Dynamics of Gene Expression Responses for Ion Transport Proteins and Aquaporins in the Gill of a Euryhaline Pupfish during Freshwater and High-Salinity Acclimation

2018 ◽  
Vol 91 (6) ◽  
pp. 1148-1171 ◽  
Author(s):  
Sean C. Lema ◽  
Paul G. Carvalho ◽  
Jennifer N. Egelston ◽  
John T. Kelly ◽  
Stephen D. McCormick
2007 ◽  
Vol 44 (11) ◽  
pp. 1146-1156 ◽  
Author(s):  
Heather E. Hallen ◽  
Marianne Huebner ◽  
Shin-Han Shiu ◽  
Ulrich Güldener ◽  
Frances Trail

1996 ◽  
Vol 18 (1-2) ◽  
pp. 23-28 ◽  
Author(s):  
H�l�ne Barbier-Brygoo ◽  
Sabine Zimmermann ◽  
S�bastien Thomine ◽  
Ian R. White ◽  
Paul Millner ◽  
...  

1975 ◽  
Vol 62 (3) ◽  
pp. 589-598
Author(s):  
RICHARD M. BAGINSKI ◽  
SIDNEY K. PIERCE

1. When stressed with high-salinity exposure, cell volume is restored in ventricles of Modiolus demissus demissus by a rapid accumulation of intracellular free amino acids. 2. Although the total amino acid pool increases and remains at a constant high level thereafter, the pattern and time course of accumulation is different for each major amino acid (glycine, alanine, taurine, and proline). 3. Initially, cell volume is restored by a rapid accumulation of alanine, but later its concentration decreases while glycine and taurine accumulate. Although at first not detected, the proline concentration increases, peaks and subsequently disappears again. 4. Isolated ventricles recover normal activity after large environmental salinity increases. 5. During recovery the intracellular free amino acid changes in isolated ventricles are similar to the initial pattern of accumulation in whole animals, i.e., alanine, and to a lesser extent, proline and glycine accumulate. 6. Finally, isolated ventricles undergo a period of decreased oxygen consumption on exposure to an increased salinity. 7. These results suggest that the initial stages of high-salinity acclimation in molluscs depends upon the synthesis of amino acids via a known anaerobic biochemical pathway. Note: Contribution No. 33 from the Tallahassee, Sopchoppy and Gulf Coast Marine Biological Association.


2020 ◽  
Vol 22 (8) ◽  
pp. 3266-3286
Author(s):  
Hermann Rath ◽  
Praveen K. Sappa ◽  
Tamara Hoffmann ◽  
Manuela Gesell Salazar ◽  
Alexander Reder ◽  
...  

2020 ◽  
Vol 18 ◽  
pp. 100423
Author(s):  
Chao Li ◽  
Na Li ◽  
Tiantian Dong ◽  
Qiang Fu ◽  
Yanting Cui ◽  
...  

2000 ◽  
Vol 88 (5) ◽  
pp. 1890-1896 ◽  
Author(s):  
Christine Clerici ◽  
Michael A. Matthay

Alveolar hypoxia occurs during ascent to high altitude but is also commonly observed in many acute and chronic pulmonary disorders. The alveolar epithelium is directly exposed to decreases in O2tension, but a few studies have evaluated the effects of hypoxia on alveolar cell function. The alveolar epithelium consists of two cell types: large, flat, squamous alveolar type I and cuboidal type II (ATII). ATII cells are more numerous and have a number of critical functions, including transporting ions and substrates required for many physiological processes. ATII cells express 1) membrane proteins used for supplying substrates required for cell metabolism and 2) ion transport proteins such as Na+channels and Na+-K+-ATPase, which are involved in the vectorial transport of Na+from the alveolar to interstitial spaces and therefore drive the resorption of alveolar fluid. This brief review focuses on gene expression regulation of glucose transporters and Na+transport proteins by hypoxia in alveolar epithelial cells. Cells exposed to severe hypoxia (0% or 3% O2) for 24 h upregulate the activity and expression of the glucose transporter GLUT-1, resulting in preservation of ATP content. Hypoxia-induced increases in GLUT-1 mRNA levels are due to O2deprivation and inhibition of oxidative phosphorylation. This regulation occurs at the transcriptional level through activation of a hypoxia-inducible factor. In contrast, hypoxia downregulates expression and activity of Na+channels and Na+-K+-ATPase in cultured alveolar epithelial cells. Hypoxia induces time- and concentration-dependent decreases of α-, β-, and γ-subunits of epithelial Na+channel mRNA and β1- and α1-subunits of Na+-K+-ATPase, effects that are completely reversed after reoxygenation. The mechanisms by which O2deprivation regulates gene expression of Na+transport proteins are not fully elucidated but likely involve the redox status of the cell. Thus hypoxia regulates gene expression of transport proteins in cultured alveolar epithelial type II cells differently, preserving ATP content.


2019 ◽  
Vol 55 (87) ◽  
pp. 13152-13155
Author(s):  
Awatef Ben Tahar ◽  
Abdelkader Zebda ◽  
Jean-Pierre Alcaraz ◽  
Landry Gayet ◽  
Abderrahim Boualam ◽  
...  

This biomimetic membrane system of Na+/H+ transport proteins in a lipid bilayer supported by polyanaline has controllable electrogenic ion transport to function as a high-speed rechargeable biocapacitor for use in bioinspired biological engineering.


2010 ◽  
Vol 298 (1) ◽  
pp. C1-C10 ◽  
Author(s):  
Sascha Kopic ◽  
Michael Murek ◽  
John P. Geibel

The parietal cell is responsible for secreting concentrated hydrochloric acid into the gastric lumen. To fulfill this task, it is equipped with a broad variety of functionally coupled apical and basolateral ion transport proteins. The concerted scientific effort over the last years by a variety of researchers has provided us with the molecular identity of many of these transport mechanisms, thereby contributing to the clarification of persistent controversies in the field. This article will briefly review the current model of parietal cell physiology and ion transport in particular and will update the existing models of apical and basolateral transport in the parietal cell.


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