Asthenozoospermia: Analysis of a Large Population

Curi, Susana Mercedes; Ariagno, Julia Irene; Chenlo, Patricia Haydee; Mendeluk, Gabriela Ruth; Pugliese, Mercedes Norma; Segovia, L. M. Sardi; Repetto, Herberto Ernesto; Blanco, A M

doi:10.1080/713828220

Cited by 23 publications

(13 citation statements)

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“…Asthenozoospermia is the most common cause of infertility in males, but its etiology remains incompletely understood (Curi et al, 2003;O'Brien, Varghese, & Agarwal, 2010). This is probably due to a relative lack of knowledge of the proteins that regulate the normal physiology of spermatozoa.…”

Section: Discussionmentioning

confidence: 99%

Proteomic analysis of seminal extracellular vesicle proteins involved in asthenozoospermia by iTRAQ

Lin

Liang

et al. 2019

Molecular Reproduction Devel

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Asthenozoospermia is a common cause of male infertility, but in most cases its etiology is unknown. The exocytic cell vesicles called seminal extracellular vesicles in the human seminal fluid have been reported to play a pivotal role in promoting the motility of spermatozoa, and functional disorder of seminal extracellular vesicles may cause male infertility. To determine whether abnormal seminal extracellular vesicles are involved in asthenozoospermia, the differential abundance proteins between normozoospermic (NSEV) and asthenozoospermic seminal extracellular vesicles (ASEV) samples were analyzed by iTRAQ coupled with two‐dimensional liquid chromatography–tandem mass spectrometry. A total of 3,699 proteins were identified in the seminal extracellular vesicles (false discovery rate <0.01). Overall, 11 proteins were significantly upregulated (>1.2) in ASEV and 80 were significantly downregulated (<0.833). Functional bioinformatic analysis showed that these proteins with differential abundance were mainly associated with transport, metabolism, and signal pathways. The changes of OPTN, SMYD2, EIF2B2, TRPV6, ACE, PRSS8, and PPAP2A in ASEV were verified by western blot analysis, and we found that the abundance of TRPV6 markedly reduced in the seminal extracellular vesicles and ejaculated spermatozoa of asthenozoospermic patients, which indicated trpv6 was important in sperm motility. This study provides deeper insight into the involvement of seminal extracellular vesicles in asthenozoospermia and should aid the search for novel biomarkers of male infertility.

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Section: Discussionmentioning

confidence: 99%

Proteomic analysis of seminal extracellular vesicle proteins involved in asthenozoospermia by iTRAQ

Lin

Liang

et al. 2019

Molecular Reproduction Devel

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“…The prevalence of these male infertility cases was 18.71% for asthenozoospermia and 63.13% for asthenozoospermia associated with oligo-and/ or terato-zoospermia. 4 However, the exact pathogenesis of oligoasthenozoospermia is not clear. TPPP2 is likely to be a potential pathogenic factor in male infertility.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of TPPP2, a factor linked to oligoasthenozoospermia, causes subfertility in male mice

Zhu

Yan

Zhang

et al. 2019

J Cellular Molecular Medi

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Oligoasthenozoospermia is a major cause of male infertility; however, its etiology and pathogenesis are unclear and may be associated with specific gene abnormalities. This study focused on Tppp2 (tubulin polymerization promoting protein family member 2), whose encoded protein localizes in elongating spermatids at stages IV‐VIII of the seminiferous epithelial cycle in testis and in mature sperm in the epididymis. In human and mouse sperm, in vitro inhibition of TPPP2 caused significantly decreased motility and ATP content. Studies on Tppp2 knockout (KO) mice demonstrated that deletion of TPPP2 resulted in male subfertility with a significantly decreased sperm count and motility. In Tppp2 −/− mice, increased irregular mitochondria lacking lamellar cristae, abnormal expression of electron transfer chain molecules, lower ATP levels, decreased mitochondrial membrane potential and increased apoptotic index were observed in sperm, which could be the potential causes for its oligoasthenozoospermia phenotype. Moreover, we identified a potential TPPP2‐interactive protein, eEf1b (eukaryotic translation elongation factor 1 beta), which plays an important role in protein translation extension. Thus, TPPP2 is probably a potential pathogenic factor in oligoasthenozoospermia. Deficiency of TPPP2 might affect the translation of specific proteins, altering the structure and function of sperm mitochondria, and resulting in decreased sperm count, motility and fertility.

