Transplacental transport and tissue distribution of biotin in mice at midgestation

Taniguchi, Atsuhiko; Watanabe, Toshiaki

doi:10.1111/j.1741-4520.2008.00179.x

Cited by 5 publications

(7 citation statements)

References 26 publications

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“…Immediately after fetal echography on E14.5, biotin was injected intravenously into the pregnant dams. To test whether maternal endogenous biotin can cross the placenta and accumulate in fetal tissues, immunofluorescent staining was conducted 51 . In non-immune pregnant mice, biotin crossed the placenta and accumulated in fetal tissues, whereas fetuses from biotin-injected immune mice had less fetal biotin accumulation (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…After abdominal shaving, chemical depilation (Nair™, Church & Dwight Co, Inc.) and application of coupling gel (37 °C), high-frequency ultrasound imaging was performed by nonlinear contrast imaging using a Vevo ® 2100 system and a MS550 transducer (32–56 MHz). After ultrasound, some animals were intravenously injected with biotin (0.25 g per kg body weight) to test maternal–fetal transport of essential nutrient 51 . Biotin is transported by its sodium-dependent multivitamin transporter 68 .…”

Section: Methodsmentioning

confidence: 99%

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Activated NK cells cause placental dysfunction and miscarriages in fetal alloimmune thrombocytopenia

et al. 2017

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Miscarriage and intrauterine growth restriction (IUGR) are devastating complications in fetal/neonatal alloimmune thrombocytopenia (FNAIT). We previously reported the mechanisms for bleeding diatheses, but it is unknown whether placental, decidual immune cells or other abnormalities at the maternal–fetal interface contribute to FNAIT. Here we show that maternal immune responses to fetal platelet antigens cause miscarriage and IUGR that are associated with vascular and immune pathologies in murine FNAIT models. Uterine natural killer (uNK) cell recruitment and survival beyond mid-gestation lead to elevated NKp46 and CD107 expression, perforin release and trophoblast apoptosis. Depletion of NK cells restores normal spiral artery remodeling and placental function, prevents miscarriage, and rescues hemorrhage in neonates. Blockade of NK activation receptors (NKp46, FcɣRIIIa) also rescues pregnancy loss. These findings shed light on uNK antibody-dependent cell-mediated cytotoxicity of invasive trophoblasts as a pathological mechanism in FNAIT, and suggest that anti-NK cell therapies may prevent immune-mediated pregnancy loss and ameliorate FNAIT.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Activated NK cells cause placental dysfunction and miscarriages in fetal alloimmune thrombocytopenia

et al. 2017

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“…C. abortus can grow in a number of hosts and tissues, but is best known for causing abortions. Pregnant animals are known to incur transient biotin deficiencies and mouse models have shown that reduced biotin levels in dams correlates with reduced levels of biotin in the fetus [57], [58]. The loss of biotin synthesis by the LLG strain might explain its reduced pathology in a pregnant mouse abortion model and small plaque phenotype and makes it an ideal candidate to test for biotin dependent phenotypes compared to “dual” biotin metabolism C. abortus strains [59].…”

Section: Discussionmentioning

confidence: 99%

Uptake of Biotin by Chlamydia Spp. through the Use of a Bacterial Transporter (BioY) and a Host-Cell Transporter (SMVT)

