Journal articles: 'Mice Fertility'

1

Boughton, Barbara. "Fertility preserved in irradiated mice." Lancet Oncology 3, no. 10 (October 2002): 584. http://dx.doi.org/10.1016/s1470-2045(02)00884-7.

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El-Fiky, B. A. "fertility in induced azoospermic mice." Journal of Bioscience and Applied Research 2, no. 9 (September 23, 2016): 626–33. http://dx.doi.org/10.21608/jbaar.2016.109004.

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Chubb, C., and L. Henry. "The fertility of hypothyroid male mice." Reproduction 83, no. 2 (July 1, 1988): 819–23. http://dx.doi.org/10.1530/jrf.0.0830819.

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Silberner, J. "Fertility Factor from the Mouths of Mice." Science News 130, no. 9 (August 30, 1986): 135. http://dx.doi.org/10.2307/3970946.

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Yamamoto, Yoshiko, Keiichi Yamamoto, and Tamaki Hayase. "Effect of Methamphetamine on Male Mice Fertility." Journal of Obstetrics and Gynaecology Research 25, no. 5 (October 1999): 353–58. http://dx.doi.org/10.1111/j.1447-0756.1999.tb01176.x.

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Rubinstein, Eric, Ahmed Ziyyat, Michel Prenant, Edyta Wrobel, Jean-Philippe Wolf, Shoshana Levy, François Le Naour, and Claude Boucheix. "Reduced fertility of female mice lacking CD81." Developmental Biology 290, no. 2 (February 2006): 351–58. http://dx.doi.org/10.1016/j.ydbio.2005.11.031.

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Gao, Qian, Li-Li Sun, Fen-Fen Xiang, Li Gao, Yin Jia, Jian-Rong Zhang, Hai-Bo Tao, Jun-Jie Zhang, and Wen-Jie Li. "Crybb2 deficiency impairs fertility in female mice." Biochemical and Biophysical Research Communications 453, no. 1 (October 2014): 37–42. http://dx.doi.org/10.1016/j.bbrc.2014.09.049.

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Evans, Maggie C., Mohammed Z. Rizwan, and Greg M. Anderson. "Insulin Action on GABA Neurons Is a Critical Regulator of Energy Balance But Not Fertility in Mice." Endocrinology 155, no. 11 (November 1, 2014): 4368–79. http://dx.doi.org/10.1210/en.2014-1412.

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Abstract Insulin signaling in the brain plays an important role in the central regulation of energy homeostasis and fertility, such that mice exhibiting brain-specific deletion of insulin receptors (InsRs) display a diet-sensitive obesogenic phenotype and hypothalamic hypogonadism. However, the specific neurons mediating insulin's central effects on fertility remain largely unidentified. The neurotransmitters γ-aminobutyric acid (GABA) and glutamate are important modulators of fertility and energy homeostasis and are widely distributed in the hypothalamus. We therefore investigated whether insulin signaling via GABAergic or glutamatergic neurons plays an important role in the metabolic regulation of fertility. We used the Cre-loxP system to generate mice with a selective inactivation of the Insr gene from GABAergic (Vgat+) or glutamatergic (Vglut2+) cells by crossing Insr-flox mice with Vgat-Cre or Vglut2-Cre mice, respectively. Multiple reproductive and metabolic parameters were then compared between male and female Insr-flox/Vgat-Cre+ (VgatIRKO), Insr-flox/Vglut2-Cre+ (VglutIRKO), and Insr-flox/Cre-negative control (CON) mice. Female VgatIRKO mice exhibited a significant increase in adult body weight, abdominal fat mass, and fasting plasma insulin and leptin concentrations, but normal fasting glucose concentration and glucose tolerance compared with CON mice. Surprisingly, VgatIRKO and VglutIRKO mice exhibited normal reproductive maturation and function compared with CONs. No differences in the age of puberty onset, estrous cyclicity, or fertility were observed between VgatIRKO, VglutIRKO, and CON mice. However, male VgatIRKO mice exhibited significantly augmented LH concentration and a trend toward reduced seminal vesicle weight compared with CON mice, which may be indicative of primary hypogonadism. Our results therefore demonstrate that insulin signaling via GABAergic and glutamatergic cells is not required for fertility in mice, but show that GABAergic neurons encompass circuitry through which insulin acts to modulate energy homeostasis.

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Kuchmiy, Anna A., Jinke D’Hont, Tino Hochepied, and Mohamed Lamkanfi. "NLRP2 controls age-associated maternal fertility." Journal of Experimental Medicine 213, no. 13 (November 23, 2016): 2851–60. http://dx.doi.org/10.1084/jem.20160900.

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Nucleotide-binding domain and leucine-rich repeat (NLR) proteins are well-known for their key roles in the immune system. Ectopically expressed NLRP2 in immortalized cell lines assembles an inflammasome and inhibits activation of the proinflammatory transcription factor NF-κB, but the physiological roles of NLRP2 are unknown. Here, we show that Nlrp2-deficient mice were born with expected Mendelian ratios and that Nlrp2 was dispensable for innate and adaptive immunity. The observation that Nlrp2 was exclusively expressed in oocytes led us to explore the role of Nlrp2 in parthenogenetic activation of oocytes. Remarkably, unlike oocytes of young adult Nlrp2-deficient mice, activated oocytes of mature adult mice developed slower and largely failed to reach the blastocyst stage. In agreement, we noted strikingly declining reproductive rates in vivo with progressing age of female Nlrp2-deficient mice. This work identifies Nlrp2 as a critical regulator of oocyte quality and suggests that NLRP2 variants with reduced activity may contribute to maternal age-associated fertility loss in humans.

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Hardy, C. M., J. F. M. ten Have, K. J. Mobbs, and L. A. Hinds. "Assessment of the immunocontraceptive effect of a zona pellucida 3 peptide antigen in wild mice." Reproduction, Fertility and Development 14, no. 3 (2002): 151. http://dx.doi.org/10.1071/rd01112.

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Immunizing laboratory mice against a short peptide to mouse zona pellucida protein 3 (mZP3; amino acids 328-342) reduces fertility in some strains. This antigen was therefore tested to see if it is suitable for use in an immunocontraceptive vaccine to control wild mice. Mouse zona pellucida protein 3 peptide conjugated to a carrier protein (keyhole limpet hemocyanin) was considerably more immunogenic and effective in reducing fertility in wild mice when compared with inbred BALB/c mice. Fertility of the immunized wild mice was reduced by over 50% compared with controls, whereas BALB/c mice showed no reduction. Variation in the responses between individual animals to mZP3 peptide was observed and infertility correlated to the presence of cross-reacting antibodies to native zona pellucida in wild, but not BALB/c, mice.

