VDAC2 (porin-2) expression pattern and localization in the bovine testis

Hinsch, Klaus‐Dieter; Asmarinah,; Hinsch, Elvira; Konrad, Lutz

doi:10.1016/s0167-4781(01)00199-3

Cited by 48 publications

(42 citation statements)

References 19 publications

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“…It has been proposed that loss of doublets 4 -7 represent sliding of microtubules during attempted motility, with extrusion of half of the axoneme (35). Although, based on the results presented here, expression of VDAC3 protein appears ubiquitous, VDAC1 and VDAC2 reportedly are expressed in a more limited fashion, with VDAC1 restricted to Sertoli cells and VDAC2 found in secondary spermatocytes and in round and elongated spermatids (36). These differences in cell FIG.…”

Section: Discussionmentioning

confidence: 58%

Immotile Sperm and Infertility in Mice Lacking Mitochondrial Voltage-dependent Anion Channel Type 3

Sampson

Decker

Beaudet

et al. 2001

Journal of Biological Chemistry

211

190

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Voltage-dependent anion channels (VDACs), also known as mitochondrial porins, are small channel proteins involved in the translocation of metabolites across the mitochondrial outer membrane. A single channelforming protein is found in yeast, whereas higher eukaryotes express multiple VDACs, with humans and mice each harboring three distinct channels (VDAC1-3) encoded by separate genes. To begin to assess the functions of each of the three isoforms, the VDAC3 gene was inactivated by targeted disruption in embryonic stem cells. Here we show that mice lacking VDAC3 are healthy, but males are infertile. Although there are normal sperm numbers, the sperm exhibit markedly reduced motility. Structural defects were found in twothirds of epididymal axonemes, with the most common abnormality being loss of a single microtubule doublet at a conserved position within the axoneme. In testicular sperm, the defect was only rarely observed, suggesting that instability of a normally formed axoneme occurs with sperm maturation. In contrast, tracheal epithelial cilia showed no structural abnormalities. In addition, skeletal muscle mitochondria were abnormally shaped, and activities of the respiratory chain complexes were reduced. These results demonstrate that axonemal defects may be caused by associated nonaxonemal components such as mitochondrial channels and illustrate that normal mitochondrial function is required for stability of the axoneme.

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Section: Discussionmentioning

confidence: 58%

Immotile Sperm and Infertility in Mice Lacking Mitochondrial Voltage-dependent Anion Channel Type 3

Sampson

Decker

Beaudet

et al. 2001

Journal of Biological Chemistry

211

190

View full text Add to dashboard Cite

show abstract

“…VDAC existed in the mitochondrial outer membrane of leukocytes. Although the presence and localization of VDAC in human reproductive system remained unclear, VDAC2 was reportedly expressed in immature germ cells [33]. Removing the non-mature cells would avoid the contamination of redundant VDAC mRNA.…”

Section: Discussionmentioning

confidence: 99%

Analysis and difference of voltage-dependent anion channel mRNA in ejaculated spermatozoa from normozoospermic fertile donors and infertile patients with idiopathic asthenozoospermia

Liu

Wang

et al. 2010

J Assist Reprod Genet

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Purpose To analyze the abundance and difference of voltagedependent anion channel (VDAC) mRNA in ejaculated spermatozoa from normozoospermic fertile donors and infertile patients with idiopathic asthenozoospermia. Methods High motile and low motile spermatozoa were separated respectively from ejaculates of 36 donors and 40 patients using a discontinuous Percoll gradient centrifugation. Real-Time PCR was performed to detect mRNA abundance and difference of three VDAC subtypes between two groups with different sperm motility.Results Real-Time PCR demonstrated that three VDAC mRNAs were present in mature spermatozoa. The VDAC2 mRNA level in ejaculated spermatozoa of patients was significantly higher than that of donors. No significant differences of VDAC1 and VDAC3 mRNA levels were found between two groups. Conclusion The high abundance of VDAC2 mRNA seemed to have a positive correlation with low sperm motility. The abnormal expression of VDAC might be related to male infertility with idiopathic asthenozoospermia.

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“…This is especially true of mitochondrial targeted nuclearencoded proteins which may use preexisting OMM-associated proteins as receptors or may associate with the OMM, as is the case with OMM-associated b-barrel proteins (Koehler 2004). Therefore, the import receptors at the OMM may be affected by nicotine (Hinsch et al 2001). As StAR's conformation remained unchanged with increasing concentrations of nicotine, it is likely that nicotine affected the conformation of the cytoplasmic proteins associated with the OMM, thereby inhibiting StAR's interaction with the OMM.…”

Section: Discussionmentioning

confidence: 99%

Folding, activity and import of steroidogenic acute regulatory protein into mitochondria changed by nicotine exposure

Bose¹,

Debnath²,

Chen³

et al. 2007

Journal of Molecular Endocrinology

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Nicotine, a pharmacologically active constituent of tobacco smoke, decreases sex steroid production and impairs reproductive function. The rate-limiting step in steroid hormone biosynthesis is the transport of substrate cholesterol from the outer to inner mitochondrial membrane by the steroidogenic acute regulatory protein (StAR). StAR is a 37 kDa cytoplasmic phosphoprotein processed as a 32 kDa intermediate to a mature 30 kDa inactive mitochondrial protein.StAR's cholesterol transport capacity is proportional to its residency time at the outer mitochondrial membrane (OMM). Nonsteroidogenic COS-1 cells transfected with StAR/F2, steroidogenic MA-10 cells induced with cAMP or transfected with StAR or the isolated steroidogenic mitochondria preincubated with nicotine reduced StAR expression, import and activity. Mitochondria isolated from steroidogenic tissues or cells, pretreated with nicotine, also reduced the association of StAR with the OMM, but had no effect on the import of signal sequence substituted SCC/N-62StAR. The fluorescence emission maximum of StAR was unchanged with nicotine, but StAR's free energy of unfolding and the surface area (m) increased in the presence of nicotine. Nicotine also blocked StAR from proteolysis with trypsin, suggesting that nicotine partially stabilised protein conformation by insertion into the molten globule conformation of StAR.

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VDAC2 (porin-2) expression pattern and localization in the bovine testis

Cited by 48 publications

References 19 publications

Immotile Sperm and Infertility in Mice Lacking Mitochondrial Voltage-dependent Anion Channel Type 3

Immotile Sperm and Infertility in Mice Lacking Mitochondrial Voltage-dependent Anion Channel Type 3

Analysis and difference of voltage-dependent anion channel mRNA in ejaculated spermatozoa from normozoospermic fertile donors and infertile patients with idiopathic asthenozoospermia

Folding, activity and import of steroidogenic acute regulatory protein into mitochondria changed by nicotine exposure

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