Ferreiro, María Eugenia; Amarilla, María Sofía; Glienke, Leilane; Méndez, Cinthia Soledad; González, Candela; Jacobo, Patricia Verónica; Sobarzo, Cristian Marcelo; Laurentiis, Andrea De; Ferraris, María Jimena; Theas, María Susana The inflammatory mediators TNFα and nitric oxide arrest spermatogonia GC-1 cell cycle (Journal Article) In: Reprod Biol, 19 (4), pp. 329–339, 2019, ISSN: 2300-732X. @article{ferreiro_inflammatory_2019,
title = {The inflammatory mediators TNFα and nitric oxide arrest spermatogonia GC-1 cell cycle},
author = {Mar\'{i}a Eugenia Ferreiro and Mar\'{i}a Sof\'{i}a Amarilla and Leilane Glienke and Cinthia Soledad M\'{e}ndez and Candela Gonz\'{a}lez and Patricia Ver\'{o}nica Jacobo and Cristian Marcelo Sobarzo and Andrea De Laurentiis and Mar\'{i}a Jimena Ferraris and Mar\'{i}a Susana Theas},
doi = {10.1016/j.repbio.2019.11.001},
issn = {2300-732X},
year = {2019},
date = {2019-01-01},
journal = {Reprod Biol},
volume = {19},
number = {4},
pages = {329--339},
abstract = {During an inflammatory process of the testis, the network of somatic, immune, and germ cell interactions is altered leading to organ dysfunction. In testicular biopsies of infertile men, spermatogenesis impairment is associated with reduced spermatogonia proliferation, increased number of immune cells, and content of pro-inflammatory cytokines. TNFα-TNFR and nitric oxide (NO)-NO synthase systems are up-regulated in models of testicular damage and in human testis with maturation arrest. The purpose of this study was to test the hypothesis that TNFα-TNFR system and NO alter the function of spermatogonia in the inflamed testis. We studied the effect of TNFα and NO on GC-1 spermatogonia cell cycle progression and death by flow cytometry. GC-1 cells expressed TNFR1 and TNFR2 (immunofluorescence). TNFα (10 and 50 ng/ml) and DETA-Nonoate (0.5 and 2 mM), a NO releaser, increased the percentage of cells in S-phase of the cell cycle and reduced the percentage in G1, inducing also cell apoptosis. TNFα effect was not mediated by oxidative stress unlike NO, since the presence of N-acetyl-l-cysteine (2.5 and 5.0 mM) prevented NO induced cell cycle arrest and death. GC-1 spermatogonia overpass NO induced cell cycle arrest but no TNFα, since after removal of NO, spermatogonia progressed through the cell cycle. We propose TNFα and NO might contribute to impairment of spermatogenesis by preventing adequate functioning of the spermatogonia population. Our results showed that TNFα and NO impaired spermatogonia cell cycle, inducing GC-1 arrest in the S phase.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
During an inflammatory process of the testis, the network of somatic, immune, and germ cell interactions is altered leading to organ dysfunction. In testicular biopsies of infertile men, spermatogenesis impairment is associated with reduced spermatogonia proliferation, increased number of immune cells, and content of pro-inflammatory cytokines. TNFα-TNFR and nitric oxide (NO)-NO synthase systems are up-regulated in models of testicular damage and in human testis with maturation arrest. The purpose of this study was to test the hypothesis that TNFα-TNFR system and NO alter the function of spermatogonia in the inflamed testis. We studied the effect of TNFα and NO on GC-1 spermatogonia cell cycle progression and death by flow cytometry. GC-1 cells expressed TNFR1 and TNFR2 (immunofluorescence). TNFα (10 and 50 ng/ml) and DETA-Nonoate (0.5 and 2 mM), a NO releaser, increased the percentage of cells in S-phase of the cell cycle and reduced the percentage in G1, inducing also cell apoptosis. TNFα effect was not mediated by oxidative stress unlike NO, since the presence of N-acetyl-l-cysteine (2.5 and 5.0 mM) prevented NO induced cell cycle arrest and death. GC-1 spermatogonia overpass NO induced cell cycle arrest but no TNFα, since after removal of NO, spermatogonia progressed through the cell cycle. We propose TNFα and NO might contribute to impairment of spermatogenesis by preventing adequate functioning of the spermatogonia population. Our results showed that TNFα and NO impaired spermatogonia cell cycle, inducing GC-1 arrest in the S phase. |
Eugenia obtained her Degree in Biotechnology in the Argentinian University of Enterprise (UADE – Argentina) in 2017. She accomplished an honours degree thesis in the University of Buenos Aires working on the molecular mechanisms driving male infertility. In between 2017 and 2019, Eugenia worked in the Centre of Tissue Engineering and Cell Therapy (Maimonides University – Argentina), developing stem cell differentiation and primary cell culture expertise. She joined the Faulkner lab in 2020, first as a research assistant and later as a PhD student. She is currently working in the Queensland Brain Institute and her project aims to understand the role of L1 retrotransposons in neurodegeneration.