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Herbison, Allan E., Robert Porteous, Jean-Rémi Pape, Jocelyn M. Mora, and Peter R. Hurst. "Gonadotropin-Releasing Hormone Neuron Requirements for Puberty, Ovulation, and Fertility." Endocrinology 149, no. 2 (November 15, 2007): 597–604. http://dx.doi.org/10.1210/en.2007-1139.

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The absolute requirement for reproduction implies that the hypothalamo-pituitary-gonadal axis, controlling fertility, is an evolutionary robust mechanism. The GnRH neurons of the hypothalamus represent the key cell type within the body dictating fertility. However, the level of functional redundancy within the GnRH neuron population is unknown. As a result of a fortuitous transgene insertion event, GNR23 mice exhibit a marked allele-dependent reduction in GnRH neuron number within their brain. Wild-type mice have approximately 600 GnRH neurons, compared with approximately 200 (34%) and approximately 70 (12%) in GNR23+/− and GNR23−/− mice, respectively. Using these mice, we examined the minimal GnRH neuron requirements for fertility. Male GNR23−/− mice exhibited normal fertility. In contrast, female GNR23−/− mice were markedly subfertile, failing to produce normal litters, have estrous cycles, or ovulate. The failure of ovulation resulted from an inability of the few existing GnRH neurons to generate the LH surge. This was not the case, however, for the first cycle at puberty that appeared normal. Together, these observations demonstrate that 12% of the GnRH neuron population is sufficient for pulsatile gonadotropin secretion and puberty onset, whereas between 12 and 34% are required for cyclical control in adult female mice. This indicates that substantial redundancy exists within the GnRH neuronal population and suggests that the great majority of GnRH neurons must be dysfunctional before fertility is affected.

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12

Zhao, Longmei, Kerstin Reim, and David J. Miller. "Complexin-I-deficient sperm are subfertile due to a defect in zona pellucida penetration." REPRODUCTION 136, no. 3 (September 2008): 323–34. http://dx.doi.org/10.1530/rep-07-0569.

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Upon adhesion to the zona pellucida, sperm undergo regulated exocytosis of the acrosome. Although it is necessary for sperm to penetrate the zona pellucida and fertilize an egg, the acrosomal membrane fusion process is poorly understood. Complexins I and II are small, cytosolic proteins that bind to a complex of proteins termed the solubleN-ethylmaleimide-sensitive factor attachment protein receptor complex to regulate synaptic vesicle exocytosis. Complexin-II-deficient mice are fertile but the fertility of sperm from complexin-I-deficient male mice is unclear because the mice have ataxia and cannot mate. Here, we show that the genes encoding complexins I and II are expressed in primary spermatocytes and spermatids. Complexin proteins were found in/near the developing acrosome in spermatids and in or around the acrosome of mature sperm. Cell fractionation demonstrated that complexins I and II were predominantly found in the cytosolic fraction. Furthermore, sperm from complexin-I-deficient mice had normal morphology, number, and only small differences in motility, as assessed by computer-assisted semen analysis. Complexin-I-deficient sperm capacitated normally and bound to the zona pellucida. But when sperm from complexin-I-deficient mice were inseminated into females, a defect in fertility was observed, in concordance with previous data showing thatin vitrofertilization rate was also reduced. If the zona pellucida was removed prior toin vitrofertilization, fertility was normal, demonstrating that zona pellucida penetration was defective, a step requiring acrosomal exocytosis. Therefore, complexin-I-deficient sperm are subfertile due to faulty zona pellucida penetration.

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Yang, Jasmine J., Claudia S. Caligioni, Yee-Ming Chan, and Stephanie B. Seminara. "Uncovering Novel Reproductive Defects in Neurokinin B Receptor Null Mice: Closing the Gap Between Mice and Men." Endocrinology 153, no. 3 (March 1, 2012): 1498–508. http://dx.doi.org/10.1210/en.2011-1949.

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Patients bearing mutations in TAC3 and TACR3 (which encode neurokinin B and its receptor, respectively) have sexual infantilism and infertility due to GnRH deficiency. In contrast, Tacr3−/− mice have previously been reported to be fertile. Because of this apparent phenotypic discordance between mice and men bearing disabling mutations in Tacr3/TACR3, Tacr3 null mice were phenotyped with close attention to pubertal development, estrous cyclicity, and fertility. Tacr3−/− mice demonstrated normal timing of preputial separation and day of first estrus, markers of sexual maturation. However, at postnatal d 60, Tacr3−/− males had significantly smaller testes and lower FSH levels than their wild-type littermates. Tacr3−/− females had lower uterine weights and abnormal estrous cyclicity. Approximately half of Tacr3−/− females had no detectable corpora lutea on ovarian histology at postnatal d 60. Despite this apparent ovulatory defect, all Tacr3−/− females achieved fertility when mated. However, Tacr3−/− females were subfertile, having both reduced numbers of litters and pups per litter. The subfertility of these animals was not due to a primary ovarian defect, because they demonstrated a robust response to exogenous gonadotropins. Thus, although capable of fertility, Tacr3-deficient mice have central reproductive defects. The remarkable ability of acyclic female Tacr3 null mice to achieve fertility is reminiscent of the reversal of hypogonadotropic hypogonadism seen in a high proportion of human patients bearing mutations in TACR3. Tacr3 mice are a useful model to examine the mechanisms by which neurokinin B signaling modulates GnRH release.

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Maccarinelli, Federica, Maria Regoni, Fernando Carmona, Maura Poli, Esther G. Meyron-Holtz, and Paolo Arosio. "Mitochondrial ferritin deficiency reduces male fertility in mice." Reproduction, Fertility and Development 29, no. 10 (2017): 2005. http://dx.doi.org/10.1071/rd16348.

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Mitochondrial ferritin (FtMt) is a functional ferritin targeted to mitochondria that is highly expressed in the testis. To investigate the role of FtMt in the testis we set up a series of controlled matings between FtMt gene-deletion mice (FtMt–/–) with FtMt+/+ mice. We found that the number of newborns per litter and the fertility rate were strongly reduced for the FtMt–/– males, but not for the females, indicating that FtMt has an important role for male fertility. The morphology of the testis and of the spermatozoa of FtMt–/– mice was normal and we did not detect alterations in sperm parameters or in oxidative stress indices. In contrast, we observed that the cauda epididymides of FtMt–/– mice were significantly lighter and contained a lower number of spermatozoa compared with the controls. Also, the ATP content of FtMt–/– spermatozoa was found to be lower than that of FtMt+/+ spermatozoa. These data show that FtMt contributes to sperm epididymis maturation and to male fertility.

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15

Wood, H. M., U. J. Lee, D. Vurbic, E. Sabanegh, J. H. Ross, T. Li, and M. S. Damaser. "Sexual Development and Fertility of Loxl1-/- Male Mice." Journal of Andrology 30, no. 4 (February 5, 2009): 452–59. http://dx.doi.org/10.2164/jandrol.108.006122.

