The role of L-type calcium channels in mouse oocyte maturation, activation and early embryonic development

He, Guifang; Yang, Leilei; Luo, Shi‐Ming; Ma, Jun‐Yu; Ge, Zhao‐Jia; Shen, Wei; Yin, Shen; Sun, Qing‐Yuan

doi:10.1016/j.theriogenology.2017.07.012

Cited by 13 publications

(4 citation statements)

References 38 publications

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“…We found that the homozygous Actl7a mutation caused the failure of oocyte activation in mice, but the arrest of embryonic development in humans. It has been reported that the duration of oocyte activation, patterns of calcium oscillations, and calcium channel blockers affect the early embryonic development in mice (14,21,22). In addition, sperms with low levels of PLC have been reported to be significantly related to higher rates of embryonic development arrest in humans (23).…”

Section: Discussionmentioning

confidence: 99%

Disruption in ACTL7A causes acrosomal ultrastructural defects in human and mouse sperm as a novel male factor inducing early embryonic arrest

Xin

Chen

et al. 2020

Sci. Adv.

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Early embryonic arrest is a challenge for in vitro fertilization (IVF). No genetic factors were previously revealed in the sperm-derived arrest of embryonic development. Here, we reported two infertile brothers presenting normal in conventional semen analysis, but both couples had no embryos for transfer after several IVF and intracytoplasmic sperm injection (ICSI). Whole-exome sequencing identified a homozygous missense mutation of ACTL7A in both brothers. This mutation is deleterious and causes sperm acrosomal ultrastructural defects. The Actl7a knock-in mouse model was generated, and male mutated mice showed sperm acrosomal defects, which were completely consistent with the observations in patients. Furthermore, the sperm from ACTL7A/Actl7a-mutated men and mice showed reduced expression and abnormal localization of PLCζ as a potential cause of embryonic arrest and failure of fertilization. Artificial oocyte activation could successfully overcome the Actl7a-mutated sperm-derived infertility, which is meaningful in the future practice of IVF/ICSI for the ACTL7A-associated male infertility.

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Section: Discussionmentioning

confidence: 99%

Disruption in ACTL7A causes acrosomal ultrastructural defects in human and mouse sperm as a novel male factor inducing early embryonic arrest

Xin

Chen

et al. 2020

Sci. Adv.

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“…The results show that amlodipine at high concentrations can cause a decrease in parthenogenetic activation and inhibit early embryonic development in mice 32 .…”

Section: Teratogenicity Testmentioning

confidence: 86%

The Review: The Discovery and Development of Amlodipine Drug

Putri¹,

Mustika²,

Asra³

2022

Asian J Pharm Res Dev

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“…The immunofluorescence staining procedure was performed as described previously . Briefly, after cultured for 8 hours, oocytes were fixed with 4% paraformaldehyde (PFA) for at least 30 minutes at room temperature (RT).…”

Section: Methodsmentioning

confidence: 99%

“…The immunofluorescence staining procedure was performed as described previously. 19 Briefly, after cultured for 8 hours, oocytes were fixed with 4% paraformaldehyde (PFA) for at least 30 minutes at room temperature (RT). After washing, oocytes were permeabilized in PBS supplemented with 1% Triton X-100 for 20 minutes and blocked in PBS containing 1% bovine serum albumin for 1 hour at RT.…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

Tributyltin oxide exposure impairs mouse oocyte maturation and its possible mechanisms

Yang

Cui

et al. 2018

J of Cellular Biochemistry

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Tributyltin oxide (TBTO) has been widely used as marine antifouling composition, preservative, biocide, and a stabilizer in plastic industry. Previous studies have indicated that TBTO can cause immunotoxicity as an environmental pollutant. However, little is known about its reproductive toxicity, especially on female oocyte maturation and the underlying mechanisms. In this study, mouse oocytes were cultured with different concentrations of TBTO in vitro, and several crucial events during meiotic maturation were evaluated. We found that the first polar body extrusion rate was significantly reduced, which reflected the disruption of meiotic maturation. The rate of abnormal spindle organization increased significantly, accompanied with a higher rate of chromosome misalignment. In addition, TBTO treatment increased reactive oxygen species generation markedly, which also accelerated the early-stage apoptosis. Moreover, heterogeneous mitochondrial distribution, mitochondrial dysfunction, and higher rate of aneuploidy were detected, which consequently disrupted in vitro fertilization. In conclusion, our results indicated that TBTO exposure could impair mouse oocyte maturation by affecting spindle organization, chromosome alignment, mitochondria functions, oxidative stress, and apoptosis.

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The role of L-type calcium channels in mouse oocyte maturation, activation and early embryonic development

Cited by 13 publications

References 38 publications

Disruption in ACTL7A causes acrosomal ultrastructural defects in human and mouse sperm as a novel male factor inducing early embryonic arrest

Disruption in ACTL7A causes acrosomal ultrastructural defects in human and mouse sperm as a novel male factor inducing early embryonic arrest

The Review: The Discovery and Development of Amlodipine Drug

Tributyltin oxide exposure impairs mouse oocyte maturation and its possible mechanisms

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