Expression of stress inducible protein 1 (Stip1) in the mouse testis

Mizrak, Sefika C.; Bogerd, Jan; López-Casas, Pedro P.; Párraga, Mario; Mazo, Jesús del; Rooij, Dirk G. de

doi:10.1002/mrd.20548

Cited by 15 publications

(13 citation statements)

References 54 publications

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“…Moreover, we found the decreased mRNA expression of Prnp, Stip1, Hsp70, and Sod genes. Stip1 provides potential to germ cells to survive in stress conditions [44] and exist in a macromolecular complex with the proteins of Hsp70 and 90 families [45]. Prnp, a cellular prion protein, cooperates with Stip1 and regulates superoxide dismutase activity in neuronal cell lines [46].…”

Section: Discussionmentioning

confidence: 99%

Genistein Induces Deleterious Effects during Its Acute Exposure in Swiss Mice

Singh

Sharma

Rath

2014

BioMed Research International

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Genistein is a soy derived isoflavone. It has wide variety of therapeutic effects against certain diseases including cancer. Although toxic effects of genistein have been studied, its effect on the gene expression and the reason behind toxicity have not been identified yet. In the present study, genistein was administered to age and body weight matched Swiss mice at the doses of 125, 250, 500 and 1000 mg/kg. The biomarkers of hepatotoxicity in serum, liver histology, oxidative stress parameters in tissue homogenates, and global gene expression were examined. Elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels and degenerated liver tissue were observed in 500, and 1000 mg/kg genistein treated groups. Oxidative stress was significant at these doses as considerable increase in lipid peroxidation (LPO) and decrease in total glutathione (GSH) were observed. Gene expression analysis showed 40 differentially expressed genes at twofold change and P < 0.05. Differentially expressed genes were corresponding to different biologically relevant pathways including metabolic and oxidative stress pathways. In 500 mg/kg group, Cyp4a14, Sult1e1, Gadd45g, Cidec, Mycs, and so forth genes were upregulated. These results suggested that the higher dose of genistein can produce several undesirable effects by affecting multiple cellular pathways.

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Section: Discussionmentioning

confidence: 99%

Genistein Induces Deleterious Effects during Its Acute Exposure in Swiss Mice

Singh

Sharma

Rath

2014

BioMed Research International

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“…STIP1 is a co-chaperone homologous to heat shock proteins 70 and 90. Its expression was previously shown to be altered in MEHP-exposed mouse testis (Mizrak et al 2006). In addition to HSPA8 and YWHAE, heat shock protein 75 kDa (TRAP1) was predictive of treatment.…”

Section: Biomarkers Of Dysgenesis In Fetal Rat Testismentioning

confidence: 99%

Novel molecular targets associated with testicular dysgenesis induced by gestational exposure to diethylhexyl phthalate in the rat: a role for estradiol

Klinefelter¹,

Laskey²,

Winnik³

et al. 2012

Reproduction

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Significant research has been focused on phthalate-induced alterations in male reproductive development. Studies on rodents have prompted the notion that a syndrome exists in the human male which includes phenotypic alterations such as hypospadias, cryptorchidism, poor semen quality, and even testicular cancer. Each phenotype in this 'testicular dysgenesis syndrome' is predicated on reduction in testosterone production by the fetal Leydig cell. We sought to examine the relationship between dysgenesis and steroidogenic capacity in the fetal rat testis more stringently by incorporating lower exposures than those typically used, conducting a comprehensive, non-targeted quantitative evaluation of the fetal testis proteome, and relating alterations in individual proteins to the capacity of the fetal Leydig cell to produce testosterone, and histopathology of the fetal testis. Pregnant dams were dosed orally from gestation day (GD) 13-19 with 0, 10, or 100 mg diethylhexyl phthalate (DEHP)/kg body weight per day. Each endpoint was represented by 16 l. Clustering of Leydig cells occurred before any significant decrease in the capacity of the GD19 Leydig cell to produce testosterone. At 100 mg DEHP/kg, testosterone production was reduced significantly, Leydig cell clusters became quite large, and additional dysgenetic changes were observed in the fetal testis. Of 23 proteins whose expression was altered significantly at both DEHP exposure levels, seven were found to be correlated with and predictive of the quantified endpoints. None of these proteins have been previously implicated with DEHP exposure. Notably, pathway analysis revealed that these seven proteins fit a pathway network in which each is regulated directly or indirectly by estradiol.

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“…An in situ hybridization protocol was applied as described earlier (Mizrak et al 2006). Initially, a postfixation step was performed with 4% paraformaldehyde for 15 min at room temperature followed by a digestion step with proteinase K at a concentration of 10 mg/ml and again a second post-fixation step.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Phosphoprotein enriched in astrocytes-15 is expressed in mouse testis and protects spermatocytes from apoptosis

Mizrak

Raffi²,

Párraga³

et al. 2007

Reproduction

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Phosphoprotein enriched in astrocytes (PEA-15) is a 15 kDa acidic serine-phosphorylated protein expressed in different cell types, especially in the CN. We initially detected the expression of PEA-15 in primary cultures of Sertoli cells. To assess the presence and localization of PEA-15 in the mouse testis, we studied the expression pattern of the PEA-15 protein by immunohistochemistry and mRNA by in situ hybridization. Both the protein and the mRNA of PEA-15 were localized in the cytoplasm of Sertoli cells, all types of spermatogonia, and spermatocytes up till zygotene phase of the meiotic prophase. Subsequently, with ongoing development of the spermatocytes, the expression decreased and was very low in the cytoplasm of diplotene spermatocytes. To analyze the possible role of PEA-15 in the developing testis, null mutants for PEA-15 were examined. As the PEA-15 C terminus contains residues for ERK binding, we studied possible differences between the localization of the ERK2 protein in wild type (WT) and PEA-15 K/K mice. In the WT testis, ERK2 was localized in the cytoplasm of Sertoli cells, B spermatogonia, preleptotene, leptotene, and zygotene spermatocytes, whereas in the KO testis, ERK2 was primarily localized in the nuclei of these cells and only little staining remained in the cytoplasm. Moreover, in PEA-15-deficient mice, significantly increased numbers of apoptotic spermatocytes were found, indicating an anti-apoptotic role of PEA-15 during the meiotic prophase. The increased numbers of apoptotic spermatocytes were not found at a specific step in the meiotic prophase.

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Expression of stress inducible protein 1 (Stip1) in the mouse testis

Cited by 15 publications

References 54 publications

Genistein Induces Deleterious Effects during Its Acute Exposure in Swiss Mice

Genistein Induces Deleterious Effects during Its Acute Exposure in Swiss Mice

Novel molecular targets associated with testicular dysgenesis induced by gestational exposure to diethylhexyl phthalate in the rat: a role for estradiol

Phosphoprotein enriched in astrocytes-15 is expressed in mouse testis and protects spermatocytes from apoptosis

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