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Preeclampsia — elucidating role of adenosine

Scientists investigated the expression of a hypoxia-associated molecule with elevated levels in a severe form of hypertension in pregnancy. Tests in cell and tissue cultures pointed to potential cellular mechanisms of reduced embryo growth.
Preeclampsia — elucidating role of adenosine
During the late second and third trimester of pregnancy babies typically grow by leaps and bounds. Sometimes complications can reduce that growth and lead to morbidity in the few weeks before and after birth, and even later in life. One potential cause could be an inadequate supply of oxygen (hypoxia or ischaemia) and nutrients to the developing embryo from abnormal vascular morphology or placental function.

Preeclampsia (PE) is a pathological condition during pregnancy characterised by an abrupt increase in blood pressure (hypertension). There is no effective treatment or cure and it is a leading cause of maternal and infant morbidity and mortality worldwide. Women with PE also have higher levels of adenosine, associated with hypoxia of tissues, as do growth-restricted infants. Furthermore, women with PE have elevated levels of proteins in the urine. Proteins are formed from amino acids and their concentration as well as placental transport is reduced in growth-restricted infants.

Taken together, the data suggest a link between diminished amino acid transport and a hypoxia-induced adenosine signal, and a role for both in growth-restricted infants. This link was investigated by scientists with EU funding of the project 'The role of adenosine in placental development and function' (ADENOSINE). Researchers investigated the hypothesis using cultures of human trophoblast cells (that play an important role in placental development) and of placental tissues.

Stimulation of the adenosine receptor A2B reduced trophoblast migration, possibly due partially to reduced activity of an enzyme associated with angiogenesis (blood vessel formation). Furthermore, hypoxia increased A2A and A2B adenosine receptor expression on trophoblast cells. Although there was no inhibition or activation effect of adenosine receptors on placental amino acid transporter activity, reduced activity was seen with decreasing oxygen concentrations.

ADENOSINE studies suggest a role of the A2B adenosine receptor in placental development. Modulation of its expression by hypoxia also diminished amino acid transport. The potential role of adenosine in PE opens the door to future research to identify other targets for therapeutic intervention in women at high-risk for PE.

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