miR-181d-5p, which is upregulated in fetal growth restriction placentas, inhibits trophoblast fusion via CREBRF

Wu, Zhi-Hong; Li, Fang-Fang; Ruan, Ling-Ling; Feng, Qian; Zhang, Shuang; Li, Zhuo-Hang; Otoo, Antonia; Tang, Jing; Fu, Li-Juan; Liu, Tai-Hang; Ding, Yu-Bin

doi:10.1007/s10815-023-02917-6

J Assist Reprod Genet

2023

DOI: 10.1007/s10815-023-02917-6

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miR-181d-5p, which is upregulated in fetal growth restriction placentas, inhibits trophoblast fusion via CREBRF

Zhi-Hong Wu,

Fang-Fang Li,

Ling-Ling Ruan

et al.

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2024

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Cited by 5 publications

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Exploring the synthesis, molecular structure and biological activities of novel Bis-Schiff base derivatives: A combined theoretical and experimental approach

Gul,

Alam,

Zainab

et al. 2024

Journal of Molecular Structure

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Exploring the synthesis, molecular structure and biological activities of novel Bis-Schiff base derivatives: A combined theoretical and experimental approach

Gul,

Alam,

Zainab

et al. 2024

Journal of Molecular Structure

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Regulatory roles of N6-methyladenosine (m6A) methylation in RNA processing and non-communicable diseases

Khan,

Nsengimana,

Awan

et al. 2024

Cancer Gene Ther

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HMGB1 regulates autophagy of placental trophoblast through ERK signaling pathway

Li,

Chen,

et al. 2024

Biology of Reproduction

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Objective The purpose of this study is to investigate the role of high mobility group protein B1 (HMGB1) in placental development and fetal growth. Methods We employed the Cre-loxP recombination system to establish a placenta-specific HMGB1 knockout mouse model. Breeding HMGB1flox/flox mice with Elf5-Cre mice facilitated the knockout, leveraging Elf5 expression in extra-embryonic ectoderm, ectoplacental cone, and trophoblast giant cells at 12.5 days of embryonic development. The primary goal of this model was to elucidate the molecular mechanism of HMGB1 in placental development, assessing parameters such as placental weight, fetal weight, and bone development. Additionally, we utilized lentiviral interference and overexpression of HMGB1 in human trophoblast cells to further investigate HMGB1’s functional role. Results Our findings indicate that HMGB1flox/floxElf5cre/+ mouse display fetal growth restriction (FGR), characterized by decreased placental and fetal weight and impaired bone development. And the absence of HMGB1 inhibits autophagosome formation, impairs lysosomal degradation, and disrupts autophagic flux. Depletion of HMGB1 in human trophoblast cells also suppresses cell viability, proliferation, migration, and invasion by inhibiting the ERK signaling pathway. Overexpression of HMGB1 observed the opposite phenotypes. Conclusions HMGB1 participates in the regulation of autophagy through the ERK signaling pathway and affects placental development.

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miR-181d-5p, which is upregulated in fetal growth restriction placentas, inhibits trophoblast fusion via CREBRF

Cited by 5 publications

References 33 publications

Exploring the synthesis, molecular structure and biological activities of novel Bis-Schiff base derivatives: A combined theoretical and experimental approach

Exploring the synthesis, molecular structure and biological activities of novel Bis-Schiff base derivatives: A combined theoretical and experimental approach

Regulatory roles of N6-methyladenosine (m6A) methylation in RNA processing and non-communicable diseases

HMGB1 regulates autophagy of placental trophoblast through ERK signaling pathway

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