Lentiviral Vector-Mediated Complementation Restored Fetal Viability but Not Placental Hyperplasia in Plac1-Deficient Mice1

Muto, Masanaga; Fujihara, Yoshitaka; Tobita, Tomohiro; Kiyozumi, Daiji; Ikawa, Masahito

doi:10.1095/biolreprod.115.133454

Cited by 16 publications

(8 citation statements)

References 19 publications

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“…In addition to the PAPPA biomarkers, the expression analysis of the novel X-linked gene PLAC-1 in FGR and normal pregnancies revealed marked differences between the two groups. Disruption of PLAC-1 can cause hyperplasia and FGR, whereas PLAC-1 is also reported to be one of the upregulated genes in the hyperplastic placenta generated by nuclear transfer ( 23 ). Although the association of PLAC-1 with the development of FGR during pregnancy has not been examined to date, previous studies demonstrated elevated levels of circulating PLAC-1 mRNA in preeclampsia that were directly related to the disease severity ( 24 – 26 ).…”

Section: Discussionmentioning

confidence: 99%

Placental expression of PAPPA, PAPPA-2 and PLAC-1 in pregnacies is associated with FGR

et al. 2018

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Fetal growth restriction (FGR) is a gynecological disorder of varying etiology. In the present study, an expression analysis of pregnancy-associated plasma protein A (PAPPA), pregnancy-associated plasma protein A2 (PAPPA2) and placenta-specific-1 (PLAC-1) was conducted in pregnancies with FGR and control pregnancies. Placental tissues were collected from pregnancies with FGR (n=16) and control pregnancies (n=16) and the expression of the genes of interest was examined by qPCR. The mean expression levels of PAPPA and PAPPA2 were significantly lower (P<0.001) in placental tissues from FGR pregnancies compared with tissues from healthy subjects, whereas the opposite pattern was observed for PLAC-1 (P<0.001). PAPPA and PLAC-1 expression in FGR and control subjects correlated with birth weight (P<0.001). The findings suggest a possible pathophysiological link between the development of FGR and the expression of PAPPA, PAPPA2 and PLAC-1.

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Section: Discussionmentioning

confidence: 99%

Placental expression of PAPPA, PAPPA-2 and PLAC-1 in pregnacies is associated with FGR

et al. 2018

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“…Then, the Plac1 expression level decreased and its distribution became restricted. Plac1 knockout in the placenta was found to be attributed to the abnormal structure of spongiotrophoblasts, and knockout of Plac1 in the embryo has been shown to induce hydrocephalus [11], which can be rescued by Plac1 overexpression [26]. Furthermore, the possible function of Plac1 in the chorioallantois, umbilical cord, and uterus during pregnancy deserves our attention because its abundance and lasting expression in the chorioallantois, umbilical cord, as well as the uterine epithelium from 13.5 dpc was observed in our study.…”

Section: Discussionmentioning

confidence: 99%

Plac1 Expression Pattern at the Mouse Fetomaternal Interface and Involvement in Trophoblast Differentiation

Wan

et al. 2017

Cell Physiol Biochem

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Background/Aims: It is well known that Plac1 is a placenta-specific gene; however, its spatiotemporal expression pattern and exact role at t h e mouse fetomaternal interface r e m a i n s unclear. Methods: In situ hybridization (ISH) was used to localize the Plac1 mRNA at the mouse fetomaternal interface. A trophoblast stem cell (TS) differentiation model with Plac1 shRNA-overexpressing lentivirus was employed to investigate the possible role of Plac1 in placentation. Real-time RT-PCR was used to detect changes in gene expression. Results: Plac1 was exclusively expressed in the ectoplacental cone (EPC) as well as in 8.5 and 9.5 days post-coitum (dpc) embryos. Subsequently, Plac1 expression was abundant in the spongiotrophoblast layer and moderately in the labyrinth layer until 13.5 dpc, and declined thereafter. Interestingly, Plac1 was also expressed by secondary trophoblast giant cells and glycogen trophoblast cells, but not in primary trophoblast giant cells. Plac1 transcription was increased during the TS differentiation (P < 0.01), and knockdown of Plac1 significantly impaired TS differentiation. Conclusion: Plac1 is abundantly expressed at the fetomaternal interface and in all trophoblast subtypes except in primary trophoblast giant cells. Plac1 knockdown retarded the progress of TS differentiation, indicating that Plac1 is necessary for normal trophoblast differentiation into various trophoblast subpopulations.

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“…Immunostaining was performed as described previously [ 42 , 43 ]. Briefly, all samples were mounted on glass slides and dried.…”

Section: Methodsmentioning

confidence: 99%

Human Globozoospermia-Related Gene Spata16 Is Required for Sperm Formation Revealed by CRISPR/Cas9-Mediated Mouse Models

Fujihara

Oji

Larasati

et al. 2017

IJMS

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A recent genetic analysis of infertile globozoospermic patients identified causative mutations in three genes: a protein interacting with C kinase 1 (PICK1), dpy 19-like 2 (DPY19L2), and spermatogenesis associated 16 (SPATA16). Although mouse models have clarified the physiological functions of Pick1 and Dpy19l2 during spermatogenesis, Spata16 remains to be determined. Globozoospermic patients carried a homozygous point mutation in SPATA16 at 848G→A/R283Q. We generated CRISPR/Cas9-mediated mutant mice with the same amino acid substitution in the fourth exon of Spata16 to analyze the mutation site at R284Q, which corresponded with R283Q of mutated human SPATA16. We found that the point mutation in Spata16 was not essential for male fertility; however, deletion of the fourth exon of Spata16 resulted in infertile male mice due to spermiogenic arrest but not globozoospermia. This study demonstrates that Spata16 is indispensable for male fertility in mice, as well as in humans, as revealed by CRISPR/Cas9-mediated mouse models.

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Lentiviral Vector-Mediated Complementation Restored Fetal Viability but Not Placental Hyperplasia in Plac1-Deficient Mice1

Cited by 16 publications

References 19 publications

Placental expression of PAPPA, PAPPA-2 and PLAC-1 in pregnacies is associated with FGR

Placental expression of PAPPA, PAPPA-2 and PLAC-1 in pregnacies is associated with FGR

Plac1 Expression Pattern at the Mouse Fetomaternal Interface and Involvement in Trophoblast Differentiation

Human Globozoospermia-Related Gene Spata16 Is Required for Sperm Formation Revealed by CRISPR/Cas9-Mediated Mouse Models

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