Experimental Evidence of Fluid Secretion of Rabbit Lacrimal Gland Duct Epithelium

2014 ◽  
Vol 55 (7) ◽  
pp. 4368
Author(s):  
Chuanqing Ding
2014 ◽  
Vol 55 (7) ◽  
pp. 4360 ◽  
Author(s):  
Máté Katona ◽  
Eszter Vizvári ◽  
Lukács Németh ◽  
Andrea Facskó ◽  
Viktória Venglovecz ◽  
...  

2013 ◽  
Vol 91 ◽  
pp. 0-0 ◽  
Author(s):  
E TOTH-MOLNAR ◽  
M KATONA ◽  
A FACSKO ◽  
V VENGLOVECZ ◽  
L NEMETH ◽  
...  

2000 ◽  
Vol 21 (1) ◽  
pp. 588-594 ◽  
Author(s):  
Chr. Albrecht May ◽  
Ulrich Welge-Lüßen ◽  
Anselm Jünemann ◽  
Hans Bloemendal ◽  
Elke Lütjen-Drecoll
Keyword(s):  

2001 ◽  
Vol 23 (3) ◽  
pp. 199-205 ◽  
Author(s):  
Yelena Paranyuk ◽  
Nidia Claros ◽  
Aija Birzgalis ◽  
Leon C. Moore ◽  
Peter R. Brink ◽  
...  

2001 ◽  
Vol 281 (2) ◽  
pp. G438-G446 ◽  
Author(s):  
Satish K. Singh ◽  
Albert Mennone ◽  
Alessandro Gigliozzi ◽  
Flavia Fraioli ◽  
James L. Boyer

Cholangiocytes absorb and secrete fluid, modifying primary canalicular bile. In several Cl−-secreting epithelia, Na+-K+-2Cl− cotransport is a basolateral Cl− uptake pathway facilitating apical Cl− secretion. To determine if cholangiocytes possess similar mechanisms independent of CO2/HCO[Formula: see text], we assessed Cl−-dependent secretion in rat liver isolated polarized bile duct units (IBDUs) by using videomicroscopy. Without CO2/HCO[Formula: see text], forskolin (FSK) stimulated secretion entirely dependent on Na+ and Cl−and inhibited by Na+-K+-2Cl−inhibitor bumetanide. Carbonic anhydrase inhibitor ethoxyzolamide had no effect on FSK-stimulated secretion, indicating negligible endogenous CO2/HCO[Formula: see text] transport. In contrast, FSK-stimulated secretion was inhibited ∼85% by K+ channel inhibitor Ba2+ and blocked completely by bumetanide plus Ba2+. IBDU Na+-K+-2Cl− cotransport activity was assessed by recording intracellular pH during NH4Cl exposure. Bumetanide inhibited initial acidification rates due to NH[Formula: see text] entry in the presence and absence of CO2/HCO[Formula: see text]. In contrast, when stimulated by FSK, a 35% increase in Na+-K+-2Cl− cotransport activity occurred without CO2/HCO[Formula: see text]. These data suggest a cellular model of HCO[Formula: see text]-independent secretion in which Na+-K+-2Cl−cotransport maintains high intracellular Cl−concentration. Intracellular cAMP concentration increases activate basolateral K+ conductance, raises apical Cl−permeability, and causes transcellular Cl− movement into the lumen. Polarized IBDU cholangiocytes are capable of vectorial Cl−-dependent fluid secretion independent of HCO[Formula: see text]. Bumetanide-sensitive Na+-K+-2Cl− cotransport, Cl−/HCO[Formula: see text] exchange, and Ba2+-sensitive K+ channels are important components of stimulated fluid secretion in intrahepatic bile duct epithelium.


2007 ◽  
Vol 292 (1) ◽  
pp. L304-L311 ◽  
Author(s):  
Jin V. Wu ◽  
Mauri E. Krouse ◽  
Jeffrey J. Wine

Cystic fibrosis (CF) airway disease arises from defective innate defenses, especially defective mucus clearance of microorganisms. Airway submucosal glands secrete most airway mucus, and CF airway glands do not secrete in response to VIP or forskolin. CFTR, the protein that is defective in CF, is expressed in glands, but immunocytochemistry finds the highest expression of CFTR in either the ciliated ducts or in the acini, depending on the antibodies used. CFTR is absolutely required for forskolin-mediated gland secretion; we used this finding to localize the origin of forskolin-stimulated, CFTR-dependent gland fluid secretion. We tested the hypothesis that secretion to forskolin might originate from the gland duct rather than or in addition to the acini. We ligated gland ducts at various points, stimulated the glands with forskolin, and monitored the regions of the glands that swelled. The results supported an acinar rather than ductal origin of secretion. We tracked particles in the mucus using Nomarski time-lapse imaging; particles originated in the acini and traveled toward the duct orifice. Estimated bulk flow accelerated in the acini and mucus tubules, consistent with fluid secretion in those regions, but was constant in the unbranched duct, consistent with a lack of fluid secretion or absorption by the ductal epithelium. We conclude that CFTR-dependent gland fluid secretion originates in the serous acini. The failure to observe either secretion or absorption from the CFTR and epithelial Na+ channel (ENaC)-rich ciliated ducts is unexplained, but may indicate that this epithelium alters the composition rather than the volume of gland mucus.


2015 ◽  
Vol 35 (5) ◽  
pp. 394-399 ◽  
Author(s):  
Alicia Galindo-Ferreiro ◽  
Hind Manaa Alkatan ◽  
Yerena Muinos-Diaz ◽  
Patricia Mitiko Akaishi ◽  
Alberto Galvez-Ruiz ◽  
...  

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