Biology subjects

Kwon, H. N.

Publications and source records attributed to Kwon, H. N..

3 recordsLinked to original sources

bioRxiv2026

Cumulus cells mediate the protective effect of the marine carotenoid fucoxanthin against postovulatory oocyte aging via NRF2 signaling

Background Oocytes awaiting insemination undergo postovulatory aging, an oxidative stress-driven loss of developmental competence. Fucoxanthin (FX), the major carotenoid of the brown alga Undaria pinnatifida, acts through NRF2, which requires a nucleus and transcription; the metaphase-II oocyte has neither, so its site of action is unresolved. Purpose To determine whether FX delays postovulatory aging of mouse oocytes and identify the mediating compartment of the cumulus-oocyte complex. Study design Ex vivo study of intact cumulus-oocyte complexes from superovulated ICR mice aged for 12 h, or 24 h for spindle analysis. Astaxanthin (AX) served as benchmark and the NRF2 inhibitor ML385 tested pathway dependence. Methods Complexes were held in M16 medium with FX (1-10 {micro}M) or AX (5 {micro}M). Mitochondrial membrane potential, reactive oxygen species (ROS) and glutathione were measured with JC-1, DCFH-DA and monochlorobimane; spindle organization and cumulus-cell NRF2 localization by immunofluorescence. Results At the optimal 5 {micro}M, FX raised the JC-1 aggregate-to-monomer ratio eight-fold over untreated aged oocytes (1.24 {+/-} 0.10 versus 0.15 {+/-} 0.02; p < 0.05), lowered ROS to 0.18 {+/-} 0.04-fold and raised glutathione to 1.80 {+/-} 0.02-fold of control (both p < 0.01), comparably to AX. ML385 abolished all three effects concentration-dependently. FX increased the cumulus-cell NRF2 nuclear-to-cytoplasmic ratio (p < 0.05) and, after 24 h, nearly halved abnormal spindles (p = 0.059). Conclusion FX preserves mitochondrial and redox status in postovulatory-aged oocytes through NRF2, which translocates in cumulus cells rather than the oocyte, identifying the cumulus cell as a target for extending oocyte usability in assisted reproduction.

cell biology↗

bioRxiv2025

Impact of gestational antibiotics on maternal and offspring gut microbiota and growth in pigs

Maternal microbiota modulates the development of the microbiota in the offspring. Effects of gestational antibiotics are not well understood, as most studies have focused on the perinatal period. We treated sows with penicillin, tetracycline or saline on days 78-80 of the 114-119-day gestation, a critical period in the fetal immune system development. Microbiotas were analyzed by 16S rRNA gene amplicon sequencing in sow feces and vagina at days 77 and 113, in colostrum, and in piglet feces at three days, three weeks and ten weeks of age. Sow fecal microbiota changed during pregnancy, but less in antibiotic groups. No significant effects on sow microbiota remained on day 113. The piglets of the antibiotic-treated sows had lower Firmicutes+Actinobacteriota to Bacteroidota+Proteobacteria ratio, lower alpha diversity and higher relative abundance of Escherichia at three days. At ten weeks, they exhibited higher alpha diversity, had higher of Prevotella and Clostridium sp. CAG-127, and smaller increase of Limosilactobacillus than the control. Increased alpha diversity at 10 weeks was associated with lower weight gain during nursing. Oliverpabstia and Mitsuokella were positively associated with growth, while CAG-127 and Campylobacter B were negatively associated. Sow antibiotic treatment decreased the positive effect of Oliverpabstia and Mitsuokella and increased the negative effects of CAG-127 and Campylobacter B. Gestational antibiotics may have had adverse effects on microbiota and growth of the offspring, even if their effects on maternal microbiota were undetectable by parturition.

microbiology↗

bioRxiv2021

Omics profiling identifies MAPK/ERK pathway as a gatekeeper of nephron progenitor metabolism

Nephron endowment is defined by fetal kidney growth and critically dictates renal health in adults. Despite the advances in understanding the molecular regulation of nephron progenitors, the causes for low congenital nephron count and contribution of basic metabolism to nephron progenitor biology remain poorly understood. Here we characterized the metabolic consequences of MAPK/ERK-deficiency in nephron progenitors, whose maintenance and propagation in developing kidney critically depends on ERK activation. Our LC/MS-based metabolomics profiling identified 42 reduced metabolites, of which 26 were further supported by in vivo transcriptional characterization of MAPK/ERK-deficient nephron progenitors. This revealed a severe shortage of energy and nucleotide biosynthesis precursors, blockage in glycolysis and diminished pyruvate and proline metabolism. Utilization of in vitro kidney cultures demonstrated a dosage-specific function for glycolytic pyruvate as an energy source that controls the shape of the ureteric bud tip kwon to serve as a niche for nephron progenitor regulation. Analysis of the proline biosynthesis effects in developing kidney in vivo revealed premature loss of nephron progenitor maintenance in the absence of Pycr1/2 functions. Our results suggest that MAPK/ERK-dependent nephron progenitor metabolism functionally contributes to progenitor preservation by controlling pyruvate availability and proline metabolism in developing kidneys.

developmental biology↗