1. Insight Into the Pathogenesis of Fetal Growth Restriction in Placental Malaria: Decreased Placental Glucose Transporter Isoform 1 Expression
- Author
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Caroline Lin Lin Chua, Ebbie Chaluluka, Philippe Boeuf, Alexandra J. Umbers, Stephen J. Rogerson, Jocelyn D. Glazier, and Upeksha P. Chandrasiri
- Subjects
medicine.medical_specialty ,Adolescent ,Placenta ,Biology ,Pathogenesis ,Young Adult ,Syncytiotrophoblast ,Pregnancy ,Internal medicine ,parasitic diseases ,Biopsy ,medicine ,Humans ,Immunology and Allergy ,Malaria, Falciparum ,Glucose Transporter Type 1 ,Fetal Growth Retardation ,medicine.diagnostic_test ,Infant, Newborn ,Glucose transporter ,Transplacental ,Basal plasma membrane ,Infectious Diseases ,medicine.anatomical_structure ,Endocrinology ,Gene Expression Regulation ,Pregnancy Complications, Parasitic ,embryonic structures ,Female - Abstract
Placental malaria, especially when complicated with intervillositis, can cause fetal growth restriction. Transplacental glucose transport by glucose transporter isoform 1 (GLUT-1) on the syncytiotrophoblast microvillous and basal plasma membranes regulates fetal growth. We found that GLUT-1 expression in the microvillous plasma membrane of Plasmodium falciparum-negative placenta biopsy specimens was comparable to that in P. falciparum-positive placenta biopsy specimens with or without intervillositis, whereas GLUT-1 expression in the basal plasma membrane was lowest in P. falciparum-positive placenta biopsy specimens with intervillositis, compared with the other 2 specimen types (P ≤ .0016). GLUT-1 expression in the basal plasma membrane also correlated negatively with monocyte infiltrate density (r = -0.43; P = .003) and positively with birth weight (r = 0.28; P = .06). These findings suggest that intervillositis, more than placental malaria per se, might cause fetal growth restriction, through impaired transplacental glucose transport.
- Published
- 2013
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