scholarly journals The Testicular Antiviral Defense System: Localization, Expression, and Regulation of 2′5′ Oligoadenylate Synthetase, Double-Stranded RNA-activated Protein Kinase, and Mx Proteins in the Rat Seminiferous Tubule

1997 ◽  
Vol 139 (4) ◽  
pp. 865-873 ◽  
Author(s):  
Nathalie Dejucq ◽  
Suzanne Chousterman ◽  
Bernard Jégou
Keyword(s):  
Protein Kinase ◽  
Sertoli Cells ◽  
Seminiferous Tubule ◽  
Sendai Virus ◽  
Antiviral Defense ◽  
Defense System ◽  
Oligoadenylate Synthetase ◽  
Double Stranded Rna ◽  
Ifn Γ ◽  
Peritubular Cells

Although the involvement of viruses in alterations of testicular function and in sexually transmitted diseases is well known, paradoxically, the testicular antiviral defense system has virtually not been studied. The well known antiviral activity of interferons (IFNs) occurs via the action of several IFN-induced proteins, among which the 2′5′ oligoadenylate synthetase (2′5′ A synthetase), the double-stranded RNA-activated protein kinase (PKR), and the Mx proteins are the best known. To explore the antiviral capacity of the testis and to study the testicular action of IFNs, we looked for the presence and regulation of these three proteins in isolated seminiferous tubule cells, cultured in the presence or in the absence of IFN α, IFN γ, or Sendai virus. In all conditions tested, the meiotic pachytene spermatocytes and the post-meiotic early spermatids lacked 2′5′ A synthetase, PKR, and Mx mRNAs and proteins. In contrast, Sertoli cells constitutively expressed these mRNAs and proteins, and their levels were greatly increased after IFN α or Sendai virus exposure. While peritubular cells were also able to markedly express 2′5′ A synthetase, PKR, and Mx mRNA and proteins after IFN α or viral exposure, only PKR was constitutively present in these cells. Interestingly, IFN γ had no effect on peritubular cells' 2′5′ A synthetase and Mx production but it enhanced Mx proteins in Sertoli cells. In conclusion, this study reveals that the seminiferous tubules are particularly well equipped to react to a virus attack. The fact that the two key tubular elements of the blood–testis barrier, namely, Sertoli and peritubular cells, were found to assume this protection allows the extension of the concept of blood–testis barrier to the testicular antiviral defense.

Increased expression of 2′5′oligoadenylate synthetase and double-stranded RNA dependent protein kinase messenger RNAs on affected skin of systemic sclerosis patients

2007 ◽  
Vol 299 (5-6) ◽  
pp. 259-262 ◽  
Author(s):  
Luiz Felipe Leomil Coelho ◽  
Jaquelline Germano de Oliveira ◽  
Danilo Bretas de Oliveira ◽  
Antônio Carlos Martins Guedes ◽  
Cristina Costa Duarte Lanna ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Protein Kinase ◽  
Messenger Rnas ◽  
Oligoadenylate Synthetase ◽  
Dependent Protein Kinase ◽  
Double Stranded Rna ◽  
Dependent Protein

scholarly journals Androgen Receptor Expression in Sertoli Cells as a Function of Seminiferous Tubule Maturation in the Human Cryptorchid Testis1

2001 ◽  
Vol 86 (1) ◽  
pp. 413-421 ◽  
Author(s):  
Javier Regadera ◽  
Francisco MartÍnez-GarcÍa ◽  
Pilar González-Peramato ◽  
Alvaro Serrano ◽  
Manuel Nistal ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Sertoli Cells ◽  
Seminiferous Tubule ◽  
Staining Intensity ◽  
Receptor Expression ◽  
Seminiferous Tubules ◽  
Adult Type ◽  
Archival Collection ◽  
Cryptorchid Testis ◽  
Peritubular Cells

Androgen receptor (AR) immunohistochemistry was performed in an archival collection of adult human cryptorchid testes to determine whether AR cellular distribution and intensity of immunostaining were functions of the severity of cellular dysgenesis. The seminiferous tubule histology of cryptorchid testes collected from adults is marked by three specific patterns. 1) Seminiferous tubules are characterized as maintaining focal areas of germinal cell differentiation (albeit incomplete) that are interspersed with 2) tubules composed of Sertoli cells only, these latter cells being principally of the adult type, although dysgenetic and immature Sertoli cells may also be detected. 3) In contrast, there is a class of tubule that is characterized as being composed exclusively of Sertoli cells that are extremely dysgenetic in appearance. The majority of adult-type Sertoli cells found in the first types of tubules exhibited either robust or moderate AR staining intensity. Peritubular cells of these tubules also expressed a similar AR staining intensity. In contrast, in the more dysgenetic and immature type Sertoli cells found in the second type of tubules, the intensity of AR staining was significantly less, if not missing altogether. Finally, in the most dysgenetic tubules, Sertoli cell AR staining was never detected. To our knowledge, this is the first report in the literature that addresses the intensity of AR immunostaining in Sertoli cells of cryptorchid testes. The results presented herein are consistent with the interpretation that the intensity of AR staining in Sertoli cells diminishes as a function of the severity to which the cells are afflicted within a cryptorchid testis and that focal absence of AR expression in Sertoli cells correlates with a lack of local spermatogenesis in the tubules.

