Latest research on PGI2

A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from prostaglandin endoperoxides in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension.

Latest findings

Vasodilator responsiveness was defined as a reduction in mean pulmonary arterial pressure of at least 10 mm Hg to a level below 40 mm Hg with no reduction in cardiac output after administration of inhaled Nitric oxide, although some centres have historically used inhaled Prostacyclin or intravenous Prostacyclin, according to local practice. [source, 2016]
An increased MPV decreases the inhibitory effectiveness of prostacyclin I2 (PGI2) on both platelet aggregation and the release reaction29. [source, 2016]
The endothelium also controls blood flow distribution around the body through the release of vasoactive substances, including Nitric oxide (NO) and prostacyclin (PGI2) [1]. [source, 2016]
However, under NO inhibition, the dilatory response to Prostacyclin in young and old subjects was similar [43], implicating loss of the NO pathway as the primary mechanism behind ageing-induced vascular dysfunction. [source, 2016]
Moreover, genetically engineered MSCs that overexpress endothelial Nitric oxide synthase, Prostacyclin, or heme oxygenase-1 had even greater reversal effects on PH [223,224]. [source, 2016]
The exact mechanisms responsible for pulmonary arterial remodeling have, however, not been fully elucidated thus far, although certain studies have demonstrated that biologically active media, such as endothelin, vascular endothelial growth factor, Nitric oxide, Prostacyclin and other factors are involved in this pathological process (19,20). [source, 2016]
PGI2, PGE2, Aβ1–42 and the inhibitors NS398, U0126, and KT5720 were obtained from Sigma-Aldrich Corp (St. Louis, MO, USA). [source, 2016]
Mice at 6 months of age were injected (i.c.v) with PGE2 (2 μg/5 μl) or PGI2 (2 μg/5 μl) in the absence or presence of Aβ antibody (1 μg/5 μl) or Aβ oligomers (1 μg/5 μl) for 24 h before determining the expression of IFNγ. [source, 2016]
NS398, PGE2, PGI2, Aβ, or anti-human Aβ or vehicle (PBS) solutions were injected (i.c.v) into WT or APP/PS1 transgenic mice as previously described25. [source, 2016]
PGI2, PGE2 or vehicle (PBS) solutions were then injected (i.c.v) into the other side of ventricle. [source, 2016]