bioRxiv Science⌕ Search

bioRxiv · 10.1101/2024.04.04.588122

Ovarian support cell in vitro maturation (OSC-IVM) results in healthy murine live births with no evidence of reprotoxicology in a multigenerational study

Abstract

Study questionDoes application of human stem cell-derived ovarian support cells (OSCs) for in vitro maturation (IVM) have a safe reproductive toxicity profile? Summary answerThe use of OSC-IVM co-culture improves blastocyst formation in a mouse model and results in healthy live births with no evidence of reprotoxicity. What is known alreadyAbbreviated stimulation to obtain immature oocytes combined with a successful IVM offers a promising alternative to traditional in vitro fertilization, reducing hormonal doses and making IVF shorter and safer. Recently, we developed an OSC platform derived from human induced pluripotent stem cells (hiPSCs) that replicate dynamic ovarian function in vitro, enhancing human oocyte maturation and yielding an improved blastocyst formation rate compared to commercial IVM options. However, the reproductive toxicity profile, commonly assessed via murine multigenerational models, for OSC-IVM remains unknown. Study design, size, durationA total of 70 B6/CBA 6-8-week-old stimulated female mice were used in this study to collect immature mouse oocytes (n=2,025) at the germinal vesicle (GV) stage. Half of these oocytes were retrieved denuded (denuded oocytes condition, n= 930), while the remaining oocytes were kept with the cumulus cells (COCs condition, n= 1,095) to simulate the two possible dispositions of oocytes during clinical practice. Oocytes from each condition, denuded oocytes and COCs, were randomly assigned to either commercially available traditional IVM media (MediCult-IVMTM, Origio) group (control group) or the same traditional IVM media supplemented with human OSCs (FertiloTM, Gameto Inc.) to form the OSC-IVM group (test group). Participants/materials, setting, methodsOocytes from each condition, denuded oocytes and COCs, were subjected to in vitro culture for 18-20 hours. After IVM, metaphase II (M2) oocytes were inseminated by intracytoplasmic sperm injection (ICSI) and cultured to assess blastocyst formation in vitro. Embryos that reached the blastocyst stage on day five were vitrified using Kitazatos protocol in preparation for embryo transfers. A group of M2 oocytes and blastocyst embryos were employed for quality analyses by immunofluorescence. Vitrified blastocysts were warmed and transferred to pseudopregnant females (4-5 embryos per uterine horn), evaluating the F1 offspring. Pup characteristics were tracked, including weight, length, sex ratio, and physiology. Weekly monitoring assessed mouse behavior and development. At reproductive age, select F1 mice were outbred to wildtype mice to produce the F2 generation, analyzing live births, sex ratio, morphology, and behavior across groups. Moreover, hormonal and organ histological analyses were performed in F1 mice to further explore the overall health of the progeny. Main results and the role of chanceIn contrast to findings in humans, in mice OSC-IVM generally led to a decreased maturation rate compared to Traditional-IVM (68.6% {+/-} 14.1% versus 80.9% {+/-} 5.9%, p=0.0101). Subsequent embryo culture yielded significantly different fertilization rates between the four groups (p=0.0055). Specifically, OSC-IVM with COCs significantly differed from Traditional-IVM with denuded oocytes (89.5 {+/-} 10.5 versus 96.5 {+/-} 4.8, p=0.0098). There were no differences in the cleavage rates (p=0.7547). However, there was a significant distinction in the blastocyst formation (p=0.0068), wherein OSC-IVM with COCs showed a greater formation rate compared to Traditional-IVM for both denuded oocytes and COCs (56.1% {+/-} 19.2% versus 41.5% {+/-} 15.9% and 38.0% {+/-} 16.2%; p=0.0408, and p=0.0063). Spindle morphology analysis demonstrated normal spindle morphology in denuded oocytes and COCs under both Traditional-IVM and OSC-IVM. Moreover, embryo analysis showed no significant difference in inner cell mass count (p=0.1550). Following embryo transfers, analysis of live births showed no significant distinctions between groups regarding delivery, sex ratio, pup length, developmental and behavioral abnormalities, hormonal values or histopathological anomalies in the F1 generation. Evaluation of the F2 generation also showed no significant differences in live births, sex ratio, or developmental/behavioral abnormalities between groups, further validating the absence of long-term implications and transgenerational effects derived from OSC-IVM culture. Limitations, reasons for cautionAlthough this study was conducted in compliance with European Medicines Agency (EMA) ICH E6 (R2) Good clinical practice scientific guidelines to demonstrate the OSC safety, human clinical studies evaluating in vivo and live birth outcomes are necessary to corroborate the findings of this study. Wider implications of the findingsThis study provides evidence of the safety of using the OSC-IVM system, as evidenced by the lack of adverse effects on in vitro embryo development post OSC-IVM and on the health and fertility of offspring across successive generations in vivo. Trial registration numberN/A

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Marchante, M., Barrachina, F., Mestres, E., Acacio, M., Potts, K. S., Piechota, S., Paulsen, B., Noblett, A. D., Figueroa, A. B., Costa-Borges, N., Kramme, C. C.. 2024-04-06. Ovarian support cell in vitro maturation (OSC-IVM) results in healthy murine live births with no evidence of reprotoxicology in a multigenerational study. https://doi.org/10.1101/2024.04.04.588122

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

PCB-Exposed Gut Microbiota Recapitulate Neurobehavioral Deficits and Reprogram Hippocampal Transcriptomic Signatures