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Daigle,Jr., Harold J., Derek N. Cole, J. Andrew Carlson, William R. Lee, and Vincent L. Wilson. "Ethylene Dichloride Disruption of Fertility in Male Mice." Open Toxicology Journal 3, no. 1 (April 20, 2009): 39–46. http://dx.doi.org/10.2174/1874340400903010039.

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Hani, Toshio, Takanori Tachibe, Saburo Shingai, Nobuo Kamada, Otoya Ueda, and Kou-ichi Jishage. "Fertility of mice receiving vitrified adult mouse ovaries." Reproduction 131, no. 4 (April 2006): 681–87. http://dx.doi.org/10.1530/rep.1.01030.

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Cryopreservation of the ovaries is a useful technology for preservation of germ cells from experimental animals, because if the female founder is infertile or has mutated mitochondrial DNA, preservation of female germ cells is necessary. Although it is possible to cryopreserve immature mouse ovaries with a high degree of viability by vitrification with a mixture of several cryoprotectants, the viability of cryopreserved adult mouse ovaries is still unknown. Here, we investigated the viability of mouse ovaries at various ages after cryopreservation by vitrification techniques. Donor ovaries were collected from 10-day-, 4-week-, 10-week- and 7-month-old, female, nulliparous, green fluorescence protein (GFP)-transgenic mice and cryopreserved by vitrification. The vitrified-warmed ovaries were orthotopically transplanted to 4- or 10-week-old mice. GFP-positive pups were obtained in all experimental groups. In the 4-week-old recipients, the percentages of GFP-positive pups among the total pups from recipients transplanted with ovaries of 10-day-, 4-week-, 10-week- and 7-month-old donors were 44%, 9%, 12% and 4% respectively. In the 10-week-old recipients, the percentages of GFP-positive pups among the total pups from recipients transplanted with ovaries of 10-day-, 4-week-, 10-week- and 7-month-old donors were 36%, 16%, 2% and 9% respectively. Furthermore, GFP-positive pups also were obtained from recipients transplanted with ovaries of donors without normal estrous cyclicity. Our results indicate that cryopreservation of mouse ovaries by vitrification is a useful method for the preservation of female germ cells from mice of various ages.

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Umesaki, Naohiko, Satoshi Uda, Masami Kawabata, and Sachio Ogita. "Significance of peritoneal macrophages on fertility in mice." American Journal of Obstetrics and Gynecology 167, no. 1 (July 1992): 261–64. http://dx.doi.org/10.1016/s0002-9378(11)91671-8.

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19

deCatanzaro, Denys. "Duration of mating relates to fertility in mice." Physiology & Behavior 50, no. 2 (August 1991): 393–95. http://dx.doi.org/10.1016/0031-9384(91)90084-2.

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Le Naour, F. "Severely Reduced Female Fertility in CD9-Deficient Mice." Science 287, no. 5451 (January 14, 2000): 319–21. http://dx.doi.org/10.1126/science.287.5451.319.

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21

Kanatsu-Shinohara, M., H. Miki, K. Inoue, N. Ogonuki, S. Toyokuni, A. Ogura, and T. Shinohara. "Germline niche transplantation restores fertility in infertile mice." Human Reproduction 20, no. 9 (May 26, 2005): 2376–82. http://dx.doi.org/10.1093/humrep/dei096.

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22

Fan, Shutong, Yuhan Zhao, Zhiwei Pan, Zhiqin Gao, Zumu Liang, Zhifang Pan, and Weiguo Feng. "ZNF185-derived peptide induces fertility suppression in mice." Journal of Peptide Science 24, no. 10 (September 17, 2018): e3121. http://dx.doi.org/10.1002/psc.3121.

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Su, Weiheng, Ying Qiao, Fei Yi, Xingang Guan, Di Zhang, Shuzhi Zhang, Feng Hao, et al. "Increased female fertility in aquaporin 8-deficient mice." IUBMB Life 62, no. 11 (November 2010): 852–57. http://dx.doi.org/10.1002/iub.398.

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Schoeller, Erica L., Maggie Chi, Andrea Drury, Ashley Bertschinger, Prabagaran Esakky, and Kelle H. Moley. "Leptin Monotherapy Rescues Spermatogenesis in Male Akita Type 1 Diabetic Mice." Endocrinology 155, no. 8 (August 1, 2014): 2781–86. http://dx.doi.org/10.1210/en.2014-1119.

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Type 1 diabetes is associated with subfertility in humans. The current treatment for type 1 diabetes, insulin monotherapy, is suboptimal to fully stabilize glycemia, potentially leading to this subfertility. Recent work has demonstrated that treatment with the energy-regulating hormone leptin, alone or in combination with insulin, can more effectively control glycemia in mouse models of type 1 diabetes. Here, we sought to determine whether the fertility defects in a type 1 diabetic mouse model, the Akita mouse, can be rescued with leptin monotherapy in the absence of any exogenous insulin. Akita homozygous mice treated with leptin alone had a larger total body size, testes, and seminal vesicles than their untreated siblings. Leptin treatment prevented testicular degeneration and rescued sperm motility to wild-type levels. Furthermore, sperm obtained from leptin-treated mice could successfully fertilize ooctyes in vitro. Despite completely rescuing spermatogenesis, the critical reproductive hormones LH and testosterone were only modestly higher than in untreated mice, indicating that a minimum threshold of these hormones must be met to maintain spermatogenesis. Cumulatively, these findings implicate the importance of leptin in maintaining fertility and support the use of leptin therapy in the treatment of type 1 diabetes.

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Singireddy, Amritha V., Megan A. Inglis, Wieteke A. Zuure, Joon S. Kim, and Greg M. Anderson. "Neither Signal Transducer and Activator of Transcription 3 (STAT3) or STAT5 Signaling Pathways Are Required for Leptin's Effects on Fertility in Mice." Endocrinology 154, no. 7 (May 21, 2013): 2434–45. http://dx.doi.org/10.1210/en.2013-1109.

