Background[1-3]
Phosphorylated epithelial natriuretic beta antibody is a type of polyclonal antibody that can specifically bind to phosphorylated epithelial natriuretic beta protein. It is mainly used in in vitro detection experiments of phosphorylated epithelial natriuretic beta protein.
Schematic diagram of ELISA detection of phosphorylated epithelial natriuretic beta
Sodium ion channels are ion channels formed by intrinsic membrane proteins that allow sodium ions (Na) to pass through the cell membrane. Sodium ion channels can be classified according to the way they are activated. One type is activated by changes in voltage (voltage-gated type), and the other type is activated after binding to other chemicals (ligands) (ligand-gated type). control type).
The epithelial sodium channel (ENaC) is a membrane ion channel permeable to Na+ ions. It is located in the apical plasma membrane of epithelial cells in the kidney, lung, colon, and other tissues, where it plays a role in transepithelial Na+ ion transport. Specifically, Na+ transport via ENaC occurs on many epithelial surfaces and plays a key role in regulating salt and water absorption.
ENaC consists of three structurally related subunits forming a tetrameric channel A, B and γ. As keratinocytes differentiate, the expression of their A and B subunits is enhanced. The B and γ-ENaC subunits exert their greatest effects on edema fluid and the clear fluid absorption of the distal lung epithelium. It has been concluded that these subunits are differentially expressed in the retina of mice with high intraocular pressure and, therefore, upregulation of A-ENaC protein may serve as a protective mechanism against elevated intraocular pressure.
Apply[4][5]
For research on the expression of renal epithelial sodium channels and sodium, potassium and chloride co-transporters in rats with chronic renal failure caused by adenine
The kidneys maintain the body’s water and salt metabolism, acid-base balance and homeostasis mainly through the regulation of water and salt metabolism through epithelial sodium channels (ENaC), sodium potassium chloride co-transporters (NKCC2) and aquaporins (AQP2). to achieve.
In order to study the changes in these proteins during chronic renal failure, this experiment established an adenine-induced chronic renal failure rat model and applied morphological observation, hematuria biochemical detection, immunohistochemical staining, RT-PCR and Werstern blotting and other methods were used to observe changes in kidney morphology and biochemical indicators, changes in the mRNA and protein levels of the kidney’s main sodium channels NKCC2, γ-ENaC, and water channel AQP2, as well as changes in the cellular localization of NKCC2 and γ-ENaC. The role of NKCC2 and γ-ENaC in chronic renal failure and their regulatory mechanisms. The research results show that when chronic renal failure occurs with polyuria and electrolytic substance disorder, the levels of NKCC2 and AQP2 mRNA and protein in renal tubular epithelial cells decrease, while the expression of γ-ENaCmRNA increases, but the protein level shows a downward trend, and is related to related to functional indicators.
The research results suggest that chronic renal failure is a gradual process from compensation to decompensation, and tubular reabsorption disorder in rats with adenine-induced renal failure precedes glomerular filtration disorder. In chronic renal failure in rats, reduced NKCC2 and γ-ENaC protein levels are one of the main reasons for increased urine output and reduced blood sodium.
