Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the cellular and molecular events associated with the increase in sodium transport across the alveolar epithelium of rats exposed to hyperoxia (85% O2 for 7 days followed by 100% O2 for 4 days). Alveolar type II (ATII) cell RNA was isolated and probed with a cDNA for one of the rat colonic epithelial sodium channel subunits (alpha rENaC). The alpha rENaC mRNA (3.7-kb transcript) increased 3-fold in ATII cell RNA isolated from rats exposed to 85% O2 for 7 days and 6-fold after 4 days of subsequent exposure to 100% O2. In situ hybridization revealed increased expression of alpha rENaC mRNA transcripts in both airway and alveolar epithelial cells of hyperoxic rats. When immunostained with a polyclonal antibody to kidney sodium channel protein, ATII cells from hyperoxic rats exhibited a significant increase in the amount of immunogenic protein present in both the plasma membrane and the cytoplasm. When patched in the whole-cell mode, ATII cells from hyperoxic rats exhibited amiloride and 5-(N-ethyl-N-isopropyl)-2',4'-amiloride (EIPA)-sensitive currents that were 100% higher compared with those obtained from air-breathing rats. Single-channel sodium currents (mean conductance of 25 pS) were seen in ATII cells patched in both the inside-out and cell-attached modes. The number and open probability of these channels increased significantly during exposure to hyperoxia. Exposure to sublethal hyperoxia up-regulated both alpha rENaC mRNA and the functional expression of sodium channels in ATII cells.
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PMID:Increased expression and activity of sodium channels in alveolar type II cells of hyperoxic rats. 766 5

We investigated whether exposure of rats to sublethal hyperoxia (85% O2 for 7 days) raises the levels of proteins antigenically related to Na+ channels in alveolar type II (ATII) cells and, if so, whether this rise was accompanied by an increase in conductive Na+ transport in vitro. ATII cells were isolated from the lungs of these rats at the end of the exposure period. In Western blot studies, a polyclonal antibody raised against Na+ channel protein (NaAb), recognized in a specific manner a 135 +/- 10 kDa polypeptide in plasma membrane vesicles of ATII cells from both control and oxygen-exposed rats. However, higher levels of immunoreactivity were seen in ATII cells from oxygen-exposed rats. When ATII cells were patched in the whole cell mode using symmetrical solutions (150 mM Na(+)-glutamate), outward rectified Na+ currents were observed. When corrected for cell capacitance, both inward and outward currents of ATII cells from rats exposed to hyperoxia were significantly higher than control. Addition of either 1 microM amiloride or 1 microM 5-(N-ethyl-N-isopropyl)-2'-4'-amiloride in the bath solution decreased the magnitude of outward currents of both control and hyperoxic ATII cells by approximately 50%. Taken together, these results indicate that exposure of rats to sublethal hyperoxia results in upregulation of ATII cell conductive pathways with low affinity to amiloride and increased Na+ transport. This may be an early adaptive response that limits the degree of alveolar edema in injured lungs.
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PMID:Upregulation of sodium conductive pathways in alveolar type II cells in sublethal hyperoxia. 830 67