Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling by array to investigate the effect of interfacial stress on rat alveolar type II cell signalling and gene expression (conventional air-liquid interface)


ABSTRACT: Many epithelia have contact with air-liquid interfaces. This applies particularly to the lung, where one of the epithelial cell types (the surfactant secreting alveolar type II [AT II] cells) even project into the air. This specific environment may be of considerable physiological relevance; however, only few data exist to provide a satisfying description. This is mainly due to the difficulty to manipulate cell-air contacts in a specific way. In previous investigations, using new microscopic approaches, we found that the presence of an air-liquid interface leads to a paradoxical situation: it is a potential threat that may cause cell injury, but also a potent stimulus for the cells: AT II cells respond promptly, and show sustained Ca2+-signals that activate exocytosis. In this report, gene chip analysis was performed to test the concept of an Air-liquid interface IAL as a mechanical stimulus, stress factor and/or regulator of the AT II cells. For this purpose, cultured AT II cells were exposed to two different interfacial conditions (inverted and conventional interface). The results support the concept that the IAL is a strong stimulus for AT II cells inducing cellular responses that seem to be closely associated with mechanotransduction, stress response, and alveolar repair.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Nina Hobi 

PROVIDER: E-MEXP-3363 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Interfacial stress affects rat alveolar type II cell signaling and gene expression.

Hobi Nina N   Ravasio Andrea A   Haller Thomas T  

American journal of physiology. Lung cellular and molecular physiology 20120518 2


Previous work from our group (Ravasio A, Hobi N, Bertocchi C, Jesacher A, Dietl P, Haller T. Am J Physiol Cell Physiol 300: C1456-C1465, 2011.) showed that contact of alveolar epithelial type II cells with an air-liquid interface (I(AL)) leads to a paradoxical situation. It is a potential threat that can cause cell injury, but also a Ca(2+)-dependent stimulus for surfactant secretion. Both events can be explained by the impact of interfacial tensile forces on cellular structures. Here, the stren  ...[more]

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