scholarly journals The PATE gene is expressed in the accessory tissues of the human male genital tract and encodes a secreted sperm-associated protein

Reproduction ◽  
2005 ◽  
Vol 129 (4) ◽  
pp. 515-524 ◽  
Author(s):  
Ángel A Soler-García ◽  
Rangan Maitra ◽  
Vasantha Kumar ◽  
Tomoko Ise ◽  
Satoshi Nagata ◽  
...  

ThePATEgene is expressed in prostate and testis. To determine if PATE is expressed in other accessory tissues of the male genital tract, RT-PCR of the epididymis and seminal vesicle was performed. PATE mRNA was highly expressed in the epididymis and seminal vesicle.In situhybridization of the testis showed PATE mRNA is strongly expressed in the spermatogonia. ThePATEgene encodes a 14-kDa protein with a predicted signal sequence and a cleavage site between residues G21 and S22. To determine if PATE is a secreted protein, 293T cells were transfected with a pcDNA-PATE-myc-His plasmid and protein immunoprecipitated with anti-myc monoclonal antibody. Western blot analysis showed the presence of PATE-myc-His protein was in the medium and the cell lysate. Confocal microscopy demonstrated that PATE-myc-His protein is found in the endoplasmic reticulum. The polyclonal antibody SOL-1 was generated by immunization of rabbits with recombinant PATE protein expressed and purified fromEscherichia coli.Western blots were performed on extracts of prostate, testis, seminal vesicle and ejaculated spermatozoa, but PATE protein was only detected in the spermatozoa. Immunostaining of sperm smears revealed that PATE is located in a band-like pattern in the sperm head. Our data indicate that PATE is made by various sexual accessory tissues and secreted into the semen where it becomes associated with sperm, suggesting that PATE is a novel sperm-associated protein with a possible role in mammalian sperm maturation.

2015 ◽  
pp. 2125-2140 ◽  
Author(s):  
Deborah J. Anderson ◽  
Jeffrey Pudney

1992 ◽  
Vol 105 (2) ◽  
pp. 75-80 ◽  
Author(s):  
Katsuji Nishi ◽  
Tatsushige Fukunaga ◽  
Yoshio Yamamoto ◽  
Mitsuko Yamada ◽  
Masateru Kane ◽  
...  

1997 ◽  
Vol 39 (1) ◽  
pp. 45-53 ◽  
Author(s):  
P. Sirigu ◽  
M. T. Perra ◽  
C. Maxia ◽  
E. Usai

2011 ◽  
Vol 60 (3) ◽  
pp. 307-316 ◽  
Author(s):  
Juan Pablo Mackern-Oberti ◽  
Mariana Maccioni ◽  
Maria Laura Breser ◽  
Adrian Eley ◽  
Thomas Miethke ◽  
...  

Chlamydia trachomatis is an intracellular pathogen that infects mucosal epithelial cells, causing persistent infections. Although chronic inflammation is a hallmark of chlamydial disease, the proinflammatory mechanisms involved are poorly understood. Little is known about how innate immunity in the male genital tract (MGT) responds to C. trachomatis. Toll-like receptors (TLRs) are a family of receptors of the innate immunity that recognize different pathogen-associated molecular patterns (PAMPs) present in bacteria, viruses, yeasts and parasites. The study of TLR expression in the MGT has been poorly investigated. The aim of this work was to investigate the keratinocyte-derived chemokine (KC) response of MGT primary cultures from C57BL/6 mice to C. trachomatis and different PAMPs. KC production by prostate, seminal vesicle and epididymis/vas deferens cell cultures was determined by ELISA in culture supernatants. TLR2, 3, 4 and 9 agonists induced the production of KC by all MGT primary cultures assayed. In addition, we analysed the host response against C. trachomatis and Chlamydia muridarum. Chlamydial LPS (cLPS) as well as C. trachomatis and C. muridarum infection induced KC secretion by all MGT cell cultures analysed. Differences in KC levels were observed between cultures, suggesting specific sensitivity against pathogens among MGT tissues. Chemokine secretion was observed after stimulation of seminal vesicle cells with TLR agonists, cLPS and C. trachomatis. To our knowledge, this is the first report showing KC production by seminal vesicle cells after stimulation with TLR ligands, C. trachomatis or C. muridarum antigens. These results indicate that different receptors of the innate immunity are present in the MGT. Understanding specific immune responses, both innate and adaptive, against chlamydial infections, mounted in each tissue of the MGT, will be crucial to design new therapeutic approaches where innate and/or adaptive immunity would be targeted.


