title: Changes of chloride channels in the lacrimal glands of a rabbit model of Sjögren syndrome.
abstract: OBJECTIVE
  To test the hypothesis that expressions of Na-K-2Cl cotransporter-1 (NKCC1), cystic fibrosis transmembrane conductance regulator (CFTR), and chloride channel 2 γ subunit (ClC2γ) in the lacrimal glands (LGs) of rabbits with induced autoimmune dacryoadenitis (IAD) are changed.
  
  
  METHODS
  LGs were obtained from adult female rabbits with IAD and age-matched female control rabbits. LGs were processed for laser capture microdissection, real-time reverse transcription-polymerase chain reaction, Western blot, and immunofluorescence.
  
  
  RESULTS
  In rabbits with IAD, messenger RNA (mRNA) abundance and protein expressions of NKCC1 and CFTR from whole LGs were significantly lower than those in controls. mRNA abundance of NKCC1, CFTR, and ClC2γ from rabbits with IAD was significantly different from that in acinar and ductal cells from controls. NKCC1 was localized to the basolateral membranes of all acinar and ductal cells, with weaker staining intensity in ductal cells, and the staining pattern from rabbits with IAD appeared similar to that from controls. CFTR was found as punctate aggregates in the apical cytoplasm of all acinar and ductal cells, with the intensity in ductal cells much stronger and no significant difference between controls and rabbits with IAD. ClC2γ was also localized to the apical cytoplasm as punctate aggregates of all acinar cells but not in ductal cells, and a similar staining pattern was observed in rabbits with IAD compared with control rabbits.
  
  
  CONCLUSIONS
  Our data demonstrated significant changes of mRNA and protein expressions of NKCC1, CFTR, and ClC2γ in rabbits with IAD, suggesting that these changes may contribute to the altered lacrimal secretion, particularly Cl transport, in rabbits with IAD.
authors.affiliation: Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089-9112, USA.
authors.forename: Prachi
authors.initials: P
authors.lastname: Nandoskar
authors.forename: Yanru
authors.initials: Y
authors.lastname: Wang
authors.forename: Ruihua
authors.initials: R
authors.lastname: Wei
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Ping
authors.initials: P
authors.lastname: Zhao
authors.forename: Michael
authors.initials: M
authors.lastname: Lu
authors.forename: Jianyan
authors.initials: J
authors.lastname: Huang
authors.forename: Padmaja
authors.initials: P
authors.lastname: Thomas
authors.forename: Melvin D
authors.initials: MD
authors.lastname: Trousdale
authors.forename: Chuanqing
authors.initials: C
authors.lastname: Ding
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases; D015153:Blotting, Western; D000090007:CLC-2 Chloride Channels; D018118:Chloride Channels / Q000378:metabolism*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000378:metabolism; D003607:Dacryocystitis / Q000209:etiology / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D005455:Fluorescent Antibody Technique; D007765:Lacrimal Apparatus / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012859:Sjogren's Syndrome / Q000150:complications*; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism; D064506:Solute Carrier Family 12, Member 2
chemical_list: D000090007:CLC-2 Chloride Channels; D018118:Chloride Channels; D012333:RNA, Messenger; D028021:Sodium-Potassium-Chloride Symporters; D064506:Solute Carrier Family 12, Member 2; D019005:Cystic Fibrosis Transmembrane Conductance Regulator