GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    In: Andrology, Wiley, Vol. 8, No. 3 ( 2020-05), p. 602-609
    Abstract: Spermatogenesis‐associated (SPATA) family of genes plays important roles in spermatogenesis, sperm maturation or fertilization. The knockout studies in mice have demonstrated that SPATA genes are crucial for fertility. Gene expression and genetic polymorphism studies have further suggested their correlation with infertility; however, methylation analysis of SPATA genes in human male infertility has not yet been undertaken. Objectives To analyze the methylation status of SPATA4, SPATA5 and SPATA6 genes in oligozoospermic male infertility. Materials and methods In the present study, we have analyzed DNA methylation pattern in the promoter regions of SPATA4, SPATA5 and SPATA6 genes in oligozoospermic patients and compared it with normozoospermic fertile controls. Semen samples were obtained from 30 oligozoospermic infertile and 19 normozoospermic fertile controls, and DNA methylation levels of the target gene promoters were analyzed by amplicon based deep sequencing methylation analysis using MiSeq. Results SPATA4 ( P   〈  0.0008), SPATA5 ( P  = 0.009) and SPATA6 (Promoter, P   〈  0.0005; Exon 1, P  = 0.0128) genes were significantly hypermethylated in oligozoospermic patients in comparison to controls. This is the first study reporting a higher methylation in the promoters of SPATA4, SPATA5 and SPATA6 in oligozoospermic infertile individuals in comparison to the normozoospermic fertile controls. Discussion Altered methylation of SPATA genes would affect pathways involved in sperm production or affect various processes linked to sperm fertility. Conclusion In conclusion, hypermethylation in the SPATA4, SPATA5 and SPATA6 genes correlates with oligozoospermic infertility.
    Type of Medium: Online Resource
    ISSN: 2047-2919 , 2047-2927
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2693844-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    In: The Prostate, Wiley, Vol. 73, No. 2 ( 2013-01), p. 146-152
    Type of Medium: Online Resource
    ISSN: 0270-4137
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 1494709-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    Wiley ; 2019
    In:  Molecular Reproduction and Development Vol. 86, No. 12 ( 2019-12), p. 1921-1939
    In: Molecular Reproduction and Development, Wiley, Vol. 86, No. 12 ( 2019-12), p. 1921-1939
    Abstract: Meiosis is the defining event of spermatogenesis. Spermatocytes undergo meiosis to give rise to round spermatids, which in turn metamorphose to flagellated spermatozoa that mature in the epididymis. To characterize the dynamics of gene expression during these important stages of spermatogenesis, we undertook transcriptome analysis in 〉 90% pure pachytene spermatocytes and round spermatids, and pure mature sperm of rat by massive parallel deep sequencing. The study has identified 10,719 total transcripts expressed in meiotic and postmeiotic cells, out of which 7,641 were present in all the three cell types. Most abundant transcripts were related to gametogenesis in spermatocytes and spermatids, and mitochondrial energy metabolism in sperm. Importantly, 108 transcripts were specific to spermatocytes, including Cpeb2 , Dpf3 , H2afy , Haus7 , Plcb1 , Taf9 , and Tdrd7 strongly linked with meiosis. Similarly, 323 transcripts unique to round spermatids included Arpc5 , Apoa1 , Cntrob , Dcaf17 , Ift88 , and Ly6k that play essential roles in spermiogenesis. Likewise, 178 transcripts unique to sperm included Camta1 , Hoxb1 , and Prdx6 having assigned roles in fertility and/or embryonic development. Levels of ~16% transcripts declined from spermatocytes to sperm while two ( Cd300e and Ddx17 ) increased. New candidate genes with possible roles in meiosis (91), spermiogenesis (298), and sperm function (171), have been identified. This study has provided new potential targets for contraception and/or treatment of male infertility. (CDRI communication number 9889).
