the only cholinergically innervated mucous cells of the sublingual gland. The first phase is characterized by overproduction and oversecretion. Possibly this results from acetylcholine overproduction, caused by the block, termed as "degeneration secretion" however of preganglionic origin. Hypersensitivity of the gland parenchyma appears to be present also, which with catecholamins as well as acetylcholine cause the ensuing "paralytic secretion". At the end of the first phase the desquamation of parts of cells, and rarely entire cells, in form of apocrine and holocrine secretion occurs and a uniform cell population is developing. When this cell population develops the second phase starts. The lack of stimulation because of acetylcholine exhaustion is discussed as the cause of the second phase. In the third phase a self regulatory involution commences. In the double innervated serous submandibular gland the effect of chorda tympani section was less severe.

Acetylcholine↗
PubMed1991

Inhibition of activity-induced parotid growth by submandibular gland ablation or autonomic denervation.

When solid chow was reintroduced for 2 days to rats previously maintained on an all-liquid diet, [3H]thymidine incorporation into rat parotid gland was 2.4-4.4 times that of chow-fed or liquid-fed animals. When the submandibular-sublingual glands were removed before the change in diet from liquid to solid food, values for [3H]thymidine incorporation of parotid gland were not statistically different from those of chow-fed rats: the increase was completely prevented. The increase in gland size that accompanied the change in dietary consistency was not prevented by prior submandibular gland ablation; [3H]uridine incorporation was also not different from that of chow controls. The removal of both the sympathetic and parasympathetic nerves to the parotid gland before the dietary manipulation also suppressed [3H]thymidine incorporation into parotid, and values did not differ from chow controls. Moreover, the return to normal gland size (chow level) also was prevented by autonomic denervation. The data show an important role of the submandibular gland in regulation of the thymidine increase associated with the enhanced parotid activity that accompanies the change from liquid to solid diet. However, the submandibular gland does not have an important role in regulation of the increase in gland size that also accompanies the dietary change, whereas the autonomic nerves have an important role in regulation of hypertrophy and hyperplasia of parotid gland.

Animal Feed↗