et al. 2012

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Chlamydia spp. are obligate intracellular Gram-negative bacterial pathogens that cause disease in humans and animals. Minor variations in metabolic capacity between species have been causally linked to host and tissue tropisms. Analysis of the highly conserved genomes of Chlamydia spp. reveals divergence in the metabolism of the essential vitamin biotin with genes for either synthesis (bioF_2ADB) and/or transport (bioY). Streptavidin blotting confirmed the presence of a single biotinylated protein in Chlamydia. As a first step in unraveling the need for divergent biotin acquisition strategies, we examined BioY (CTL0613) from C. trachomatis 434/Bu which is annotated as an S component of the type II energy coupling-factor transporters (ECF). Type II ECFs are typically composed of a transport specific component (S) and a chromosomally unlinked energy module (AT). Intriguingly, Chlamydia lack recognizable AT modules. Using 3H-biotin and recombinant E. coli expressing CTL0613, we demonstrated that biotin was transported with high affinity (a property of Type II ECFs previously shown to require an AT module) and capacity (apparent K(m) of 3.35 nM and V(max) of 55.1 pmol×min−1×mg−1). Since Chlamydia reside in a host derived membrane vacuole, termed an inclusion, we also sought a mechanism for transport of biotin from the cell cytoplasm into the inclusion vacuole. Immunofluorescence microscopy revealed that the mammalian sodium multivitamin transporter (SMVT), which transports lipoic acid, biotin, and pantothenic acid into cells, localizes to the inclusion. Since Chlamydia also are auxotrophic for lipoic and pantothenic acids, SMVT may be subverted by Chlamydia to move multiple essential compounds into the inclusion where BioY and another transporter(s) would be present to facilitate transport into the bacterium. Collectively, our data validates the first BioY from a pathogenic organism and describes a two-step mechanism by which Chlamydia transport biotin from the host cell into the bacterial cytoplasm.

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“…Detection of holocarboxylase and biotinidase activity. The holocarboxylases (biotinylated carboxylases in vivo) were separated by SDS-PAGE in 8% polyacrylamide gels and detected by Western blotting analysis with streptavidin peroxidase (11,28,35).…”

Section: Animals and Dietsmentioning

confidence: 99%

“…In experimental animals, biotin deficiency has been demonstrated to have teratogenic effects (e.g. cleft palate, micrognathia, and micromelia) in mice (7)(8)(9)(10)(11)(12)(13)(14). Biotin deficiency also causes metabolic disorders, for example, increased urinary excretion of 3-hydroxyisovaleric acid (3-HIA) due to decreased MCC activity (15).…”

mentioning

confidence: 99%

Effects of Biotin Deficiency on Biotinylated Proteins and Biotin-Related Genes in the Rat Brain

Yuasa

Aoyama

Shimada

et al. 2016

J Nutr Sci Vitaminol

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Biotin is a water-soluble vitamin that functions as a cofactor for biotin-dependent carboxylases. The biochemical and physiological roles of biotin in brain regions have not yet been investigated sufficiently in vivo. Thus, in order to clarify the function of biotin in the brain, we herein examined biotin contents, biotinylated protein expression (e.g. holocarboxylases), and biotin-related gene expression in the brain of biotin-deficient rats. Three-week-old male Wistar rats were divided into a control group, biotin-deficient group, and pair-fed group. Rats were fed experimental diets from 3 wk old for 8 wk, and the cortex, hippocampus, striatum, hypothalamus, and cerebellum were then collected. In the biotin-deficient group, the maintenance of total biotin and holocarboxylases, increases in the bound form of biotin and biotinidase activity, and the expression of an unknown biotinylated protein were observed in the cortex. In other regions, total and free biotin contents decreased, holocarboxylase expression was maintained, and bound biotin and biotinidase activity remained unchanged. Biotin-related gene (pyruvate carboxylase, sodium-dependent multivitamin transporter, holocarboxylase synthetase, and biotinidase) expression in the cortex and hippocampus also remained unchanged among the dietary groups. These results suggest that biotin may be related to cortex functions by binding protein, and the effects of a biotin deficiency and the importance of biotin differ among the different brain regions.

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Transplacental transport and tissue distribution of biotin in mice at midgestation

Cited by 5 publications

References 26 publications

Activated NK cells cause placental dysfunction and miscarriages in fetal alloimmune thrombocytopenia

Activated NK cells cause placental dysfunction and miscarriages in fetal alloimmune thrombocytopenia

Uptake of Biotin by Chlamydia Spp. through the Use of a Bacterial Transporter (BioY) and a Host-Cell Transporter (SMVT)

Effects of Biotin Deficiency on Biotinylated Proteins and Biotin-Related Genes in the Rat Brain

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