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Abstract The hormone leptin is critical for the regulation of energy balance and fertility. The long-form leptin receptor (LepR) regulates multiple intracellular signaling cascades, including the classic Janus kinase-signal transducer and activator of transcription (STAT) pathways. Previous studies have shown that deletion of STAT3 or the closely related STAT5 from the brain results in an obese phenotype, but their roles in fertility regulation are not clear. This study tested whether STAT3 and STAT5 pathways of leptin signaling are required for fertility, and whether absence of one pathway might be compensated for by the other in a redundant manner. A Cre-loxP approach was used to generate 3 models of male and female transgenic mice with LepR-specific deletion of STAT3, STAT5, or both STAT3 and STAT5. Body weight, puberty onset, estrous cyclicity, and fertility were measured in all knockout (KO) mice and their control littermates. Knocking out STAT3 or both STAT3 and 5 from LepR expressing cells, but not STAT5 alone, led to significant increase in body weight. All STAT3 and STAT5 single KO mice exhibited normal puberty onset and subsequent fertility compared to their control littermates. Surprisingly, all STAT3 and STAT5 double KO mice also exhibited normal puberty onset, estrous cyclicity, and fertility, although they had severely disrupted body weight regulation. These results suggest that, although STAT3 signaling is crucial for body weight regulation, neither STAT3 nor STAT5 is required for the regulation of fertility by leptin. It remains to be determined what other signaling molecules mediate this effect of leptin, and whether they interact in a redundant manner.

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Chen, Yinghong, Chao Liu, Yongliang Shang, Liying Wang, Wei Li, and Guoping Li. "Adam21 is dispensable for reproductive processes in mice." PeerJ 9 (September 23, 2021): e12210. http://dx.doi.org/10.7717/peerj.12210.

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Background As a group of membrane-anchored proteins, the proteins containing a disintegrin and metalloprotease domain (ADAMs) control many biological processes, especially for male fertility. Mouse Adam21 was previously found to be specifically expressed in the somatic cells and germ cells of testes, but its functional role during spermatogenesis and male reproductive processes is still unknown. Methods Adam21-null mice were created using the CRISPR/Cas9 system. Quantitative real-time PCR was used for analyzing of gene expression. Histological, cytological and immunofluorescence staining were performed to analyze the phenotypes of mouse testis and epididymis. Intracellular lipid droplets (LDs) were detected by Oil red O (ORO) staining and BODIPY staining. Fertility and sperm characteristics were also detected. Results Here, we successfully generated an Adam21 conventional knockout mouse model via CRISPR/Cas9 technology so that we can explore its potential role in male reproduction. We found that male mice lacking Adam21 have normal fertility without any detectable defects in spermatogenesis or sperm motility. Histological analysis of the seminiferous epithelium showed no obvious spermatogenesis difference between Adam21-null and wild-type mice. Cytological analysis revealed no detectable defects in meiotic progression, neither Sertoli cells nor Leydig cells displayed any defect compared with that of the control mice. All these results suggest that Adam21 might not be essential for male fertility in mice, and its potential function still needs further investigation.

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Burton, Kimberly A., and G. Stanley McKnight. "PKA, Germ Cells, and Fertility." Physiology 22, no. 1 (February 2007): 40–46. http://dx.doi.org/10.1152/physiol.00034.2006.

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Temporal and spatial regulation of PKA activity are essential for vigorous sperm motility and for the resumption of meiosis in oocytes, two events required for successful fertilization. Genetic mutations in mice that affect PKA signaling in germ cells lead to infertility and illustrate the importance of this pathway in mammalian reproduction.

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Jacob, Jens, Grant R. Singleton, and Lyn A. Hinds. "Fertility control of rodent pests." Wildlife Research 35, no. 6 (2008): 487. http://dx.doi.org/10.1071/wr07129.

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Ricefield rats (Rattus argentiventer) in south-east Asian rice fields and house mice (Mus domesticus) in Australian grain fields are major pest species. They cause damage before and after harvest and carry zoonotic diseases. For both species, management techniques have been pursued using the approach of immunocontraceptive vaccination. We review results from a series of enclosure and field studies conducted with these species to assess the effects of fertility control in small rodents. In the experiments, fertility control was simulated by tubal ligation, ovariectomy or progesterone treatment. A once-off sterilisation of 50–75% of enclosed founder females considerably reduced reproductive output of ricefield rat populations until the end of the reproductive period. In house mice, similar success was achieved when a sterility level of 67% of female founders and offspring was maintained. Repeated antifertility treatments are required because of the much longer breeding period of house mice versus ricefield rats. Comparing the results of enclosure trials with the outcome of simulation models suggests that partial compensation of treatment effects can occur through enhanced reproduction of the remaining fertile females and improved survival of juveniles. However, such compensatory effects as well as behavioural consequences of sterility in field populations are not likely to prevent the management effect at the population level. The challenge for effective fertility control of small rodents in the field is the wide-scale delivery of an antifertility treatment to founders at the beginning of the breeding season and to fertile immigrants that are recruited into the population, which otherwise contribute to the reproductive output at the population level. Future research efforts should focus on species-specific techniques and on agents that can be effectively delivered via bait.

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Xiao, Yuhang, Baojun Xu, Matteo Bordiga, Haiwei Li, Fabiano Travaglia, Shun Bai, Jiali Chen, and Weibin Bai. "Cyanidin-3-O-Glucoside Supplement Improves Sperm Quality and Spermatogenesis in a Mice Model of Ulcerative Colitis." Nutrients 14, no. 5 (February 25, 2022): 984. http://dx.doi.org/10.3390/nu14050984.

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Impaired fertility and low sperm quality are the global health problem with high attention. It has been noted that inflammation may impact fertility by affecting testicular spermatogenesis. Cyanidin-3-O-glucoside is a natural functional pigment with various health benefits. Nevertheless, studies on the mechanism by which C3G protects male reproduction in mice with ulcerative colitis remain scarce. The purpose of this study is to illustrate the potential mechanism of C3G for improving impaired fertility caused by colitis. A DSS-induced colitis model was applied to assess the effects of sperm quality with colitis and the health benefit role of C3G. Results indicated that C3G-treated mice exhibited higher body weight, longer colon length, less crypt damage and focal inflammation infiltration. Being consistent with that, low sperm count, low testis weight, high inflammation levels and abnormal thickness of seminiferous epithelium also observed in the DSS group were significantly recovered upon C3G treatment. These findings suggested that colitis has a close link to impaired fertility. Further analysis found that C3G could significantly suppress the inflammatory mediators in serum. Results conjointly indicated that C3G might improve the impaired fertility of mice with colitis by inhibiting inflammatory cytokines through the blood–testis barrier. C3G could be a promising daily supplement for ameliorating impaired fertility caused by colitis.

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Abbasi, Ferheen, Mayo Kodani, Chihiro Emori, Daiji Kiyozumi, Masashi Mori, Yoshitaka Fujihara, and Masahito Ikawa. "CRISPR/Cas9-Mediated Genome Editing Reveals Oosp Family Genes are Dispensable for Female Fertility in Mice." Cells 9, no. 4 (March 28, 2020): 821. http://dx.doi.org/10.3390/cells9040821.

