【 TITLE 】Stabilization of F‐Actin Cytoskeleton by Paclitaxel Improves the Blastocyst Developmental Competence through P38 MAPK Activity in Porcine Embryos

【 JOURNAL 】Biomedicines

​【 NAME 】Seung-Yeon Joe, Seul-Gi Yang, Jae-Ho Lee, Hyo-Jin Park and Deog-Bon Koo

【 PUBLISHED 】02 August 2022

【 ISSN 】2227-9059

【 DOI 】https://doi.org/10.3390/biomedicines10081867

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【 ABSTRACT 】

 Changes in F‐actin distribution and cortical F‐actin morphology are important for blastocyst

developmental competence during embryogenesis. However, the effect of paclitaxel as a microtubule

stabilizer on embryonic development in pigs remains unclear. We investigated the role of

F‐actin cytoskeleton stabilization via P38 MAPK activation using paclitaxel to improve the developmental

potential of blastocysts in pigs. In this study, F‐actin enrichment and adducin expression

based on blastomere fragment rate and cytokinesis defects were investigated in cleaved embryos

after in vitro fertilization (IVF). Adducin and adhesive junction F‐actin fluorescence intensity were

significantly reduced with increasing blastomere fragment rate in porcine embryos. In addition,

porcine embryos were cultured with 10 and 100 nM paclitaxel for two days after IVF. Adhesive

junction F‐actin stabilization and p‐P38 MAPK activity in embryos exposed to 10 nM paclitaxel increased

significantly with blastocyst development competence. However, increased F‐actin aggregation,

cytokinesis defects, and over‐expression of p‐P38 MAPK protein by 100 nM paclitaxel exposure

disrupted blastocyst development in porcine embryos. In addition, exposure to 100 nM

paclitaxel increased the misaligned α‐tubulin of spindle assembly and adhesive junction F‐actin aggregation

at the blastocyst stage, which might be caused by p‐P38 protein over‐expression‐derived

apoptosis in porcine embryos.

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【 KEYWORDS 】paclitaxel; F‐actin; cytoskeleton; adducin; P38 MAPK; porcine embryo