Background: Authors demonstrated that gestational low-protein (LP) intake offspring presents a lower birthweight, reduced nephrons numbers and renal salt excretion, arterial hypertension and renal failure development when compared to normal protein (NP) intake rats in adulthood. The current study evaluated the miRNAs and predicted gene expression patterns in the 17-days LP (17-DG) fetal kidney to elucidate the molecular pathways and renal cell proliferation and differentiation profile. Methods: Pregnant Wistar rats were allocated into two groups, according to protein supply during pregnancy: NP (normal protein diet- 17%) or LP (low protein diet-6%). miRNA transcriptome sequencing (miRNA-Seq) was performed on the MiSeq platform and, RT-qPCR of predicted target genes, immunohistochemistry and morphological quantification from 17-DG offspring kidneys using previously described methods. Results: Forty-four expressed miRNAs, which 19 miRNA were up- and 25 downregulated, were identified in 17-DG LP fetuses compared to age-matched NP offspring. The study selected 7 miRNAs related to proliferation, differentiation, and cellular apoptosis processes. The study showed a reduced cell number, Six-2 and c-Myc immunoreactivity in metanephros cap (CM) and ureter bud (UB) in 17-DG LP fetuses. Also, Ki-67 immunoreactivity in CM was 48% lesser in LP compared to NP age-matched fetus. Conversely, in LP CM and UB β-catenin was 154% and 85% markedly enhanced, respectively and, mTOR immunoreactivity was also higher in LP CM (139%) and UB (104%) compared to the NP offspring. UB TGFβ-1 staining cells increased (about 30%) in the LP offspring. Otherwise, Zeb1 metanephros-stained, enhanced 30% in LP offspring without Zeb2 staining in both groups. Conclusions: The present study demonstrates that maternal protein restriction change miRNAs, mRNAs, and critical proteins expression involved in the processes of proliferation, differentiation, and apoptosis that occurs during renal development. The renal ontogenic dysfunction caused by maternal protein restriction promotes a reduced reciprocal interaction between CM and UB, and consequently, a programmed and expressive decrease in the nephron number fetuses.
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