    Type of Medium: Online Resource
    ISSN: 1040-452X , 1098-2795
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1493888-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    In: American Journal of Reproductive Immunology, Wiley, Vol. 83, No. 2 ( 2020-02)
    Abstract: Vitamin D is well‐known for having anti‐inflammatory and immunomodulatory properties. Impaired maternal vitamin D status has been known to increase the risk of adverse pregnancy outcomes like pre‐term birth. The present study aims to evaluate the impact of fetal cord serum 25‐hydroxyvitamin D‐mediated signaling in mediating inflammatory responses in placenta during pre‐term birth. Method of study For the above purpose, cord serum 25 hydroxyvitamin D 25(OH)D were measured in term (n = 20) and pre‐term (n = 20) born babies using ELISA. Vitamin D downstream signaling has also been checked in placenta (VDR, CYP27B1, cathelicidin LL37) along with expression of inflammatory markers (S100A8, HMGB1, TLR2, p‐NF‐kappaB) using Western blotting and immunohistochemistry. Pearson correlation model was used to do correlation study. Results Compared with term born babies (59.31 ± 3.476), decline in cord serum 25(OH)D levels is observed in pre‐term born babies (22.26 ± 1.083, P  =  〈 0.0001) that showed strong positive correlation with gestational age ( r  = .9368***) and birthweight ( r  = .9559***). On the other hand, vitamin D signaling markers were found to be downregulated and inflammatory markers were upregulated in placental tissue of pre‐term born babies. Conclusion Thus, our study demonstrated that insufficient cord 25(OH)D levels may disturb the homeostasis of inflammation in placenta. Altered cord serum 25(OH)D mediated anti‐inflammatory signaling may be acting as trigger signals in modulating inflammatory responses in placenta and eliciting premature activation of spontaneous labor in pre‐term birth.
    Type of Medium: Online Resource
    ISSN: 1046-7408 , 1600-0897
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2024667-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    In: American Journal of Reproductive Immunology, Wiley, Vol. 81, No. 2 ( 2019-02)
    Abstract: Decline in myeloid‐derived suppressor cells (MDSCs) and Th2 cytokines levels lead to early miscarriage (EM) but how the hormonal milieu of the body regulates MDSCs and Th1/Th2 cytokine balance is still a matter of investigation. Method of study Peripheral blood and decidua samples were collected from 20 EM patients, and 20 healthy pregnant women opted for elective abortion. MDSCs and G‐MDSCs levels were analyzed in peripheral blood mononuclear cells, and Th1/Th2 cytokines levels were determined in serum via flow cytometry. Estrogen (E2), Progesterone (P4), and Testosterone levels were measured via ELISA. Further, proliferation and apoptosis in decidual samples were checked via immunoblot/immunohistochemistry of estrogen receptor ‐α (ER‐α), STAT‐3/pSTAT‐3, and caspase‐3, respectively. Results Our results clearly indicate that in EM patients; decline in E2 and P4 significantly correlates with decline in MDSCs, particularly with subtype granulocytic MDSCs (G‐MDSCs) and skewness of the Th1/Th2 cytokines balance toward Th1 response. Downregulation of ER‐ α and increased caspase‐3 expression in endometrium decidua signifies poor endometrial receptivity in EM. STAT‐3 activation regulates proliferation, differentiation and suppressive potency of MDSCs. In decidua of EM, significantly lower expression of pSTAT‐3 indicates that these processes pertaining to MDSCs are compromised. Conclusion Altogether, this unfavorable systemic milieu may drive toward early breakdown of maternal‐fetal tolerance in EM. Therefore, regulated crosstalk of E2, P4 with MDSCs and balanced Th1/Th2 cytokines is prerequisite for successful pregnancy.
