A chromosome 19 cluster of galectins has emerged in anthropoid primates, species with deep placentation and long gestation.
Three of the five human cluster galectins are solely expressed in the placenta, where they may confer additional immunoregulatory functions to enable deep placentation. Two polymorphic PP 13 variants have been identified: (1 The promoter PP 13 variant with an “A/A†genotype in the -98 position (versus “A/C†or “C/Câ€. Having the “A/A†genotype is coupled to lower PP 13 expression, mainly during placental syncytiotrophoblast differentiation and, if associated with obesity and history of previous preeclampsia, it accurately predicts higher risk for developing the disorder. (2 A thymidine deletion at position 221 causes a frame shift in the open reading frame, and the formation of an early stop codon resulting in the formation of DelT221, a truncated variant of PP 13. In pregnant rodents, both short- and long- term replenishment of PP 13 causes reversible hypotension and vasodilation of uterine vessels. It affects ten million pregnant women globally and additionally causes fetal loss and major newborn disabilities. The syndrome's origin is multifactorial, and anti-hypertensive drugs are ineffective in treating it. Biomarkers are helpful for predict its development. Generic drugs, such as low dose aspirin, were proven effective in preventing preterm PE.
However, it does not cure the majority of cases and many studies are underway for fighting PE with extended use of additional generic drugs, or through new drug development programs.This review focuses on placental protein 13 ( PP 13. This protein is only expressed in the placenta.
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