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There are over 200 genes that are predicted to be solely expressed in the oocyte and ovary, and thousands more that have expression patterns in the female reproductive tract. Unfortunately, many of their physiological functions, such as their roles in oogenesis or fertilization, have yet to be elucidated. Previous knockout (KO) mice studies have proven that many of the genes that were once thought to be essential for fertility are dispensable in vivo. Therefore, it is extremely important to confirm the roles of all genes before spending immense time studying them in vitro. To do this, our laboratory analyzes the functions of ovary and oocyte-enriched genes in vivo through generating CRISPR/Cas9 KO mice and examining their fertility. In this study, we have knocked out three Oosp family genes (Oosp1, Oosp2, and Oosp3) that have expression patterns linked to the female reproductive system and found that the triple KO (TKO) mutant mice generated exhibited decreased prolificacy but were not infertile; thus, these genes may potentially be dispensable for fertility. We also generated Cd160 and Egfl6 KO mice and found these genes are individually dispensable for female fertility. KO mice with no phenotypic data are seldom published, but we believe that this information must be shared to prevent unnecessary experimentation by other laboratories.

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Guo, Tao, Liang Zhang, Dong Cheng, Tao Liu, Liguo An, Wei-Ping Li, and Cong Zhang. "Low-density lipoprotein receptor affects the fertility of female mice." Reproduction, Fertility and Development 27, no. 8 (2015): 1222. http://dx.doi.org/10.1071/rd13436.

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Low-density lipoprotein receptor (LDLR) has been demonstrated to play a central role in lipoprotein metabolism, with Ldlr-deficient (Ldlr–/–) mice developing severe dyslipidemia. In the present study we investigated whether Ldlr knockout could harm female reproduction and explored the mechanisms involved. The results indicate that although the number of litters born to Ldlr–/– mice did not differ significantly from that born to controls, the number of pups per litter was significantly lower in the former group. Interestingly, although Ldlr–/– mice were obese, the weight of their ovaries was lower than that in control mice. Serum cholesterol levels was significantly higher in Ldlr–/– mice than in their wild-type counterparts. In contrast, there were significant decreases in cholesterol, triglyceride and total lipid levels in ovaries of Ldlr–/– mice. Both ovarian lipid deposition, as detected by Oil red O staining, and lipid droplets, as evaluated by transmission electron microscopy, supported decreased lipid levels in ovaries from Ldlr–/– mice. In addition, Ldlr–/– mice had fewer ovarian follicles, more atretic follicles, lower oestrogen levels and spent significantly less time in oestrus than did the controls. Superovulation assays indicated immature Ldlr–/– mice ovulated fewer ova than controls. These results indicate that lack of Ldlr results in dyslipidaemia and poor fertility.

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Rodrigo, Natassia, Hui Chen, Carol A. Pollock, and Sarah J. Glastras. "Preconception weight loss improves fertility and maternal outcomes in obese mice." Journal of Endocrinology 253, no. 1 (April 1, 2022): 27–38. http://dx.doi.org/10.1530/joe-21-0399.

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Women with obesity have higher incidences of infertility, with longer time to conception and increased risk of pregnancy complications compared to women with normal body weight. There is a lack of evidence demonstrating the benefit of preconception maternal weight loss on fertility and pregnancy outcomes. We aimed to determine if preconception weight loss, either with diet modification or glucose-like peptide 1 receptor agonist liraglutide, improves maternal weight, fertility, and pregnancy outcomes. C57BL/6 female mice were fed either a high-fat diet (HFD) or chow for 8 weeks. HFD-fed dams were administered liraglutide (0.3 mg/kg, s.c., for 4 weeks) or switched to chow to induce weight loss. Prior to mating, liraglutide was ceased and mice continued on HFD. Mice in the ‘diet switch’ group continued on chow. Pregnancy rates were recorded. Maternal anthropometry and glucose tolerance were measured before and after the intervention and at late gestation. Offspring outcomes were assessed. Liraglutide or diet switch led to weight reduction, improved insulin resistance (P< 0.001), and enhanced fertility, particularly in the liraglutide group (P< 0.005). Liraglutide-treated mice had significantly higher gestational weight gain (GWG) compared to the diet switch group (P< 0.05), with similar weight and glucose tolerance in late gestation to HFD mice. In contrast, diet switch maintained similar weight and glucose tolerance in late gestation to control mice. Pre-pregnancy weight intervention with liraglutide was effective at restoring fertility. Diet modification also improved fertility and avoided catch up weight gain in pregnancy. Liraglutide may be a therapeutic strategy for weight loss to prepare for pregnancy. However, our study provides caution about the potential for excessive GWG without diet intervention in pregnancy.

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Navarro-Pando, José M., Elísabet Alcocer-Gómez, Beatriz Castejón-Vega, Elena Navarro-Villarán, Mónica Condés-Hervás, María Mundi-Roldan, Jordi Muntané, et al. "Inhibition of the NLRP3 inflammasome prevents ovarian aging." Science Advances 7, no. 1 (January 2021): eabc7409. http://dx.doi.org/10.1126/sciadv.abc7409.

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Inflammation is a hallmark of aging and is negatively affecting female fertility. In this study, we evaluate the role of the NLRP3 inflammasome in ovarian aging and female fertility. Age-dependent increased expression of NLRP3 in the ovary was observed in WT mice during reproductive aging. High expression of NLRP3, caspase-1, and IL-1β was also observed in granulosa cells from patients with ovarian insufficiency. Ablation of NLRP3 improved the survival and pregnancy rates and increased anti-Müllerian hormone levels and autophagy rates in ovaries. Deficiency of NLRP3 also reduced serum FSH and estradiol levels. Consistent with these results, pharmacological inhibition of NLRP3 using a direct NLRP3 inhibitor, MCC950, improved fertility in female mice to levels comparable to those of Nlrp3−/− mice. These results suggest that the NLRP3 inflammasome is implicated in the age-dependent loss of female fertility and position this inflammasome as a potential new therapeutic target for the treatment of infertility.

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Sitasiwi, Agung Janika, Sri Isdadiyanto, and Siti Muflichatun Mardiati. "Pelacakan eskpresi protein pada testis mencit (Mus musculus) setelah paparan esktrak etanol daun mimba (Azadirachta indica)." Jurnal Sain Veteriner 37, no. 1 (August 5, 2019): 90. http://dx.doi.org/10.22146/jsv.43027.

