Known as a degenerative joint disorder of advanced age affecting predominantly females, osteoarthritis can develop in younger and actively working people because of activities involving loading and injuries of joints. Collagenase-induced osteoarthritis (CIOA) in a mouse model allowed us to investigate for the first time its effects on key cytoskeletal structures (meiotic spindles and actin distribution) of ovulated mouse oocytes. Their meiotic spindles, actin caps, and chromatin were analyzed by immunofluorescence. A total of 193 oocytes from mice with CIOA and 209 from control animals were obtained, almost all in metaphase I (M I) or metaphase II (MII). The maturation rate was lower in CIOA (26.42% M II) than in controls (55.50% M II). CIOA oocytes had significantly larger spindles (average 37 μm versus 25 μm in controls, ), with a proportion of large spindles more than 64% in CIOA versus up to 15% in controls ( ). Meiotic spindles were wider in 68.35% M I and 54.90% M II of CIOA oocytes (mean 18.04 μm M I and 17.34 μm M II versus controls: 11.64 μm M I and 12.64 μm M II), and their poles were approximately two times broader (mean 6.9 μm) in CIOA than in controls (3.6 μm). CIOA oocytes often contained disoriented microtubules. Actin cap was visible in over 91% of controls and less than 20% of CIOA oocytes. Many CIOA oocytes without an actin cap had a nonpolarized thick peripheral actin ring (61.87% of M I and 52.94% of M II). Chromosome alignment was normal in more than 82% in both groups. In conclusion, CIOA affects the cytoskeleton of ovulated mouse oocytes—meiotic spindles are longer and wider, their poles are broader and with disorganized fibers, and the actin cap is replaced by a broad nonpolarized ring. Nevertheless, meiotic spindles were successfully formed in CIOA oocytes and, even when abnormal, allowed correct alignment of chromosomes.

Serum antibodies against the small heat shock protein Hsp27 (HspB1) have been associated with certain diseases but have not been studied in infertility. Sera from 73 infertile patients were tested for antisperm antibodies using agglutination and immobilization tests and ELISA, and for anti-Hsp27 antibodies using ELISA. Of these sera, 31 (42.5%) were positive for anti-Hsp27 antibodies, and 46 (63%) were positive for antisperm antibodies through analysis with at least one method. A total of 17 sera (23.3%) were positive for both anti-Hsp27 and antisperm antibodies. When sera containing both anti-Hsp27 and antisperm antibodies were used for immunofluorescence, the neck and tail of spermatozoa were stained, where the related sperm-specific protein HspB10 (ODF1) is localized. These data suggest that anti-Hsp27 antibodies are elevated in a certain proportion of infertile patients, which, in some of them, could be due to cross-reactivity between Hsp27 and the related sperm cytoskeletal component ODF1.

According to recent data, prostaglandin F2 alpha can have a negative influence on meiosis during oogenesis. Previously, we have found that this prostaglandin may accelerate in a dosage-dependent way the postovulatory aging in ovulated mature oocytes, compromising the integrity of their meiotic spindles. Aim. The study aimed to investigate the effects of prostaglandin F2α on the course and outcome of oocyte meiosis in a mouse model. Materials and Methods. Mouse oocytes were matured in vitro in the presence of prostaglandin F2α in a concentration of 100 ng/ml. Their meiotic stage, spindle morphology and chromosome arrangement were assessed by immunofluorescent labeling of tubulin and fluorescent staining of DNA. Results. We obtained a higher percentage of immature oocytes in metaphase I after the treatment than in untreated control oocytes. In addition, there were specific morphological changes in the meiotic spindles of oocytes exposed to prostaglandin F2α associated with a reduced number of fibers. Conclusion. It is probable that prostaglandin F2α has an impact on the microtubule dynamics of the meiotic spindle that can prevent the transition of maturing oocytes to the second meiotic division, most likely by triggering the spindle assembly checkpoint.

Background/Objectives: Osteoarthritis has been increasingly described as associated with systemic inflammation, raising the question of how it would affect fertility in young women with or without reproductive hormone administration. We studied oogenesis in mice with collagenase-induced osteoarthritis (CIOA) as a model system with fewer ethical limitations after estradiol (E2) or follicle-stimulating hormone (FSH) treatment. Methods: Oocytes have been isolated from mice subjected to various treatment regimens. The meiotic spindle, the chromatin, and the actin cap were fluorescently labeled and analyzed. Results: In addition to reduced maturation rates, specific oocyte abnormalities were registered when CIOA, FSH, or E2 were applied in isolation. Combined treatments showed that the spindle, chromatin, and actin cytoskeleton parameters were differently affected in oocytes from groups with CIOA treated by estradiol and those treated with FSH. Enlarged spindles, ooplasmic tubulin asters, aligned metaphases, and predominantly normal actin caps, often with an actin halo, were typical for groups with CIOA combined with estradiol. The groups with CIOA and FSH had slightly enlarged spindles, unaligned metaphases with degenerated chromatin surrounded by a cloud of depolymerized tubulin, and small actin caps. Conclusions: Our results show that experimental osteoarthritis with or without exogenous reproductive hormones negatively affects oogenesis, presumably due to systemic inflammatory factors making the ovarian microenvironment less capable of supporting oocyte maturation. Estradiol supplementation does not benefit oogenesis. FSH treatment induced cytoskeletal and chromatin abnormalities that presumably disturb the fertilization and development potential of affected oocytes. These data can have implications for assisted reproduction in cases of patients with osteoarthritis.