Morphometric image analysis of vascular endothelial growth factor receptor-3 in preeclamptic, HIV infected women

Abstract

ObjectiveTo ascertain the expression of vascular endothelial growth factor receptor-3 (VEGFR-3) in placental conducting and exchange villi from normotensive, preeclamptic (PE) and antiretroviral treated pregnant women, using morphometric image analysis. Study designThis study utilizes retrospectively collected, paraffin wax-embedded, placental samples (n = 90) that were immuno-stained for VEGFR-3. During selection of the retrospective study, women with chronic illnesses were filtered out, to exclusively allow for the examination of VEGFR-3 immuno-expression in HIV and preeclamptic women. The study population consisted of normotensive (n = 30) and preeclamptic (n = 60) groups which were further divided on the basis of HIV status (negative – and positive +), and early and late onset preeclampsia (EOPE and LOPE respectively). The resulting groups were as follows; N- (n = 15), N+ (n = 15), EOPE- (n = 15), EOPE+ (n = 15), LOPE- (n = 15) and LOPE+ (n = 15). Microscopic examination and morphometric image analysis were performed on the immuno-stained placental tissue samples. ResultsAnalysis on HIV status did not yield a significant difference in conducting (p = 0.3015) or exchange (p = 0.4535) villi, regardless of pregnancy type. The N vs. PE analysis showed a reduced immuno-expression of VEGFR-3 in both conducting (p = 0.0107) and exchange (p < 0.0001) villi. Results from a multiple group comparative analysis of N vs. EOPE vs. LOPE VEGFR-3 immuno-expression, showed a significant difference between the N vs. EOPE groups. ConclusionThe results presented provide compelling evidence that HIV infection does not significantly alter angiogenesis in placental villi. PE however, has caused angiogenic dysregulation and trophoblast pathology was observed. We report a severe downregulation of VEGFR-3 in placental villi from EOPE woman, regardless of HIV status. Hence we suggest a future investigation into EOPE’s aetiology and its downstream effects on pregnancy.