title: The acute and regulatory phases of time-course changes in gill mitochondrion-rich cells of seawater-acclimated medaka (Oryzias dancena) when exposed to hypoosmotic environments.
abstract: The recent model showed that seawater (SW) mitochondrion-rich (MR) cells with hole-type apical openings secrete Cl(-) through the transporters including the Na(+), K(+)-ATPase (NKA), Na(+), K(+), 2Cl(-) cotransporter (NKCC), and cystic fibrosis transmembrane conductance regulator (CFTR). The present study focused on the dynamic elimination of the Cl(-) secretory capacity and illustrated different phases (i.e., acute and regulatory phases) of branchial MR cells in response to hypoosmotic challenge. Time-course remodeling of the cell surfaces and the altered expressions of typical ion transporters were observed in the branchial MR cells of SW-acclimated brackish medaka (Oryzias dancena) when exposed to fresh water (FW). On the 1st day post-transfer, rapid changes were shown in the acute phase: the flat-type MR cells with large apical surfaces replaced the hole-type cells, the gene expression of both Odnkcc1a and Odcftr decreased, and the apical immunostaining signals of CFTR protein disappeared. The basolateral immunostaining signals of NKCC1a protein decreased throughout the regulatory phase (>1day post-transfer). During this period, the size and number of NKA-immunoreactive MR cells were significantly reduced and elevated, respectively. Branchial NKA expression and activity were maintained at constant levels in both phases. The results revealed that when SW-acclimated brackish medaka were transferred to hypoosmotic FW for 24h, the Cl(-) secretory capacity of MR cells was eliminated, whereas NKCC1a protein was retained to maintain the hypoosmoregulatory endurance of the gills. The time-course acute and regulatory phases of gill MR cells showed different strategies of the euryhaline medaka when subjected to hypoosmotic environments.
authors.affiliation: Department of Life Sciences, National Chung-Hsing University, Taichung 402, Taiwan.
authors.forename: Chao-Kai
authors.initials: CK
authors.lastname: Kang
authors.forename: Wen-Kai
authors.initials: WK
authors.lastname: Yang
authors.forename: Shang-Tao
authors.initials: ST
authors.lastname: Lin
authors.forename: Chin-Cheng
authors.initials: CC
authors.lastname: Liu
authors.forename: Huei-Ming
authors.initials: HM
authors.lastname: Lin
authors.forename: Hong-Huan
authors.initials: HH
authors.lastname: Chen
authors.forename: Chien-Wen
authors.initials: CW
authors.lastname: Cheng
authors.forename: Tsung-Han
authors.initials: TH
authors.lastname: Lee
authors.forename: Pung-Pung
authors.initials: PP
authors.lastname: Hwang
mesh_terms: D000064:Acclimatization; D000818:Animals; D002452:Cell Count; D048429:Cell Size; D002712:Chlorides / Q000378:metabolism; D016616:Cryoultramicrotomy; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000378:metabolism; D029941:Fish Proteins / Q000235:genetics / Q000378:metabolism; D005618:Fresh Water; D015971:Gene Expression Regulation, Enzymologic; D005880:Gills / Q000201:enzymology / Q000648:ultrastructure; D007150:Immunohistochemistry; D008855:Microscopy, Electron, Scanning; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism*; D008954:Models, Biological; D009990:Oryzias / Q000033:anatomy & histology / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D054712:Salinity; D012623:Seawater; D028021:Sodium-Potassium-Chloride Symporters / Q000235:genetics / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013997:Time Factors
chemical_list: D002712:Chlorides; D029941:Fish Proteins; D028021:Sodium-Potassium-Chloride Symporters; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D000254:Sodium-Potassium-Exchanging ATPase