2000 ◽  
Vol 157 (6) ◽  
pp. 2011-2021 ◽  
Author(s):  
Annukka Paju ◽  
Anders Bjartell ◽  
Wan-Ming Zhang ◽  
Stig Nordling ◽  
Anders Borgström ◽  
...  

2005 ◽  
Vol 175 (6) ◽  
pp. 4127-4136 ◽  
Author(s):  
Zina Moldoveanu ◽  
Wen-Qiang Huang ◽  
Rose Kulhavy ◽  
Mitchell S. Pate ◽  
Jiri Mestecky

1983 ◽  
Vol 130 (2) ◽  
pp. 386-391 ◽  
Author(s):  
J. Gu ◽  
J.M. Polak ◽  
L. Probert ◽  
K.N. Islam ◽  
P.J. Marangos ◽  
...  

2015 ◽  
Vol 89 (11) ◽  
pp. 5772-5787 ◽  
Author(s):  
G. Matusali ◽  
N. Dereuddre-Bosquet ◽  
A. Le Tortorec ◽  
M. Moreau ◽  
A.-P. Satie ◽  
...  

ABSTRACTA number of men receiving prolonged suppressive highly active antiretroviral therapy (HAART) still shed human immunodeficiency virus (HIV) in semen. To investigate whether this seminal shedding may be due to poor drug penetration and/or viral production by long-lived cells within male genital tissues, we analyzed semen and reproductive tissues from macaques chronically infected with simian immunodeficiency virus mac251 (SIVmac251) who were treated for 4 months with HAART, which was intensified over the last 7 weeks with an integrase inhibitor. We showed that a subset of treated animals continued shedding SIV in semen despite efficient HAART. This shedding was not associated with low antiretroviral drug concentrations in semen or in testis, epididymis, seminal vesicles, and prostate. HAART had no significant impact on SIV RNA in the urethra, whereas it drastically reduced SIV RNA levels in the prostate and vas deferens and to a lesser extent in the epididymis and seminal vesicle. The only detectable SIV RNA-positive cells within the male genital tract after HAART were urethral macrophages. SIV DNA levels in genital tissues were not decreased by HAART, suggesting the presence throughout the male genital tract of nonproductively infected cells. In conclusion, our results demonstrate that 4 months of HAART induced variable and limited control of viral infection in the male reproductive organs, particularly in the urethra, and suggest that infected long-lived cells in the male genital tract may be involved in persistent seminal shedding during HAART. These results pave the way for further investigations of male genital organ infection in long-term-treated infected individuals.IMPORTANCEA substantial subset of men receiving prolonged HAART suppressing viral loads in the blood still harbor HIV in semen, and cases of sexual transmission have been reported. To understand the origin of this persistence, we analyzed the semen and male reproductive tissues from SIV-infected macaques treated with HAART. We demonstrated that persistent seminal shedding was not linked to poor drug penetration in semen or semen-producing prostate, seminal vesicle, epididymis, and testis. We revealed that HAART decreased SIV RNA to various extents in all male genital organs, with the exception of the urethra, in which SIV RNA+macrophages were observed despite HAART. Importantly, HAART did not impact SIV DNA levels in the male genital organs. These results suggest that infection of male genital organs, and particularly the urethra, could be involved in the release of virus in semen during HAART.


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