scholarly journals SARS-CoV-2 induces double-stranded RNA-mediated innate immune responses in respiratory epithelial derived cells and cardiomyocytes

2020 ◽  
Author(s):  
Yize Li ◽  
David M Renner ◽  
Courtney E Comar ◽  
Jillian N Whelan ◽  
Hanako M Reyes ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Immune Responses ◽  
Innate Immune ◽  
Alveolar Type ◽  
Rnase L ◽  
Innate Immune Responses ◽  
Oligoadenylate Synthetase ◽  
Protein Kinase R ◽  
Double Stranded Rna ◽  
Ribonuclease L

SummaryCoronaviruses are adept at evading host antiviral pathways induced by viral double-stranded RNA, including interferon (IFN) signaling, oligoadenylate synthetase–ribonuclease L (OAS-RNase L), and protein kinase R (PKR). While dysregulated or inadequate IFN responses have been associated with severe coronavirus infection, the extent to which the recently emerged SARS-CoV-2 activates or antagonizes these pathways is relatively unknown. We found that SARS-CoV-2 infects patient-derived nasal epithelial cells, present at the initial site of infection, induced pluripotent stem cell-derived alveolar type 2 cells (iAT2), the major cell type infected in the lung, and cardiomyocytes (iCM), consistent with cardiovascular consequences of COVID-19 disease. Robust activation of IFN or OAS-RNase L is not observed in these cell types, while PKR activation is evident in iAT2 and iCM. In SARS-CoV-2 infected Calu-3 and A549ACE2 lung-derived cell lines, IFN induction remains relatively weak; however activation of OAS-RNase L and PKR is observed. This is in contrast to MERS-CoV, which effectively inhibits IFN signaling as well as OAS-RNase L and PKR pathways, but similar to mutant MERS-CoV lacking innate immune antagonists. Remarkably, both OAS-RNase L and PKR are activated in MAVS knockout A549ACE2 cells, demonstrating that SARS-CoV-2 can induce these host antiviral pathways despite minimal IFN production. Moreover, increased replication and cytopathic effect in RNASEL knockout A549ACE2 cells implicates OAS-RNase L in restricting SARS-CoV-2. Finally, while SARS-CoV-2 fails to antagonize these host defense pathways, which contrasts with other coronaviruses, the IFN signaling response is generally weak. These host-virus interactions may contribute to the unique pathogenesis of SARS-CoV-2.SignificanceSARS-CoV-2 emergence in late 2019 led to the COVID-19 pandemic that has had devastating effects on human health and the economy. Early innate immune responses are essential for protection against virus invasion. While inadequate innate immune responses are associated with severe COVID-19 diseases, understanding of the interaction of SARS-CoV-2 with host antiviral pathways is minimal. We have characterized the innate immune response to SARS-CoV-2 infections in relevant respiratory tract derived cells and cardiomyocytes and found that SARS-CoV-2 activates two antiviral pathways, oligoadenylate synthetase–ribonuclease L (OAS-RNase L), and protein kinase R (PKR), while inducing minimal levels of interferon. This in contrast to MERS-CoV which inhibits all three pathways. Activation of these pathways may contribute to the distinctive pathogenesis of SARS-CoV-2.

Effect of nitric oxide on Sertoli cell microtubule of piglets

2009 ◽  
Vol 6 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Yang Li ◽  
Wang Xian-zhong ◽  
Yang Meng-bo ◽  
Zhang Jia-hua
Keyword(s):  
Nitric Oxide ◽  
Enzyme Activity ◽  
Protein Kinase ◽  
Cell Viability ◽  
Sodium Nitroprusside ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
High Concentration ◽  
Treatment Results ◽  
Anti Oxidant

AbstractTo illustrate the effect of nitric oxide (NO) on the microtubules of Sertoli cells (SC), SCs of piglets were treated with sodium nitroprusside (SNP). Changes in cell viability, anti-oxidant activity, enzyme activity and p38 mutagen-activated protein kinase (p38MAPK) activation were detected. The results were as follows. A low concentration of NO can keep SC microtubule and cell viability normal, and a high concentration of NO could increase p38MAPK activation, decrease anti-oxidant activity and transferrin secretion, and destroy the structure and distribution of the microtubules. The results suggest that SNP treatment results in an increase in NO in SCs and decreased cell anti-oxidant activity. The high concentration of NO destroys cell microtubules by activating p38MAPK.

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