Abstract
Placental aquaporin 9 (AQP9) does not participate directly in the transfer of water between mother and fetus, its role in the human placenta is still unknown1. In other tissues, its participation in lactate transport as an alternative energy source to promote cell survival has been reported2,3. In this sense, our objective was to evaluate the participation of placental AQP9 in lactate transfer. Explants from normal term placentas were cultured in low glucose conditions with or without L-lactate, and in presence and absence of AQP9 inhibitor (0.5mM Phloretin). Cell viability and apoptotic parameters were evaluated (MTT and LDH assay, Bax / Bcl-2 expression and apoptotic nuclei). MTT levels decreased in low glucose cultured explants and apoptotic parameters increased compared to controls (n=5, p<0.02). However, when the medium was supplemented with L-lactate, the MTT values and apoptotic parameters were similar to the controls, suggesting that L-lactate could substitute for glucose. And the blockade of AQP9 resulted in increased cell death (n=4, p<0.05). The LDH release did not change in any situation. Our results suggest that AQP9 could mediate the passage of lactate through the placenta as an alternative source of energy.
2. Miki A, Kanamori A, Negi A, Naka M, Nakamura M. Loss of aquaporin 9 expression adversely affects the survival of retinal ganglion cells. Am J Pathol. 2013;182(5):1727-1739.
3. Juel G, Halestrap AP. Lactate transport in skeletal muscle - Role and regulation of the monocarboxylate transporter. J Physiol. 1999;517(3):633-642.
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