Related Experiment Video
Updated: Nov 20, 2025

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
Published on: April 24, 2021
MicroRNA-210 Regulates Endoplasmic Reticulum Stress and Apoptosis in Porcine Embryos
Muhammad Rosyid Ridlo1,2, Eui Hyun Kim1, Geon A Kim3
1Department of Theriogenology and Biotechnology, Research Institute for Veterinary Science, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Abstract:
Endoplasmic reticulum (ER) stress can be triggered during in vitro embryo production and is a major obstacle to embryo survival. MicroRNA (miR)-210 is associated with cellular adaptation to cellular stress and inflammation. An experiment was conducted to understand the effects of miR-210 on in vitro embryo development, ER stress, and apoptosis; to achieve this, miR-210 was microinjected into parthenogenetically activated embryos. Our results revealed that miR-210 inhibition significantly enhanced the cleavage rate, blastocyst formation rate, and total cell number (TCN) of blastocysts, and reduced expression levels of XBP1 (p < 0.05). miR-210 inhibition greatly reduced the expression of ER stress-related genes (uXBP1, sXBP1, ATF4, and PTPN1) and Caspase 3 and increased the levels of NANOG and SOX2 (p < 0.05). A miR-210-mimic significantly decreased the cleavage, blastocyst rate, TCN, and expression levels of XBP1 compared with other groups (p < 0.05). The miR-210-mimic impaired the expression levels of uXBP1, sXBP1, ATF4, PTPN1, and Caspase 3 and decreased the expression of NANOG and SOX2 (p < 0.05). In conclusion, miR-210 plays an essential role in porcine in vitro embryo development. Therefore, we suggest that miR-210 inhibition could alleviate ER stress and reduce apoptosis to support the enhancement of in vitro embryo production.
Insights
In vitro embryo production is hindered by endoplasmic reticulum (ER) stress. Inhibiting microRNA-210 (miR-210) improves embryo development by reducing ER stress and apoptosis.
Area of Science:
- Reproductive Biology
- Molecular Biology
- Developmental Biology
Background:
- Endoplasmic reticulum (ER) stress impedes in vitro embryo production and survival.
- MicroRNA-210 (miR-210) is implicated in cellular stress adaptation and inflammation.
Purpose of the Study:
- To investigate the role of miR-210 in porcine in vitro embryo development.
- To determine the effects of miR-210 on ER stress and apoptosis during early embryonic development.
Main Methods:
- Microinjection of miR-210 inhibitor or mimic into parthenogenetically activated porcine embryos.
- Assessment of embryo developmental rates (cleavage and blastocyst formation).
- Quantification of total cell number (TCN) in blastocysts.
- Analysis of gene expression related to ER stress (XBP1, uXBP1, sXBP1, ATF4, PTPN1), apoptosis (Caspase 3), and pluripotency (NANOG, SOX2).
Main Results:
- miR-210 inhibition significantly improved cleavage rates, blastocyst formation, and TCN, while reducing XBP1 expression.
- Inhibition of miR-210 decreased ER stress markers (uXBP1, sXBP1, ATF4, PTPN1), apoptosis (Caspase 3), and increased pluripotency markers (NANOG, SOX2).
- Conversely, miR-210 mimic injection impaired embryo development, downregulated ER stress and apoptosis markers, and reduced pluripotency markers.
Conclusions:
- miR-210 plays a critical role in regulating porcine in vitro embryo development.
- Inhibiting miR-210 can alleviate ER stress and reduce apoptosis, thereby enhancing in vitro embryo production outcomes.
Related Concept Videos
Regulation of the Unfolded Protein Response
MicroRNAs
MicroRNAs
The Unfolded Protein Response