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Abstract Azadirachta indica (Neem) has been shown to affect the fertility of mice by interfering with the synthesis of testosterone in mice. The aim of this study was to detect the testes protein expression of mice after exposure to the ethanolic Neem leaf extract. The laboratory animals of this study were 20 male Swiss Webster mice with three months in age and body weight ranging from 27.5 grams. The mice were divided into two treatment groups, namely K (control group, exposed with distilled water) and P (treatment group, exposed to etahnolic Neem leaf extract with 14 mg/animal /day). The treated were given for 21 days and the testicular protein was carried out on the 22nd day. The variables observed were testes weight, concentration and expression of proteins isolated from the testes. The protein concentration is determined by a spectrophotometer at a wavelength of 450nm. The protein expression was observed and determined based on the results of protein electrophoresis (SDS-PAGE). The results showed that protein expression in the treatment group has a lower concentration compared to the control group. Those results was confirmed by thinner bands in SDS-PAGE result. Those proteins thought to be a fertility determinant in mammals. Keywords : anti-fertility; Neem; protein expression Abstrak Azadirachta indica (Mimba) telah terbukti mempengaruhi fertilitas mencit dengan cara mengganggu sintesis hormon testoteron pada mencit. Penelitian ini bertujuan untuk melacak ekspresi protein pada testis mencit setelah paparan ekstrak etanol daun Mimba. Hewan uji penelitian ini adalah 20 ekor mencit Swiss Webster jantan dengan umur tiga bulan dan bobot badan berkisar 27.5 gram. Hewan uji dibagi menjadi 2 kelompok perlakuan, yaitu K (kelompok kontrol, dipapar akuades) dan P (kelompok perlakuan, dipapar dengan ekstrak etanol daun Mimba dengan dosis 14 mg/ekor/hari). Pemberian bahan uji dilakukan secara oral selama 21 hari. Variabel yang diamati adalah bobot testes, konsentrasi serta eskpresi protein yang diisolasi dari testis. Isolasi protein testis dilakukan pada hari ke-22. Konsentrasi protein ditentukan dengan spectrofotometer pada panjang gelombang 450nm. Ekspresi protein diamati dan ditentukan berdasar hasil elektroforesa protein. Hasil penelitian menunjukkan bahwa ekspresi protein pada kelompok perlakuan menunjukkan konsentrasi yang lebih rendah dengan pita yang lebih tipis jika dibandingkan dengan kelompok kontrol. Kesimpulan penelitian ini adalah paparan ekstrak etanol daun Nimba menyebabkan gangguan ekspresi protein yang diduga berperan dalam menentukan fertilitas mamalia. Kata kunci : Mimba; anti-fertilitas; eskpresi protein;

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Wang, Yi-Bo, Chen-Yang Zhai, Guan-Ping Yao, Ting-Bao Chen, Lu-Lu Xue, Lin Zhou, Liu-Lin Xiong, and Ting-Hua Wang. "ATP5D Is a Potential Biomarker for Male Fertility." Oxidative Medicine and Cellular Longevity 2023 (January 11, 2023): 1–13. http://dx.doi.org/10.1155/2023/4923614.

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Background. Infertility is a global medical and social problem that affects human health and social development. At present, about 15% of couples of the right age in the world are infertile. As all we know, genetic defects are the most likely underlying cause of the pathology. ATP5D is also known as the delta subunit of mitochondrial ATP synthase. Mitochondria maintain sperm vitality, capacitation, acrosome reaction, and DNA integrity through ATP. Mitochondrial damage can trigger energy synthesis disorders, resulting in decreased sperm quality and function or even disappearance. The specific role of ATP5D in regulation of the male reproductive system remains elusive. Methods. In this study, semen from normal and infertile males were collected and their indicators were examined by analysis of routine sperm parameters; ATP5D protein content in semen was examined by ELISA. Singer sequencing was used to detect whether there was a mutated of ATP5D in semen. Meanwhile, ATP5D knockout (KO) and knockin (KI) male mice were selected at 8-12 weeks of age and mated with adult wild-type (WT) female mice for more than two months to assess their fertility and reproductive ability. Morphological changes in tissues such as testes and epididymis were observed by HE staining; spermatozoa were taken from the epididymis of the mice; sperm counts were performed and morphological changes were observed by Diff-Quik staining. Results. The results showed that the expression of ATP5D in infertile males was significantly lower than that in normal males ( P < 0.001 ) and the normal morphology rate of spermatozoa was much lower than that of normal males, and the sequencing results showed no mutations. The animal reproductive experiments showed no significant changes in the number of fertility in KO/KI mice compared with WT mice, but the duration of fertility was significantly longer ( P = 0.02 ). The testicular cells in KO mice were loosely arranged and disorganized, the lumen was larger, the interstitial cells were atrophied, and the number of spermatozoa was reduced and the malformation rate was higher in WT males. This suggests that ATP5D is an essential protein for sperm formation and fertility in male mice and may be used as a biomarker of male fertility. Conclusion. This study found ATP5D correlated with male infertility and the expression levels were significantly reduced in the seminal plasma of all male infertile patients without gene mutations. KO male significantly prolonged fertility time and impaired testicular histomorphology. This suggests that ATP5D may be associated with spermatogenic function and fertility in male mice and may be used as a biomarker for male fertility. Future studies are required to elucidate the potential mechanisms. The trial registration number is KLL-2021-266.

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Kobayashi, Kiyonori, Tsutomu Endo, Takafumi Matsumura, Yonggang Lu, Zhifeng Yu, Martin M. Matzuk, and Masahito Ikawa. "Prss55 but not Prss51 is required for male fertility in mice†." Biology of Reproduction 103, no. 2 (April 17, 2020): 223–34. http://dx.doi.org/10.1093/biolre/ioaa041.

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Abstract Mammalian spermatozoa are produced in the testis through spermatogenesis and matured in the epididymis to acquire fertilizing ability. Spermatozoa are ejaculated and migrate from the uterus to the oviducts to fuse with oocytes. Although over 2000 genes are expressed abundantly in mouse testes, the genes responsible for male fertility are not yet fully clarified. Here, we focused on two testis-enriched serine protease genes, Serine protease (Prss) 51 and Prss55, which overlap their gene loci partially in both mice and humans. To characterize their functions in male fertility, we first generated Prss51 and Prss55 double knockout (DKO) mice by CRISPR/Cas9 system and found that the DKO mice were sterile. DKO spermatozoa exhibit impaired migration from the uterus to the oviduct and impaired ability to bind the zona pellucida (ZP) of oocytes. Moreover, a sperm membrane protein, ADAM3 (a disintegrin and metalloprotease 3), which plays a role in sperm migration through uterotubal junction (UTJ) and sperm–ZP binding, disappeared in the DKO spermatozoa from the epididymis. We next generated single knockout (KO) mice lacking Prss51 and found that Prss51 KO mice are fertile. We also generated single KO mice lacking Prss55 and found that Prss55 KO mice phenocopy the DKO mice, demonstrating impaired sperm migration and sperm–ZP binding and a severe defect in fertility. We conclude that Prss55, but not Prss51, is required for male fertility in mice, by stabilizing ADAM3 protein for efficient sperm–UTJ migration and sperm–ZP binding. Our findings have implications for understanding additional genetic causes of the idiopathic male infertility and for the development of male or female contraceptives.

