Proteomic pattern changes associated with obesity‐induced asthenozoospermia

Liu, Y.; Guo, Yi; Song, Ning; Fan, Yong; Li, K.; Teng, Xiaoming; Guo, Qingsheng; Ding, Zhide

doi:10.1111/andr.289

Cited by 46 publications

(42 citation statements)

References 78 publications

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“…It was demonstrated recently that the amount of PDIA3 is reduced in the spermatozoa of male individuals with obesity-associated asthenozoospermia (Liu et al, 2015). Interestingly, PDIA3 also binds to the hydroxylated, hormonal form of vitamin D3,1a,25-dihydroxycholecalciferol (1a,25-(OH)2D3, calcitriol), and therefore may be involved in hormonal signaling processes (Nemere et al, 2004;Turano et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

GnRH immunization alters the expression and distribution of protein disulfide isomerases in the epididymis

et al. 2016

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SUMMARYHypogonadism is defined as the inadequate gonadal production of testosterone. Low serum testosterone leads to infertility by impairing spermatogenesis and reducing sperm count, however, the impact of hypogonadism in epididymal sperm maturation is poorly understood. From the testis, spermatozoa are transported into the epididymis where they find a specific microenvironment composed of a complex mixture of proteins that facilitate sperm storage and maturation. Inside the epididymal ductule, spermatozoa undergo several changes, resulting in their becoming capable of fertilizing eggs. Protein disulfide isomerases (PDIs) are known to participate in the folding and assembly of secreted proteins in the endoplasmic reticulum. However, little is known about the control and function of PDIs in the testis and epididymis, particularly during male development. The aim of this work was to compare the expression and distribution of PDI and PDIA3 (ERp57) in the testis and epididymis of healthy and GnRH-immunized boars. We detected higher amounts of PDIA3 and PDI in sperm preparations and fluid from the proximal regions of the epididymis of healthy boars. However, we observed an increase in PDIA3 expression in the testis and cauda epididymis in the immunocastrated group. GnRH-immunized boars showed a marked increase in PDI content in cauda spermatozoa and fluid, indicating a possible endocrine dysregulation of PDI. The results of our study suggest that PDIs are associated with epididymal sperm maturation and may be attractive candidates for monitoring male fertility.

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Section: Introductionmentioning

confidence: 99%

GnRH immunization alters the expression and distribution of protein disulfide isomerases in the epididymis

et al. 2016

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“…For example, maternal obesity is associated with numerous markers of reduced oocyte quality, including impaired maturation (17,35), increased lipid content (86,87), cellular lipotoxicity (87), alterations to mitochondria including ultrastructure (30), membrane potential (32), and mitochondrial DNA (mtDNA) content (32,88), as well as increased reactive oxygen species and depleted glutathione (indicative of oxidative stress) (32,52) and alterations to DNA methylation patterns of key metabolic and imprinting genes in oocytes (29), resulting from reduced DNA methyltransferase levels (28,29). In males, paternal obesity increases sperm oxidative stress and DNA damage (3,38,69,81) and alters sperm microRNA content (23,55), lipid content (20), protein composition (39,51,70,77), and active and repressive chromatin state (68) and global DNA hypomethylation (23). Importantly, since both maternal and paternal obesity have been independently correlated with programming perturbed metabolic health in offspring, the potential compounding effect of two obese parents must be examined.…”

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confidence: 99%

When two obese parents are worse than one! Impacts on embryo and fetal development

