Immunohistochemical localization of podoplanin in the placentas of HIV-positive preeclamptic women

Abstract

Background/aim: Impaired lymphatic function is associated with pathological conditions. The presence of placental lymphatics is still under debate. This study evaluates the placental podoplanin expression in normotensive and preeclamptic women with and without HIV. Materials and methods: Normotensive (n = 60) and preeclamptic (n = 120) pregnant women were stratified into early and late onset preeclampsia and further divided by HIV status. Immunostaining was performed using the podoplanin antibody prior to the morphometric image analysis. Results: Podoplanin was immunolocalized in a reticular-like stroma complex within the exchange and conducting villi. The immunoexpression of podoplanin was significantly upregulated in the exchange villi (P = 0.001) irrespective of the pregnancy type and HIV status. Based on pregnancy type, podoplanin was downregulated in early onset preeclampsia (15.33 ± 4.27%) compared to late onset preeclampsia in the exchange villi (17.85 ± 4.74%; P = 0.04). Podoplanin was upregulated in HIV+ vs. HIV-cases regardless of pregnancy and villi type. Irrespective of pregnancy type, podoplanin immunoexpression within exchange villi was different (P = 0.008) between the HIV+ and HIV-groups. Conclusion: Placental fluid homeostasis is maintained by a podoplanin reticular-like complex within conducting and exchange villi, being upregulated in HIV-positive pregnancies.

Biological importance of podoplanin expression in chorionic villous stromal cells and its relationship to placental pathologies

“…The CLEC-2/ podoplanin interaction induces endothelial activation, platelet activation/aggregation, and inflammation. These effects play a role in the pathogenesis of preeclampsia 14,23,30,32 . Therefore, the development of pharmacological agents that modulate the activity of podoplanin would provide a new option for the treatment of preeclampsia.…”

Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus

“…CEBPB (CCAAT enhancer binding protein beta) [38], ACSL4 [39], MBD2 [40], ULK1 [41], NUCB2 [42], TWIST1 [43], HOOK2 [44], CLDN7 [45], TBK1 [46], YIPF6 [47], TFRC (transferrin receptor) [48], ENPP2 [49], SLIT2 [50], MFGE8 [51], FAT1 [52], GPC4 [53], COL6A3 [54], EGFL6 [55], AOC3 [56], CCN2 [57], LYVE1 [58], RARA (retinoic acid receptor alpha) [59], COL18A1 [60], THY1 [61], CD36 [62], PEMT (phosphatidylethanolamine N-methyltransferase) [63], AIF1L [64], OXTR (oxytocin receptor) [65], LMNA (lamin A/C) [66], CXCL14 [67], DKK3 [68], ANGPTL2 [69] and CMTM7 [70] were reported to be associated with obesity, but these genes might be linked with progression of GDM. AHR (aryl hydrocarbon receptor) [71], STS (steroid sulfatase) [72], PLAC1 [73], CYP11A1 [74], PSG11 [75], STAT5B [76], TLR3 [77], FOLR1 [78], HSPB1 [79], HSP90AA1 [80], ANXA4 [81], ATF3 [82], DAPK1 [83], ENTPD1 [84], ABL1 [85], VSIG4 [86], CD99 [87], VWF (von Willebrand factor) [88], PODXL (podocalyxin like) [89], PDPN (podoplanin) [90], RND3 [91], VCAN (versican) [92], AXL (AXL receptor tyrosine kinase) [93], PIEZO1 [94], GAS6 [93], LAMA4 [95], CAV1 [96], DLL1 [97], CD44 [98], CD81 [99], SMAD3 [100], NES (nestin) [101], DCN (decorin) [102], AGTR1 [103], SLIT3 [104], B2M [105], STAT3 [106], STC1 [107] and ADAMTS1 [108] were shown to participate in facilitating the preeclampsia. Majchrzak-Celiń ka et al [109] ...…”