» Articles » PMID: 34150047

MiR-335 Targets CRIM1 to Promote the Proliferation and Inhibit the Apoptosis of Placental Trophoblast Cells in Preeclamptic Rats

Overview
Journal Am J Transl Res
Specialty General Medicine
Date 2021 Jun 21
PMID 34150047
Citations 2
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: To investigate the role of miRNA-335 on the proliferation and apoptosis of placental trophoblast cells in preeclamptic rats and its potential mechanism.

Methods: Placental trophoblast cells were isolated from preeclamptic model rats and normal ones. Trophoblast cells from the model group were divided into six groups for transfection: the blank (empty vector) group, the NC (negative control) group, the miRNA-335 mimic group, the miRNA-335 inhibitor group, the CRIM1 (overexpressed recombinant plasmid) group, and the miRNA-335 inhibitor + CRIM1 group. The miRNA-335 expressions after the transfection were determined using qRT-PCR. The mRNA and protein expressions of CRIM1, the transforming growth factor (TGF-β1), and the apoptosis-related factors (Bax and Bcl-2) in each group were determined using qRT-PCR and Western blotting. The cell proliferation and apoptosis were determined using MTT assays and flow cytometry, respectively.

Results: Compared with normal rats, the systolic blood pressure, diastolic blood pressure, and urinary protein levels were increased in the model rats, which had increased miRNA-335 expressions, but a decreased CRIM1 expressions (all P<0.05). The inhibition of miRNA-335 promoted the expressions of CRIM1, TGF-β1, and Bcl-2 and inhibited the expression of Bax in trophoblast cells (all P<0.05). miRNA-335 inhibition or CRIM1 over-expression promoted the proliferation and reduced the apoptosis of trophoblast cells. The combined effect of miRNA-335 inhibition or CRIM1 over-expression had an even more significant effect on the changes in the above indicators (all P<0.05).

Conclusion: miRNA-335 inhibition can enhance the expression of CRIM1 to promote the proliferation and reduce the apoptosis of trophoblast cells in preeclamptic rats.

Citing Articles

Micro-RNAs in Human Placenta: Tiny Molecules, Immense Power.

Jin M, Xu Q, Li J, Xu S, Tang C Molecules. 2022; 27(18).

PMID: 36144676 PMC: 9501247. DOI: 10.3390/molecules27185943.


SNHG22 promotes migration and invasion of trophoblasts via miR-128-3p/PCDH11X axis and activates PI3K/Akt signaling pathway.

Wei X, Yuan Y, Yang Q Clinics (Sao Paulo). 2022; 77:100055.

PMID: 35679761 PMC: 9188964. DOI: 10.1016/j.clinsp.2022.100055.

References
1.
Herzog E, Eggink A, Reijnierse A, Kerkhof M, de Krijger R, Roks A . Impact of early- and late-onset preeclampsia on features of placental and newborn vascular health. Placenta. 2016; 49:72-79. DOI: 10.1016/j.placenta.2016.11.014. View

2.
Luo R, Shao X, Xu P, Liu Y, Wang Y, Zhao Y . MicroRNA-210 contributes to preeclampsia by downregulating potassium channel modulatory factor 1. Hypertension. 2014; 64(4):839-45. DOI: 10.1161/HYPERTENSIONAHA.114.03530. View

3.
Jiang F, Li J, Wu G, Miao Z, Lu L, Ren G . Upregulation of microRNA‑335 and microRNA‑584 contributes to the pathogenesis of severe preeclampsia through downregulation of endothelial nitric oxide synthase. Mol Med Rep. 2015; 12(4):5383-90. DOI: 10.3892/mmr.2015.4018. View

4.
Ospina-Prieto S, Chaiwangyen W, Herrmann J, Groten T, Schleussner E, Markert U . MicroRNA-141 is upregulated in preeclamptic placentae and regulates trophoblast invasion and intercellular communication. Transl Res. 2016; 172:61-72. DOI: 10.1016/j.trsl.2016.02.012. View

5.
Cushen S, Goulopoulou S . New Models of Pregnancy-Associated Hypertension. Am J Hypertens. 2017; 30(11):1053-1062. DOI: 10.1093/ajh/hpx063. View