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“…A sthenozoospermia, or low sperm motility, is a common cause of human male infertility. About 20% of male infertility is associated with asthenozoospermia (Curi et al, 2003). However, the molecular mechanism of low sperm motility is not fully understood.…”

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confidence: 99%

Functional Expression of Ropporin in Human Testis and Ejaculated Spermatozoa

Chen

Wang

Wei

et al. 2010

Journal of Andrology

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Asthenozoospermia is a common cause of human male infertility, but the molecular mechanism is not fully understood. With Affymetrix Genechips, ropporin, a component of sperm flagella, was identified by comparing the expression profiles in ejaculated spermatozoa from normozoospermic men and patients with asthenozoospermia. Immunohistochemistry was used to analyze the expression characteristic of ropporin in human testis. Reverse transcription-polymerase chain reaction, Western blotting, and indirect immunofluorescence assay were used to determine the expression of ropporin in ejaculated spermatozoa from normozoospermic and asthenozoospermic men. The results showed that ropporin was predominantly expressed in round spermatids in human testis, and located in the principal piece and the end piece of spermatozoa flagella. The expression level of ropporin was significantly lower in asthenozoospermic men than in normozoospermic controls. These data suggested that ropporin may be involved in sperm motility and its decreased expression may contribute to the low sperm motility in asthenozoospermic patients.Key words: microarray analysis, asthenozoospermia, spermatozoa motility, Rho.J Androl 2011;32:26-32A sthenozoospermia, or low sperm motility, is a common cause of human male infertility. About 20% of male infertility is associated with asthenozoospermia (Curi et al, 2003). However, the molecular mechanism of low sperm motility is not fully understood. During the last decade, a complex population collection of RNAs was well documented as being present in human mature sperm and playing key roles in sperm motility, capacitation, and acrosomal reaction (Ostermeier et al, 2002;Martins et al, 2005;Lalancette et al, 2008;Dadoune, 2009). The identification of the genes involved in sperm motility provides novel insight into the understanding for the mechanisms of asthenozoospermia.Many genes have been identified as being involved in asthenozoospermia, and their aberrant expression contributes to the impaired sperm motility. With microarray techniques, Wang et al (2004) identified 149 highly expressed genes in both testis and ejaculated spermatozoa, and the expression of testis-specific protein 1 and lactate dehydrogenase C in the spermatozoa of normal semen samples was significantly higher than that in motility-impaired sperm. Jedrzejczak et al (2007) reported that the expression of spermatid-specific linker histone H1-like protein, transition proteins 1 and 2, and protamines 1 and 2 was significantly lower in spermatozoa from asthenozoospermic men compared to normozoospermic men. Huo et al (2008) identified 10 proteins expressed lower in asthenozoospermic patients, and these were Rho GDP dissociation inhibitor, outer dense fiber protein, isocitrate dehydrogenase subunit a, phosphoglycerate mutase 2, triosephosphate isomerase, glutamate oxaloacetate transaminase-1, carbonic anhydrase II, semenogelin-1 precursor, glutamine synthetase, and 26S protease regulatory subunit 7. Our previous data has shown that the expression...

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Asthenozoospermia: Analysis of a Large Population

Cited by 23 publications

References 0 publications

Proteomic analysis of seminal extracellular vesicle proteins involved in asthenozoospermia by iTRAQ

Proteomic analysis of seminal extracellular vesicle proteins involved in asthenozoospermia by iTRAQ

Deficiency of TPPP2, a factor linked to oligoasthenozoospermia, causes subfertility in male mice

Functional Expression of Ropporin in Human Testis and Ejaculated Spermatozoa

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