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The mechanisms responsible for development of PE remain to be elucidated. Using proteomics, we discovered unique amyloid-like aggregation signatures (misfoldome) in the urine of women with PE. Yet, the tissue origin of proteins composing the PE misfoldome is not known. This study was undertaken to examine the potential contribution of kidney and placental transcripts to the urine misfoldome in PE.
Urine from 92 pregnant women was classified by strict clinical criteria in 6 groups: pregnant controls (CRL, n=11, GA: 30±5 wks), mild PE (mPE, n=15, GA: 33±4 wks), severe PE (sPE, n=21, GA: 32±4 wks), superimposed PE (spPE, n=16, GA: 32±6 wks), atypical PE (HELLP±IUGR, n=16, GA: 30±5 wks), and non-PE isolated proteinuria (n=13, GA: 28±6 wks). Misfoldome proteins were enriched by Congo Red precipitation and subjected to UPLC/MS/MS. Deep RNA sequencing (RNA-seq) was performed on decidua basalis (n=5) and villous trophoblast (n=5) of women with preterm severe PE (GA: 32±1 wks). These reads, together with RNA-Seq data from the Illumina Human BodyMap 2.0 database (n=16, adult tissues including kidney), were used to intersect specific transcripts that may contribute to aberrant proteinuria in PE.
646 unique proteins IDs comprised the urinary misfoldome of PE women. Our intersection analysis showed a potential contribution of villous trophoblast, decidua and kidney to the misfoldome (Figure). Villous trophoblast was a larger contributor than either kidney or decidua (Table). Kidney-specific transcripts such as solute carrier family 22 (SLC22A12, a urate transporter), SMIM24 (an uncharacterized small integral membrane protein), MMP7 (matrilysin), and CALB1 (calbindin 1, a protein linked to Huntington disease) mapped to distinct PE subphenotypes.
The urinary misfoldome harbors a considerable number of peptides of placental and kidney origin which may interact to play key pathogenic roles in various PE subphenotypes.