Skip to search formSkip to main contentSkip to account menu

Hypoxia downregulates expression and activity of epithelial sodium channels in rat alveolar epithelial cells.

It is concluded that hypoxia induced a downregulation of expression and activity of epithelial Na channels and Na,K-ATPase in alveolar cells and this was associated with complete functional recovery.
View on PubMed (opens in a new tab)

Hypoxia upregulates VEGF expression in alveolar epithelial cells in vitro and in vivo.

Findings suggest that release of VEGF synthesized by AEC may target not only endothelial cells but also other alveolar cells, including macrophages and epithelial cells, as well as bronchoalveolar lavage fluid.
View on PubMed (opens in a new tab)

Inhibition of Na-K-ATPase activity after prolonged hypoxia in an alveolar epithelial cell line.

It is indicated that prolonged hypoxic exposure impairs Na-K-ATPase activity in SV40 ATII cells and may therefore decrease the vectorial sodium transport by alveolar epithelium.
View on PubMed (opens in a new tab)

Defective ENaC Processing and Function in Tissue Kallikrein-deficient Mice*

It is demonstrated that TK, like several other proteases, can activate ENaC in the kidney and the colon, and was able to promote γ-ENaC cleavage in vitro.
View on Publisher (opens in a new tab)

Obstructive sleep apnoea and related comorbidities in incident idiopathic pulmonary fibrosis

Severe sleep apnoea syndrome is associated with cardiovascular disease in incident idiopathic pulmonary fibrosis and severe OSA is strongly associated with the presence of CVD, particularly IHD.
View on Publisher (opens in a new tab)

Importance of ENaC-Mediated Sodium Transport in Alveolar Fluid Clearance Using Genetically-Engineered Mice

The role of ENaC in alveolar lung liquid clearance is focused on and recent data from mouse models with altered activity of epithelial sodium channel function in the lung are discussed, illustrating the impaired lung fluid clearance in these adult mice.
View on PubMed (opens in a new tab)

Hypoxia and beta 2-agonists regulate cell surface expression of the epithelial sodium channel in native alveolar epithelial cells.

It is established that hypoxia-induced inhibition of amiloride-sensitive sodium channel activity is mediated by decreased apical expression of ENaC subunits and that beta(2)-agonists reverse this effect by enhancing the insertion of ENc subunits into the membrane of hypoxic alveolar epithelial cells.
View on PubMed (opens in a new tab)

Mesenchymal stem cells reduce hypoxia-induced apoptosis in alveolar epithelial cells by modulating HIF and ROS hypoxic signaling.

Investigation of whether hMSC-conditioned medium (hMSC -CM) would protect AECs from hypoxia-induced apoptosis and the mechanisms involved in this cytoprotective effect found it to be partially dependent on keratinocyte growth factor and hepatocytes growth factor secretion, preventing ROS and HIF-1α accumulation.
View on PubMed (opens in a new tab)

Regulation of the epithelial Na+ channel by peptidases.

View on PubMed (opens in a new tab)

Gene regulation in the adaptive process to hypoxia in lung epithelial cells.

This review focuses on the role of HIF isoforms expressed in alveolar epithelial cells exposed to hypoxia and on the specific hypoxic gene regulation that takes place in alvesolar epithelium either through HIF-dependent or -independent pathways.
View on PubMed (opens in a new tab)
...
By clicking accept or continuing to use the site, you agree to the terms outlined in our Privacy Policy (opens in a new tab), Terms of Service (opens in a new tab), and Dataset License (opens in a new tab)