McPherson

Bell

Zander-Fox

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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McPherson NO, Bell VG, Zander-Fox DL, Fullston T, Wu LL, Robker RL, Lane M. When two obese parents are worse than one! Impacts on embryo and fetal development. Am J Physiol Endocrinol Metab 309: E568 -E581, 2015. First published July 21, 2015; doi:10.1152/ajpendo.00230.2015.-The prevalence of overweight and obesity in reproductive-age adults is increasing worldwide. While the effects of either paternal or maternal obesity on gamete health and subsequent fertility and pregnancy have been reported independently, the combination of having both parents overweight/ obese on fecundity and offspring health has received minimal attention. Using a 2 ϫ 2 study design in rodents we established the relative contributions of paternal and maternal obesity on fetal and embryo development and whether combined paternal and maternal obesity had an additive effect. Here, we show that parental obesity reduces fetal and placental weights without altering pregnancy establishment and is not dependent on an in utero exposure to a high-fat diet. Interestingly combined parental obesity seemed to accumulate both the negative influences of paternal and maternal obesity had alone on embryo and fetal health rather than an amplification, manifested as reduced embryo developmental competency, reduced blastocyst cell numbers, impaired mitochondrial function, and alterations to active and repressive embryonic chromatin marks, resulting in aberrant placental gene expression and reduced fetal liver mtDNA copy numbers. Further understanding both the maternal cytoplasmic and paternal genetic interactions during this early developmental time frame will be vital for understanding how developmental programming is regulated and for the proposition of interventions to mitigate their effects. blastocyst; oocyte; sperm; embryo; fertility; infertility; obesity THE PREVALENCE OF OVERWEIGHT and obesity in reproductive-age adults is increasing worldwide (62). For example, in America it is estimated that 70.9% of males and 61.9% of women are classified as overweight/obese (62). The comorbidities associated with obesity have been well defined; however, until recently the impact on pregnancy and fetal development has been less recognized. Although the effects of either paternal or maternal obesity on gamete health and subsequent fertility and pregnancy have been reported independently, the combination of having both parents overweight/obese on fecundity and offspring health has received minimal attention. This information is essential, as the percentage of couples of reproductive age with both partners overweight/ obese is increasing and is the predominant situation in many countries (62).To date, there have only been three studies that have assessed the combined effects of maternal and paternal obesity on pregnancy and fetal health, two in human-assisted reproductive technology (ART) cohorts and one using a rodent high-fat diet model (41,67,76). These studies found no effect of maternal and paternal obesity on pregnancy establishment (41, 67, 76); however, when ...

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“…Protein immunoprecipitation was characterized using the Pierce Direct IP kit (Thermo scientific) according to the manual instructions. The LC-MS analysis was performed as described (Liu et al 2015). All MS/MS spectra were searched using Proteome Discoverer2.2 software against the mouse UniProt database.…”

Section: Methodsmentioning

confidence: 99%

Functional importance of JMY expression by Sertoli cells in mediating mouse spermatogenesis

Fan

Yan

et al. 2018

Preprint

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3Sertoli cells are crucial for spermatogenesis in the seminiferous epithelium because 2 4 their actin cytoskeleton supports vesicle transport, cell junction, protein anchoring and 2 5 spermiation. Here, we show that junction-mediating and regulatory protein (JMY), an 2 6 actin regulating protein, also affects endocytic vesicle trafficking and Sertoli cell 2 7 junction remodeling since disruption of these functions induced male subfertility in 2 8Sertoli cell-specific Jmy knockout mice. Specifically, these mice have: a) impaired 2 9 BTB integrity and spermatid adhesion in the seminiferous tubules; b) high incidence 3 0 of sperm structural deformity; c) reduced sperm count and poor sperm motility. 3 1 Moreover, the cytoskeletal integrity in Sertoli cell-specific Jmy knockout mice was 3 2 compromised along with endocytic vesicular trafficking. These effects impaired 3 3 junctional protein recycling and reduced Sertoli cell junctions. In addition, JMY 3 4 interaction with α -actinin1 and Sorbs2 was related to JMY activity and in turn actin 3 5 cytoskeletal organization. In summary, JMY affects control of spermatogenesis 3 6 through regulating actin filament organization and endocytic vesicle trafficking in 3 7 Sertoli cells. 3 8 3 9

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Proteomic pattern changes associated with obesity‐induced asthenozoospermia

Cited by 46 publications

References 78 publications

GnRH immunization alters the expression and distribution of protein disulfide isomerases in the epididymis

GnRH immunization alters the expression and distribution of protein disulfide isomerases in the epididymis

When two obese parents are worse than one! Impacts on embryo and fetal development

Functional importance of JMY expression by Sertoli cells in mediating mouse spermatogenesis

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