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We are analyzing https://link.springer.com/article/10.1007/s43032-019-00098-1.

Title:
Declining BRCA-Mediated DNA Repair in Sperm Aging and its Prevention by Sphingosine-1-Phosphate | Reproductive Sciences
Description:
Abstract Recent data suggest that paternal age can have major impact on reproductive outcomes, and with increased age, there is increased likelihood of chromosomal abnormalities in the sperm. Here, we studied DNA damage and repair as a function of male aging and assessed whether sphingosine-1-phosphate (S1P), a ceramide-induced death inhibitor, can prevent sperm aging by enhancing DNA double-strand breaks (DSB) repair. We observed a significant increase in DNA damage with age and this increase was associated with a decline in the expression of key DNA DSB repair genes in mouse sperm. The haploinsufficiency of BRCA1 male mice sperm showed significantly increased DNA damage and apoptosis, along with decreased chromatin integrity when compared to similar age wild type (WT) mice. Furthermore, haploinsufficiency of BRCA1 male mice had lower sperm count and smaller litter size when crossed with WT females. The resulting embryos had a higher probability of growth arrest and reduced implantation. S1P treatment decreased genotoxic-stress-induced DNA damage in sperm and enhanced the expressions of key DNA repair genes such as BRCA1. Co-treatment with an ATM inhibitor reversed the effects of S1P, implying that the impact of S1P on DNA repair is via the ATM-mediated pathway. Our findings indicate a key role for DNA damage repair mechanism in the maintenance of sperm integrity and suggest that S1P can improve DNA repair in sperm. Further translational studies are warranted to determine the clinical significance of these findings and whether S1P can delay male reproductive aging. Summary There is mounting evidence that sperm quality declines with age, similar to that of the oocyte. However, the reasons behind this decline are poorly understood and there is no medical intervention to improve sperm quality. Our study suggests a strong role for DNA damage repair in maintenance of sperm quality, and for the first time, a potential pharmaceutical approach to prevent sperm aging
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
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Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {πŸ’Έ}

The income method remains a mystery to us.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {πŸ”}

pubmed, article, google, scholar, dna, cas, sperm, damage, repair, central, aging, age, human, reprod, brca, oktay, male, breaks, darzynkiewicz, hum, cells, reproductive, sphingosinephosphate, titus, paternal, doublestrand, ovarian, fragmentation, privacy, cookies, content, analysis, stobezki, halicka, mice, access, res, fertil, steril, cell, function, data, publish, research, search, increased, mouse, apoptosis, effects, quality,

Topics {βœ’οΈ}

month download article/chapter activation-dependent dna-reactive carcinogens dna double-strand breaks ceramide-induced death inhibitor dna damage repair dna strand breaks tumor necrosis factor-alpha breast/ovarian cancer risks sperm dna damage zona-free hamster oocytes studied dna damage improve dna repair murine brca1 gene full article pdf consistent age-dependent declines sperm dna fragmentation dna fragmentation extent acid sphingomyelinase gene privacy choices/manage cookies atm-mediated pathway decreased chromatin integrity williams gm dna damage constitutive oxidative damage sphingosine-1-phosphate therapy dna repair assisted reproductive outcome brca1 male mice matrix metalloproteinase-2 expression brca germline mutations abnormal sperm function sperm quality declines human sperm cells brca1/2 mutation carriers premature ovarian aging lower sperm count sperm progressive motility prevent sperm aging atm inhibitor reversed improve sperm quality dna fragmentation male biological clock european economic area smaller litter size potential pharmaceutical approach gamma-irradiation hypersensitivity tk6 lymphoblastoid cells fluorochrome-labeled inhibitors unexplained recurrent miscarriage van der heijden

