OBJECTIVETo investigate the expression and relationship of programmed cell death 5 (PDCD5) and cell apoptosis in the parotid gland after leading duct ligation in rat and elucidate the role of PDCD5 on the atophy of parotid gland.

METHODSThe Wistar rat model of leading duct ligation was established, and the samples of parotid gland were obtained from different time point (0, 1, 3, 5, 7, 14, 21, 30, 60, 90 and 120 d). The expression of PDCD5 protein was examined by immunohistochemistry. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL).

RESULTSThe distribution of PDCD5 protein in normal parotid was in cytoplasm with uniformity. The expression of PDCD5 protein was significantly increased and reached the peak at 3 d (1.261 ± 0.048) following main duct ligation. PDCD5 was located both in cytoplasm and nuclear of parotid gland cells. The PDCD5 density in acinar cells was higher than that in duct cells at day 1 and 3 after duct ligation (P < 0.01). The apoptotic cells were obviously upregulated at 3 d after duct ligation. The apoptosis index observed in acinar cells [(21.750 ± 0.119)%] was more than that in duct cells [(5.720 ± 0.205)%]. The difference of apoptosis index between acinar cells and duct cells was statistically significant (P < 0.01). The increased PDCD5 levels were positively correlated with cell apoptosis induced by duct ligation.

CONCLUSIONSThe expression of PDCD5 is associated with the atophy of the parotid gland after rat parotid duct ligation, indicating that PDCD5 might play an important role in apoptotic pathways after parotid duct ligation.

Acinar Cells ; metabolism ; Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Atrophy ; Cell Nucleus ; metabolism ; Cytoplasm ; metabolism ; Ligation ; Male ; Parotid Gland ; cytology ; metabolism ; pathology ; Rats ; Rats, Wistar ; Salivary Ducts

Synaptotagmin is a Ca2+ sensing protein, which triggers a fusion of synaptic vesicles in neuronal transmission. Little is known regarding the expression of Ca2+ - dependent synaptotagmin isoforms and their contribution to the release of secretory vesicles in mouse and rat parotid acinar cells. We investigated a type of Ca2+ - dependent synaptotagmin and Ca2+ signaling in both rat and mouse parotid acinar cells using RT-PCR, microfluorometry, and amylase assay. Mouse parotid acinar cells exhibited much more sensitive amylase release in response to muscarinic stimulation than did rat parotid acinar cells. However, transient [Ca2+]i increases and Ca2+ influx in response to muscarinic stimulation in both cells were identical, suggesting that the expression or activity of the Ca2+ sensing proteins is different. Seven Ca2+ - dependent synaptotagmins, from 1 to 7, were expressed in the mouse parotid acinar cells. However, in the rat parotid acinar cells, only synaptotagmins 1, 3, 4 and 7 were expressed. These results indicate that the expression of Ca2+ - dependent synaptotagmins may contribute to the release of secretory vesicles in parotid acinar cells.
Synaptotagmins/*metabolism ; Signal Transduction ; Rats ; Protein Isoforms/metabolism ; Parotid Gland/cytology/*metabolism ; Muscarinic Agonists/pharmacology ; Mice ; Exocytosis/drug effects/physiology ; Carbachol/pharmacology ; Calcium/metabolism/*physiology ; Animals ; Amylases/secretion

PURPOSE: In non-excitable cells, which include parotid and pancreatic acinar cells, Ca(2+) entry is triggered via a mechanism known as capacitative Ca(2+) entry, or store-operated Ca(2+) entry. This process is initiated by the perception of the filling state of endoplasmic reticulum (ER) and the depletion of internal Ca(2+) stores, which acts as an important factor triggering Ca(2+) entry. However, both the mechanism of store-mediated Ca(2+) entry and the molecular identity of store-operated Ca(2+) channel (SOCC) remain uncertain. MATERIALS AND METHODS: In the present study we investigated the Ca(2+) entry initiation site evoked by depletion of ER to identify the localization of SOCC in mouse parotid and pancreatic acinar cells with microfluorometeric imaging system. RESULTS: Treatment with thapsigargin (Tg), an inhibitor of sarco/endoplasmic reticulum Ca(2+)-ATPase, in an extracellular Ca(2+) free state, and subsequent exposure to a high external calcium state evoked Ca(2+) entry, while treatment with lanthanum, a non-specific blocker of plasma Ca(2+) channel, completely blocked Tg-induced Ca(2+) entry. Microfluorometric imaging showed that Tg-induced Ca(2+) entry started at a basal membrane, not a apical membrane. CONCLUSION: These results suggest that Ca2+ entry by depletion of the ER initiates at the basal pole in polarized exocrine cells and may help to characterize the nature of SOCC.
Animals ; Calcium/*metabolism ; Calcium Channels/drug effects/metabolism ; Cells, Cultured ; Endoplasmic Reticulum/drug effects/*metabolism ; Mice ; Mice, Inbred ICR ; Microscopy, Fluorescence ; Pancreas/cytology/drug effects/*metabolism ; Parotid Gland/cytology/drug effects/*metabolism ; Thapsigargin/pharmacology

We report the case of a patient who presented with cystic lymphoid hyperplasia of the right parotid gland as the index diagnosis of HIV infection. Histological examination of the excised parotid gland revealed a solid-cystic lymphoepithelial lesion with a non-keratinous squamous epithelium, which grew into the lymphoid component via anastomosing cords and islands. These anastomosing cords and islands contained variably abundant B cells, several subepithelial multinucleated histiocytes, salivary ducts infiltrated by small lymphocytes, and a dense lymphoid infiltrate containing lymphoid follicles with enlarged, irregular germinal centres.
Adult ; B-Lymphocytes ; cytology ; Biopsy ; Epithelial Cells ; cytology ; Epithelium ; metabolism ; HIV Infections ; diagnosis ; Humans ; Hyperplasia ; pathology ; virology ; Immunohistochemistry ; Lymphocytes ; cytology ; Male ; Parotid Gland ; pathology ; virology ; Salivary Glands ; pathology ; Tomography, X-Ray Computed