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Kanellopoulos, Dimitrios, Dimitra Karagianni, Vasilios Pergialiotis, Nikolaos Nikiteas, Andreas C. Lazaris, and Dimitrios Iliopoulos. "The effect of endometriosis on fertility in an animal model." Journal of Medicine and Life 15, no. 9 (September 2022): 1170–75. http://dx.doi.org/10.25122/jml-2021-0391.

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The present experimental model aimed to investigate the possible effect of endometriosis on ovarian function by altering follicular maturation and development. This single-blind, randomized study included twenty-four female Sprague Dawley mice, 2.5 months old, weighing 160–200 grams. The animals were randomly separated into four groups on the day of the surgery. Each group consisted of 6 mice. The first group (A) consisted of healthy female mice (control group). The second group (B) consisted of mice subjected to surgical insertion of ovarian endometrioma. The third group (C) consisted of mice subjected to surgically induced diffuse intraperitoneal endometriosis, and the fourth group (D) consisted of mice subjected to surgically induced extraperitoneal endometriosis. According to our experimental model, endometriosis may affect ovarian function by increasing the number of luteinized unruptured follicles (follicles that have undergone luteinization without prior rupture).

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Krajnc-Franken, Magda A. M., Ad J. M. van Disseldorp, Jasper E. Koenders, Sietse Mosselman, Marcel van Duin, and Jan A. Gossen. "Impaired Nipple Development and Parturition in LGR7 Knockout Mice." Molecular and Cellular Biology 24, no. 2 (January 15, 2004): 687–96. http://dx.doi.org/10.1128/mcb.24.2.687-696.2004.

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ABSTRACT LGR7 is a G-protein coupled receptor with structural homology to the gonadotrophin and thyrotrophin receptors. Recently, LGR7 was deorphanized, and it was shown that relaxin is the ligand for LGR7. To further study the function of this receptor, mice deficient for LGR7 were generated by replacing part of the transmembrane-encoding region with a LacZ reporter cassette. Here we show that LGR7 is expressed in various tissues, including the uterus, heart, brain, and testis. Fertility studies using female LGR7−/− mice showed normal fertility and litter size. However, some females were incapable of delivering their pups, and several pups were found dead. Moreover, all offspring died within 24 to 48 h after delivery because female LGR7−/− mice were unable to feed their offspring due to impaired nipple development. In some male LGR7−/− mice, spermatogenesis was impaired, leading to azoospermia and a reduction in fertility. Interestingly, these phenomena were absent in mutant mice at older ages or in later generations. Taken together, results from LGR7 knockout mice indicate an essential role for the LGR7 receptor in nipple development during pregnancy. Moreover, a defect in parturition was observed, suggesting a role for LGR7 in the process of cervical ripening.

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Al-Hamood, M. H., A. Elbetieha, and H. Bataineh. "Sexual maturation and fertility of male and female mice exposed prenatally and postnatally to trivalent and hexavalent chromium compounds." Reproduction, Fertility and Development 10, no. 2 (1998): 179. http://dx.doi.org/10.1071/r97001.

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The reproductive toxicity of trivalent and hexavalent chromium compounds was investigated in male and female mice exposed to 1000 ppm chromium chloride and potassium dichromate via their mother during gestational and lactational periods. Fertility was reduced in male offspring exposed to either trivalent or hexavalent chromium compounds. Body weights and weights of testes, seminal vesicles and preputial glands were reduced in trivalent-exposed male offspring. The exposure of female mice offspring to trivalent and hexavalent chromium compounds delayed sexual maturation. Fertility was reduced in female offspring exposed to either trivalent or hexavalent chromium compounds. The exposure of female mice to hexavalent chromium compound reduced the number of implantations and viable fetuses respectively. Body weight and weights of ovaries and uteri were reduced in trivalent-exposed female offspring. The results indicate that under our experimental conditions, the exposure of male and female mice offspring to either trivalent or hexavalent chromium compounds during gestational and lactational periods impair reproductive functions and fertility in adulthood.

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Wang, Tao, Binbin Cao, Yao Cai, Si Chen, Baozhu Wang, Yan Yuan, and Quan Zhang. "Plcz1 Deficiency Decreased Fertility in Male Mice Which Is Associated with Sperm Quality Decline and Abnormal Cytoskeleton in Epididymis." International Journal of Molecular Sciences 24, no. 1 (December 24, 2022): 314. http://dx.doi.org/10.3390/ijms24010314.

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Phospholipase C zeta1 (Plcz1) was known to be a physiological factor in sperm that activates oocytes to complete meiosis by triggering Ca2+ oscillations after fertilisation. However, the role of male Plcz1 in spermatogenesis and early embryo development in progeny has been controversial. Plcz1 knockout (Plcz1−/−) mouse model (Plcz1m3 and Plcz1m5) was generated by using the CRISPR-Cas9 system. The fertility of Plcz1−/− mice was evaluated by analysing the number of offsprings, sperm quality, pathological changes in the testis and epididymis. RNA-seq and RT-PCR were performed to screen differentially expressed genes and signalling pathways related to fertility in Plcz1−/− mice. Further mechanism was explored by using Plcz1−/− cells. Plcz1 knockout led to hypofertility in male mice. In particular, a significant time delay in development and polyspermy was found in eggs fertilized by both Plcz1m3 and Plcz1m5 sperm. Interestingly, a decline in sperm quality combined with pathological changes in epididymis was found in Plcz1m3 mice but not in Plcz1m5 mice. Notably, abnormal cytoskeleton appears in epididymis of Plcz1m3 mice and Plcz1−/− cells. Cytoskeleton damage of epididymis is involved in fertility decline of males upon Plcz1 deficiency in this model.

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Tsutsumi, O., Y. Taketani, and T. Oka. "The uterine growth-promoting action of epidermal growth factor and its function in the fertility of mice." Journal of Endocrinology 138, no. 3 (September 1993): 437—NP. http://dx.doi.org/10.1677/joe.0.1380437.