Questions {❓}

  • Premature ovarian aging in BRCA carriers: a prototype of systemic precocious aging?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Declining BRCA-Mediated DNA Repair in Sperm Aging and its Prevention by Sphingosine-1-Phosphate
         description:Recent data suggest that paternal age can have major impact on reproductive outcomes, and with increased age, there is increased likelihood of chromosomal abnormalities in the sperm. Here, we studied DNA damage and repair as a function of male aging and assessed whether sphingosine-1-phosphate (S1P), a ceramide-induced death inhibitor, can prevent sperm aging by enhancing DNA double-strand breaks (DSB) repair. We observed a significant increase in DNA damage with age and this increase was associated with a decline in the expression of key DNA DSB repair genes in mouse sperm. The haploinsufficiency of BRCA1 male mice sperm showed significantly increased DNA damage and apoptosis, along with decreased chromatin integrity when compared to similar age wild type (WT) mice. Furthermore, haploinsufficiency of BRCA1 male mice had lower sperm count and smaller litter size when crossed with WT females. The resulting embryos had a higher probability of growth arrest and reduced implantation. S1P treatment decreased genotoxic-stress-induced DNA damage in sperm and enhanced the expressions of key DNA repair genes such as BRCA1. Co-treatment with an ATM inhibitor reversed the effects of S1P, implying that the impact of S1P on DNA repair is via the ATM-mediated pathway. Our findings indicate a key role for DNA damage repair mechanism in the maintenance of sperm integrity and suggest that S1P can improve DNA repair in sperm. Further translational studies are warranted to determine the clinical significance of these findings and whether S1P can delay male reproductive aging. There is mounting evidence that sperm quality declines with age, similar to that of the oocyte. However, the reasons behind this decline are poorly understood and there is no medical intervention to improve sperm quality. Our study suggests a strong role for DNA damage repair in maintenance of sperm quality, and for the first time, a potential pharmaceutical approach to prevent sperm aging
         datePublished:2020-01-08T00:00:00Z
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            Embryology
            Obstetrics/Perinatology/Midwifery
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      headline:Declining BRCA-Mediated DNA Repair in Sperm Aging and its Prevention by Sphingosine-1-Phosphate
      description:Recent data suggest that paternal age can have major impact on reproductive outcomes, and with increased age, there is increased likelihood of chromosomal abnormalities in the sperm. Here, we studied DNA damage and repair as a function of male aging and assessed whether sphingosine-1-phosphate (S1P), a ceramide-induced death inhibitor, can prevent sperm aging by enhancing DNA double-strand breaks (DSB) repair. We observed a significant increase in DNA damage with age and this increase was associated with a decline in the expression of key DNA DSB repair genes in mouse sperm. The haploinsufficiency of BRCA1 male mice sperm showed significantly increased DNA damage and apoptosis, along with decreased chromatin integrity when compared to similar age wild type (WT) mice. Furthermore, haploinsufficiency of BRCA1 male mice had lower sperm count and smaller litter size when crossed with WT females. The resulting embryos had a higher probability of growth arrest and reduced implantation. S1P treatment decreased genotoxic-stress-induced DNA damage in sperm and enhanced the expressions of key DNA repair genes such as BRCA1. Co-treatment with an ATM inhibitor reversed the effects of S1P, implying that the impact of S1P on DNA repair is via the ATM-mediated pathway. Our findings indicate a key role for DNA damage repair mechanism in the maintenance of sperm integrity and suggest that S1P can improve DNA repair in sperm. Further translational studies are warranted to determine the clinical significance of these findings and whether S1P can delay male reproductive aging. There is mounting evidence that sperm quality declines with age, similar to that of the oocyte. However, the reasons behind this decline are poorly understood and there is no medical intervention to improve sperm quality. Our study suggests a strong role for DNA damage repair in maintenance of sperm quality, and for the first time, a potential pharmaceutical approach to prevent sperm aging
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         Gene expression
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         DNA fragmentation
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         Embryology
         Obstetrics/Perinatology/Midwifery
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            name:Zbigniew Darzynkiewicz
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                  name:Yale University School of Medicine
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                     name:Department of Obstetrics and Gynecology, Laboratory of Molecular Reproduction and Fertility Preservation, Yale University School of Medicine, New Haven, USA
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            address:
               name:Department of Obstetrics and Gynecology, Laboratory of Molecular Reproduction and Fertility Preservation, Yale University School of Medicine, New Haven, USA
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      name:Zbigniew Darzynkiewicz
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               name:Department of Pathology and Brander Cancer Research Institute, New York Medical College, Valhalla, USA
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      name:Kutluk Oktay
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