Objectives: 

Expression of aquaporin 1 (AQP1) has been associated with tumor formation, particularly with angiogenesis, cell migration and proliferation. In the adult carotid body (CB), an oxygen-sensing organ that grows under chronic hypoxia, expression of AQP1 was detected in type I chemoreceptor cells and in endothelial cells of small CB blood vessels. In the present work we explore the role of AQP1 in the cell proliferation process that occurs in the CB upon exposure to chronic hypoxia, comparing wild type animals for AQP1 expression (AQP1 +/+) to nock out ones (AQP1 -/-).

Materials: 

Methods: Mice were either let in normoxia (21% of O2), or maintained for 12 and 21 days in a hypoxic atmosphere (10% of O2), and received BrdU treatment as a proliferation cell marker. Immunohistological analysis of the CB was used to quantify the number of TH+, BrdU+ and TH plus BrdU double-positive cells in normoxia and hypoxia conditions. Parenchyma CB total volume and TH+ cell volume were also measured.

Results: 

Lower number of total BrdU+ and TH-BrdU+ cells were observed in AQP1 -/- mice after quantification at the two times of hypoxia indicated. By other hand, proliferation rate and cell cycle phases analysis were performed in wild type PC12 cells and PC12 cells with stable over expression of AQP1 and results showed that higher cell proliferation rate and larger percentage of cells in phase S and G2 were associated to AQP1 over expression.

Conclusions: 

These results indicate that AQP1 play a significant role in cell proliferation processes. Further studies are necessary to understand the molecular basis that underline to this phenomenon.