Elektrophysiologie / Electrophysiology (Leitung: Prof. Dr.
Wolf-Michael Weber)
Regulatory differences of ENaC from human nasal epithelium in CF and non-CF tissue (Project 3)
Cystic fibrosis (CF) is the most common lethal lung disease in the Caucasian population. The main reason of the pathogenesis is the drastically increased Na+
absorption caused by the human amiloride-sensitive epithelial sodium channel (hENaC). It was shown that ENaC from human nasal epithelia (hnENaC) seems to differ
from other epithelia in several pharmacological aspects. Furthermore, regulation might be different in respiratory epithelia. It is known that proteases play a significant role
in the regulation of ENaC. Modifications such as proteolytic cleavage of the channel may cause increased open probability of the channels or recruiting them from
intracellular compartments to the plasma membrane. These differences could be due to an alternative structure of hnENaC. To study whether the functional differences of
hENaC and hnENaC in the pharmacological profile are due to structural discrepancies we cloned and sequenced the α-subunit of hnENaC from specimens of CF and
non-CF patients. Furthermore, we compared the nucleotide sequences among each other and found no crucial varieties. For the determination of the presence and
abundance of ENaC in human nasal epithelium from CF and non-CF tissue we carried out western blot analyses with a specific anti-α-ENaC antibody. We detected
apparent differences revealed by a second band probably being dependent on a proteolytic cleavage. We suppose that this is a grade of maturation in these epithelia,
implicating a new manner of ENaC regulation by proteolytic processing.
More information: http://www.uni-muenster.de/Biologie.Zoophysiologie/electrophys/ElectroHome.htm
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