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ABSTRACT Epidermal growth factor (EGF) levels in the submandibular glands and plasma are increased in pregnant and aged female mice. The possible role of EGF in fertility was studied in virgin and pregnant mice ranging in age from 10 to 90 weeks of age, employing sialoadenectomy, administration of EGF antibody and EGF replacement. The uterine weight in pregnant, 10-week-old, sialoadenectomized mice was significantly less than in normal mice and the administration of EGF antibody to these mice further decreased uterine weight, resulting in an increased rate of abortion. Replacement EGF treatment in the sialoadenectomized mice prevented these changes. Uterine weight was about 70 mg at 10 weeks of age, and significantly increased from 30 to 80 weeks when it reached a plateau level of 275 mg. These changes closely followed the increase in the concentration of EGF in the submandibular glands and plasma and coincided with the decline in fertility. In contrast, uterine weight in the sialoadenectomized mice decreased immediately after the operation and remained at about 50–60 mg throughout the experimental period. Pregnancy, as judged by implantation, was achieved in the sialoadenectomized mice at later ages than in the controls. These findings suggest that elevated EGF levels may have a dual function in the control of fertility via uterine growth, depending on the age of mice. Journal of Endocrinology (1993) 138, 437–443

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Sato, Ban, Seiya Kanai, Daiki Sakaguchi, Kodai Yajima, Yu Matsumoto, Kazunori Morohoshi, Shinji Kagaya, et al. "Suppressive Role of Lactoferrin in Overweight-Related Female Fertility Problems." Nutrients 14, no. 5 (February 22, 2022): 938. http://dx.doi.org/10.3390/nu14050938.

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The secretory glycoprotein lactoferrin (LF) is suggested to ameliorate overweight regardless of non-genetic or genetic mechanisms. Although maternal overweight represents a key predictor of offspring growth, the efficacy of LF on fertility problems in overweight and obese mothers remains unknown. To address this issue, we examined the effect of LF ingestion by analyzing overweight mice (Institute of Cancer Research (ICR) mice with high-fat diets; HF mice) and obese mice (leptin-deficient mice with type II diabetes; ob/ob mice). Plasma insulin, leptin, glucose, and cholesterol levels were measured, and thermal imaging and histological analysis were employed. The litter size of HF females was reduced due to miscarriage, which was reversed by LF ingestion. In addition, LF ingestion suppressed overweight prevalence in their offspring. The component analysis of the maternal blood demonstrated that glucose concentration in both HF females and their offspring was normalized by LF ingestion, which further standardized the concentration of insulin, but not leptin. LF ingestion was unable to reverse female infertility in ob/ob mice, although their obesity and uterine function were partially improved. Our results indicate that LF upregulates female fertility by reinforcing ovarian and uterine functions in females that are overweight due to caloric surplus.

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Powers, Natalie R., Beth L. Dumont, Chihiro Emori, Raman Akinyanju Lawal, Catherine Brunton, Kenneth Paigen, Mary Ann Handel, Ewelina Bolcun-Filas, Petko M. Petkov, and Tanmoy Bhattacharyya. "Sexual dimorphism in the meiotic requirement for PRDM9: A mammalian evolutionary safeguard." Science Advances 6, no. 43 (October 2020): eabb6606. http://dx.doi.org/10.1126/sciadv.abb6606.

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In many mammals, genomic sites for recombination are determined by the histone methyltransferase PRMD9. Some mouse strains lacking PRDM9 are infertile, but instances of fertility or semifertility in the absence of PRDM9 have been reported in mice, canines, and a human female. Such findings raise the question of how the loss of PRDM9 is circumvented to maintain fertility. We show that genetic background and sex-specific modifiers can obviate the requirement for PRDM9 in mice. Specifically, the meiotic DNA damage checkpoint protein CHK2 acts as a modifier allowing female-specific fertility in the absence of PRDM9. We also report that, in the absence of PRDM9, a PRDM9-independent recombination system is compatible with female meiosis and fertility, suggesting sex-specific regulation of meiotic recombination, a finding with implications for speciation.

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Feng, Tianhao, Shushu Zhou, Xiaodan Shi, Xin Zhang, Jintao Zhang, Shuqin Zhao, Xiaoyu Yang, Xuhui Meng, and Mingxi Liu. "Eef2k is not required for fertility in male mice." Translational Andrology and Urology 10, no. 5 (May 2021): 1988–99. http://dx.doi.org/10.21037/tau-21-18.

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Wang, ZhiXin, Zi Teng, ZeLin Wang, Zhan Song, Peng Zhu, Ning Li, YuSheng Zhang, XueXia Liu, and FuJun Liu. "Melatonin ameliorates paclitaxel‐induced mice spermatogenesis and fertility defects." Journal of Cellular and Molecular Medicine 26, no. 4 (January 9, 2022): 1219–28. http://dx.doi.org/10.1111/jcmm.17177.

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Zudova, Dagmar, Andrew J. Wyrobek, Jack Bishop, and Francesco Marchetti. "Impaired fertility in T-stock female mice after superovulation." Reproduction 128, no. 5 (November 2004): 573–81. http://dx.doi.org/10.1530/rep.1.00333.

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Superovulation of female mice with exogenous gonadotrophins is routinely used for increasing the number of eggs ovulated by each female in reproductive and developmental studies. We report an unusual effect of superovulation on fertilization in mice.In vivomatings of superovulated T-stock females with B6C3F1 males resulted in a two-fold reduction (P< 0.001) in the frequencies of fertilized eggs compared with control B6C3F1 matings. In addition, approximately 22 h after mating, only 15% of fertilized eggs recovered in T-stock females had reached the metaphase stage of the first cleavage division versus 87% in B6C3F1 females (P< 0.0001). Matings with T-stock males did not improve the reproductive performance of T-stock females. To investigate the possible cause(s) for the impaired fertilization and zygotic development, the experiments were repeated usingin vitrofertilization. Under these conditions, the frequencies of fertilized eggs were not different in superovulated T-stock and B6C3F1 females (51.7 ± 6.0 and 64.5 ± 3.8%,P= 0.10). There was a seven-fold increase in the frequencies of fertilized eggs that completed the first cell cycle of development afterin vitroversusin vivofertilization in T-stock females. These results rule out an intrinsic deficiency of the T-stock oocyte as the main reason for the impaired fertility afterin vivomatings, and suggest that superovulation of T-stock females may induce a hostile oviductal and uterine environment with dramatic effects on fertilization and zygotic development.

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Thomas, A. "Growth hormone and fertility in oMt1a-oGH transgenic mice." Reproduction 122, no. 4 (October 1, 2001): 537–44. http://dx.doi.org/10.1530/reprod/122.4.537.

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Song, Ning, Fei Sun, Yu-Bing Dai, and Yu Lin. "LncRNA4667 is dispensable for spermatogenesis and fertility in mice." Reproductive and Developmental Medicine 3, no. 1 (2019): 18. http://dx.doi.org/10.4103/2096-2924.255985.

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Suzuki, Taichi A., and Michael W. Nachman. "Speciation and reduced hybrid female fertility in house mice." Evolution 69, no. 9 (September 2015): 2468–81. http://dx.doi.org/10.1111/evo.12747.

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Sainsbury, A. "Y4 receptor knockout rescues fertility in ob/ob mice." Genes & Development 16, no. 9 (May 1, 2002): 1077–88. http://dx.doi.org/10.1101/gad.979102.

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Journal articles on the topic 'Mice Fertility'

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