    Type of Medium: Online Resource
    ISSN: 1046-7408 , 1600-0897
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2024667-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    In: International Journal of Urology, Wiley, Vol. 28, No. 2 ( 2021-02), p. 225-240
    Abstract: To identify the sequence of inflammation‐driven signaling cascades and other molecular events that might cause tumor‐like transformation of prostatic cells. Methods Cytokine array analysis, Reactome and STRING analysis, immunoblotting, and immunocytochemistry were used to investigate the molecular mechanisms governing inflammation‐driven adverse changes in human prostatic cells caused by the sexually transmitted infection, Trichomonas vaginalis , resulting in prostatitis, benign prostatic hyperplasia and prostate cancer. Results Array analysis showed upregulation of 23 cytokines within 24 h of infection of human prostatic epithelial RWPE‐1 cells with the parasite, in vitro . Reactome and STRING analysis of array data identified interleukin‐6, interleukin‐8, nuclear factor kappa B, signal transducer and activator of transcription 3 and cyclooxygenase 2 as chief instigators of prostatic anomaly, which were found to be significantly upregulated by immunofluorescence and western blotting analyses. STRING further connected these instigators with macrophage migration inhibitory factor, PIM‐1 and prostate‐specific antigen; which was confirmed by their marked stimulation in infected prostatic cells by immunoblotting and immunocytochemistry. Upregulated proliferation markers, such as Ki67, proliferating cell nuclear antigen and B‐cell lymphoma 2, suggested tumor‐like signaling in infected RWPE‐1 cells, which was further supported by downregulation of E‐cadherin, upregulation of vimentin and activation of focal adhesion kinase. Prostate tumor DU145 cells were more sensitive to parasite invasion, and showed rapid upregulation with nuclear translocation of sensitive parameters, such as nuclear factor kappa B, signal transducer and activator of transcription 3, and macrophage migration inhibitory factor. The migration of DU145 cells augmented when incubated in spent media from parasite‐infected RWPE‐1 cells. Conclusion The initiation of inflammation driven tumor‐like cell signaling in parasite‐infected human prostatic epithelial cells is apparent, with the prostate tumor (DU145) cells being more sensitive to T. vaginalis than normal (RWPE‐1) prostatic cells.
    Type of Medium: Online Resource
    ISSN: 0919-8172 , 1442-2042
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2009793-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    In: Molecular Carcinogenesis, Wiley, Vol. 55, No. 11 ( 2016-11), p. 1843-1857
    Abstract: Estrogen Receptor‐β (ER‐β), a tumor‐suppressor in prostate cancer, is epigenetically repressed by hypermethylation of its promoter. DNA‐methyltransferases (DNMTs), which catalyze the transfer of methyl‐groups to CpG islands of gene promoters, are overactive in cancers and can be inhibited by DNMT‐inhibitors to re‐express the tumor suppressors. The FDA‐approved nucleoside DNMT‐inhibitors like 5‐Azacytidine and 5‐Aza‐deoxycytidine carry notable concerns due to their off‐target toxicity, therefore non‐nucleoside DNMT inhibitors are desirable for prolonged epigenetic therapy. Disulfiram (DSF), an antabuse drug, inhibits DNMT and prevents proliferation of cells in prostate and other cancers, plausibly through the re‐expression of tumor suppressors like ER‐β. To increase the DNMT‐inhibitory activity of DSF, its chemical scaffold was optimized and compound‐339 was discovered as a doubly potent DSF‐derivative with similar off‐target toxicity. It potently and selectively inhibited cell proliferation of prostate cancer (PC3/DU145) cells in comparison to normal (non‐cancer) cells by promoting cell‐cycle arrest and apoptosis, accompanied with inhibition of total DNMT activity, and re‐expression of ER‐β (mRNA/protein). Bisulfite‐sequencing of ER‐β promoter revealed that compound‐339 demethylated CpG sites more efficaciously than DSF, restoring near‐normal methylation status of ER‐β promoter. Compound‐339 docked on to the MTase domain of DNMT1 with half the energy of DSF. In xenograft mice‐model, the tumor volume regressed by 24% and 50% after treatment with DSF and compound‐339, respectively, with increase in ER‐β expression. Apparently both compounds inhibit prostate cancer cell proliferation by re‐expressing the epigenetically repressed tumor‐suppressor ER‐β through inhibition of DNMT activity. Compound‐339 presents a new lead for further study as an anti‐prostate cancer agent. © 2015 Wiley Periodicals, Inc.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2001984-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...