Polychlorinated biphenyls (PCBs) are persistent environmental pollutants associated with developmental neurotoxicity and autism spectrum disorder (ASD). However, whether PCB-induced alterations in gut microbiota contribute to neurodevelopmental toxicity independently of direct chemical exposure remains unclear. Here, we investigated whether transplantation of PCB-associated gut microbiota produces early neurobehavioral alterations and disrupts brain molecular pathways in offspring. Gut microbiota from conventional dams exposed to the Fox River PCB mixture (FRM; 6.0 mg/kg/day) or vehicle were transplanted into germ-free recipient females without direct PCB administration. At postnatal day 7 (P7), offspring underwent ultrasonic vocalization (USV) testing, whole-brain RNA sequencing (n = 4/sex/group), and untargeted serum metabolomics. Untargeted serum metabolomics were also performed in donor dams. PCB-associated fecal microbiota transplantation (FMT) significantly reduced offspring USVs, reproducing effects observed following direct maternal PCB exposure. Brain transcriptomics in offspring identified substantially more differentially expressed genes in males (9,339) than females (1,082), including 512 shared genes. Concordantly regulated genes revealed downregulation of neurotransmitter signaling and ion channel pathways alongside upregulation of RNA processing pathways. Male-associated responses involved altered protein synthesis and neuronal signaling, whereas female-associated responses involved DNA repair and extracellular matrix remodeling. Despite these molecular differences, behavioral responses showed no significant sex-dependent effect. Maternal metabolomics revealed increased bile acids and decreased indole-3-propionic acid, highlighting potential AhR-NF{kappa}B and bile acid-associated signaling mechanisms. Offspring metabolomics further identified alterations in lipid-associated metabolites and metabolic profiles. Collectively, these findings show that transferring PCB-exposed microbiota reproduces early neurobehavioral alterations and induces shared and sex-biased molecular responses, identifying the maternal gut microbiome as a candidate mediator linking PCB exposure to developmental neurotoxicity.

pharmacology and toxicology↗

Cisplatin-triggered sensory dysfunction in NER-defective C. elegans involves GABAergic and cholinergic signaling

Cisplatin (CisPt) is a widely used anticancer drug that causes neurotoxicity as a dose-limiting adverse effect. DNA damage contributes to CisPt-induced neurotoxicity, yet the molecular mechanisms involved remain unclear. Here, we aim to identify pathophysiological mechanisms contributing to DNA damage-driven development of sensory neuronal dysfunction using the 3R-compliant model organism Caenorhabditis elegans. To this end, we employed the nucleotide excision repair (NER)-deficient ercc-1 mutant, which shows enhanced CisPt-induced sensory dysfunction as monitored by the chemotaxis assay, to elucidate drug-induced alterations in neurotransmission and transcriptome. We found that CisPt reduces gamma-aminobutyric acid (GABA) levels in the nematode and that GABA supplementation rescues ercc-1 mutants from CisPt-evoked sensory neurotoxicity, pointing to a neuroprotective function of GABA in the context of our study. Moreover, CisPt impairs the morphological integrity of GABAergic neurons particularly in ercc-1 mutants, which again is rescued by GABA substitution. Conversely, the cholinergic agonist carbachol impairs sensory function and exacerbates the neurotoxic effects of CisPt in ercc-1 mutants, indicating detrimental effects resulting from cholinergic excitation. Transcriptome analysis revealed that CisPt treatment stimulates a broard transcriptional response, including pathways involved in the regulation of neuronal communication, including acetylcholine-mediated neurotransmission, with pronounced effects occurring in the absence of ERCC-1. Based on these finding we suggest impaired GABAergic signaling and the loss of neuronal integrity GABAergic neurons as well as excessive cholinergic excitation as key mechanisms linking CisPt-induced DNA damage in NER defective nematodes to sensory dysfunction. Hence, targeting the balance between GABAergic inhibition and cholinergic excitation is suggested to counteract sensory neurotoxicity triggered by CisPt.

pharmacology and toxicology↗

Mathematical model of phenotypic plasticity predicts interconversion is a drug target for neuroblastoma.

Neuroblastoma is a paediatric cancer arising from the sympathetic nervous system as neural crest cells, made up of noradrenergic (NOR/ADRN/N), mesenchymal like (MES/S), and intermediate (I-type/I) cell types. These cells can interconvert between types, contributing to treatment resistance and relapse. We developed a mathematical model to investigate how interconversion patterns affect the efficacy of phenotype-specific inhibitors. We used three ordinary differential equations to describe the dynamics of the three populations, including logistic growth, interconversion, and drug-induced death. Of the 64 possible interconversion patterns, five reduced the target population: two for N cells and three for S cells. N targeting patterns were more effective with higher interconversion rates, while mesenchymal targeting patterns were more effective with lower interconversion rates. Stability analysis revealed that natural tumour growth was always unstable, but during treatment, N-suppressing patterns combined with an S inhibitor gave the most consistently stable origin. Testing multi-stage and cyclic treatment schedules revealed that N-suppressing patterns with an S inhibitor, followed by an S-suppressing pattern with an N inhibitor, achieved more reliable remission. Three of the five patterns of interest correspond to reported biological plausibility, and known compounds exist to induce most of the required transitions, supporting the clinical relevance of these strategies for improving neuroblastoma treatment outcomes.

pharmacology and toxicology↗