Margarita L Martinez-Fierro1, Jose Gerardo Carrillo-Arriaga2, Martha Luevano3, Angel Lugo-Trampe4, Ivan Delgado-Enciso5, Iram Pablo Rodriguez-Sanchez6, Idalia Garza-Veloz7. 1. Molecular Medicine Laboratory, Unidad Academica de Medicina Humana y Ciencias de la Salud, Universidad Autonoma de Zacatecas, Campus UAZ siglo XXI, Carretera Zacatecas-Guadalajara Km 6, Ejido la Escondida, 98160 Zacatecas, Mexico. Electronic address: margaritamf@uaz.edu.mx. 2. Instituto Tecnologico de Estudios Superiores Monterrey, Campus Monterrey, Avenida Ignacio Morones Prieto 3000 Poniente, Los Doctores, 64710 Monterrey, Nuevo Leon, Mexico. 3. Miltenyi Biotec GmbH, Bergisch Gladbach, Germany. 4. Escuela de Medicina Humana, Campus IV, Universidad Autonoma de Chiapas, Tapachula, Chiapas 30700, Mexico. 5. School of Medicine, University of Colima, Av. Universidad # 333, Colonia Las Viboras, 28040 Colima, Colima, Mexico. 6. Laboratorio de Fisiologia Molecular y Estructural, Facultad de Ciencias Biologicas, Universidad Autonoma de Nuevo Leon, Avenida Pedro de Alba s/n, Ciudad Universitaria, 66451 San Nicolás de los Garza, Nuevo Leon, Mexico. 7. Molecular Medicine Laboratory, Unidad Academica de Medicina Humana y Ciencias de la Salud, Universidad Autonoma de Zacatecas, Campus UAZ siglo XXI, Carretera Zacatecas-Guadalajara Km 6, Ejido la Escondida, 98160 Zacatecas, Mexico.
Abstract
OBJECTIVE: Preeclampsia pathogenesis involves imbalances of oxidative stress networks including the heat shock protein (HSP) pathway. Micro-RNAs regulate gene networks associated with preeclampsia. Hsp90 and Runx2 are transcriptional targets of miR-628-3p. Considering that potential participation of hsa-miR-628-3p in PE development is still not elucidated, the aim of this study was to evaluate serum microRNA expression of hsa-miR-628-3p and hsa-miR-628-5p and their association with the preeclampsia development. STUDY DESIGN: A retrospective nested cohort case-control study was conducted. Serum samples from 16 pregnant women who developed preeclampsia (WWD-PE) during the follow-up period were selected and individually matched to that from 18 women in the cohort who had healthy pregnancies without complications (controls). MAIN OUTCOME MEASURES: The levels of hsa-miR-628-3p and hsa-miR-628-5p were measured in serum samples from study groups at 12, 16, and 20 weeks of gestation (WG) using TaqMan probes. Additionally serum levels were measured at the moment of diagnosis, in women with preeclampsia. RESULTS: Serum levels of hsa-miR-628-3p were higher than controls in WWD-PE at 12 WG (RQ = 7.7; P = 0.020), and of hsa-miR-628-5p at 20 WG (RQ = 3.4; P = 0.008). An increase in hsa-miR-628-3p serum levels at 12 WG (RQ = 12.01; P = 0.001) and of hsa-miR-628-5p at 20 WG (RQ = 2.95; P = 0.033) was also observed in women who developed mild preeclampsia, and severe preeclampsia, respectively. CONCLUSIONS: Serum hsa-miR-628-3p and hsa-miR-628-5p were differentially expressed between WWD-PE and controls, suggesting a participation of these miRNAs in the development of preeclampsia. Future studies are needed to validate hsa-miR628-3p and -5p as early predictors of preeclampsia.
OBJECTIVE: Preeclampsia pathogenesis involves imbalances of oxidative stress networks including the heat shock protein (HSP) pathway. Micro-RNAs regulate gene networks associated with preeclampsia. Hsp90 and Runx2 are transcriptional targets of miR-628-3p. Considering that potential participation of hsa-miR-628-3p in PE development is still not elucidated, the aim of this study was to evaluate serum microRNA expression of hsa-miR-628-3p and hsa-miR-628-5p and their association with the preeclampsia development. STUDY DESIGN: A retrospective nested cohort case-control study was conducted. Serum samples from 16 pregnant women who developed preeclampsia (WWD-PE) during the follow-up period were selected and individually matched to that from 18 women in the cohort who had healthy pregnancies without complications (controls). MAIN OUTCOME MEASURES: The levels of hsa-miR-628-3p and hsa-miR-628-5p were measured in serum samples from study groups at 12, 16, and 20 weeks of gestation (WG) using TaqMan probes. Additionally serum levels were measured at the moment of diagnosis, in women with preeclampsia. RESULTS: Serum levels of hsa-miR-628-3p were higher than controls in WWD-PE at 12 WG (RQ = 7.7; P = 0.020), and of hsa-miR-628-5p at 20 WG (RQ = 3.4; P = 0.008). An increase in hsa-miR-628-3p serum levels at 12 WG (RQ = 12.01; P = 0.001) and of hsa-miR-628-5p at 20 WG (RQ = 2.95; P = 0.033) was also observed in women who developed mild preeclampsia, and severe preeclampsia, respectively. CONCLUSIONS: Serum hsa-miR-628-3p and hsa-miR-628-5p were differentially expressed between WWD-PE and controls, suggesting a participation of these miRNAs in the development of preeclampsia. Future studies are needed to validate hsa-miR628-3p and -5p as early predictors of preeclampsia.