Vectorial Secretion of Perivitelline Membrane Glycoprotein ZPC of Japanese Quail (Coturnix japonica) in Polarized Madin-Darby Canine Kidney Cells

2005 ◽  
Vol 180 (3) ◽  
pp. 169-177 ◽  
Author(s):  
Tomohiro Sasanami ◽  
Kayoko Matsushima ◽  
Mamoru Ohtsuki ◽  
Norio Kansaku ◽  
Gen Hiyama ◽  
...  
Keyword(s):  
Japanese Quail ◽  
Coturnix Japonica ◽  
Membrane Glycoprotein ◽  
Kidney Cells ◽  
Madin Darby Canine Kidney ◽  
Darby Canine Kidney ◽  
Perivitelline Membrane ◽  
Canine Kidney

scholarly journals Inhibition by brefeldin A of protein secretion from the apical cell surface of Madin-Darby canine kidney cells.

1991 ◽  
Vol 266 (27) ◽  
pp. 17729-17732 ◽  
Author(s):  
S.H. Low ◽  
S.H. Wong ◽  
B.L. Tang ◽  
P. Tan ◽  
V.N. Subramaniam ◽  
...  
Keyword(s):  
Cell Surface ◽  
Protein Secretion ◽  
Apical Cell ◽  
Brefeldin A ◽  
Kidney Cells ◽  
Madin Darby Canine Kidney ◽  
Darby Canine Kidney ◽  
Canine Kidney

MST3 is involved in ENaC-mediated hypertension

2019 ◽  
Vol 317 (1) ◽  
pp. F30-F42
Author(s):  
Te-Jung Lu ◽  
Wei-Chih Kan ◽  
Sung-Sen Yang ◽  
Si-Tse Jiang ◽  
Sheng-Nan Wu ◽  
...  
Keyword(s):  
Kidney Cells ◽  
Hypertensive Rats ◽  
Madin Darby Canine Kidney ◽  
Spontaneously Hypertensive ◽  
Hypomorphic Mutation ◽  
And Oxidative Stress ◽  
Darby Canine Kidney ◽  
Canine Kidney

Liddle syndrome is an inherited form of human hypertension caused by increasing epithelial Na+ channel (ENaC) expression. Increased Na+ retention through ENaC with subsequent volume expansion causes hypertension. In addition to ENaC, the Na+-K+-Cl− cotransporter (NKCC) and Na+-Cl− symporter (NCC) are responsible for Na+ reabsorption in the kidneys. Several Na+ transporters are evolutionarily regulated by the Ste20 kinase family. Ste20-related proline/alanine-rich kinase and oxidative stress-responsive kinase-1 phosphorylate downstream NKCC2 and NCC to maintain Na+ and blood pressure (BP) homeostasis. Mammalian Ste20 kinase 3 (MST3) is another member of the Ste20 family. We previously reported that reduced MST3 levels were found in the kidneys in spontaneously hypertensive rats and that MST3 was involved in Na+ regulation. To determine whether MST3 is involved in BP stability through Na+ regulation, we generated a MST3 hypomorphic mutation and designated MST3+/− and MST3−/− mice to examine BP and serum Na+ and K+ concentrations. MST3−/− mice exhibited hypernatremia, hypokalemia, and hypertension. The increased ENaC in the kidney played roles in hypernatremia. The reabsorption of more Na+ promoted more K+ secretion in the kidney and caused hypokalemia. The hypernatremia and hypokalemia in MST3−/− mice were significantly reversed by the ENaC inhibitor amiloride, indicating that MST3−/− mice reabsorbed more Na+ through ENaC. Furthermore, Madin-Darby canine kidney cells stably expressing kinase-dead MST3 displayed elevated ENaC currents. Both the in vivo and in vitro results indicated that MST3 maintained Na+ homeostasis through ENaC regulation. We are the first to report that MST3 maintains BP stability through ENaC regulation.

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