scholarly journals Microcystin-Leucine Arginine Causes Cytotoxic Effects in Sertoli Cells Resulting in Reproductive Dysfunction in Male Mice

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yabing Chen ◽  
Yuan Zhou ◽  
Jing Wang ◽  
Lihui Wang ◽  
Zou Xiang ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Male Mice ◽  
Cytotoxic Effects ◽  
Reproductive Dysfunction

scholarly journals Kindlin-2 in Sertoli cells is essential for testis development and male fertility in mice

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Xiaochun Chi ◽  
Weiwei Luo ◽  
Jiagui Song ◽  
Bing Li ◽  
Tiantian Su ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Male Fertility ◽  
Nuclear Translocation ◽  
Hippo Pathway ◽  
Reproductive Organs ◽  
Male Reproduction ◽  
Barrier Structure ◽  
Male Mice ◽  
Sperm Development

AbstractKindlin-2 is known to play important roles in the development of mesoderm-derived tissues including myocardium, smooth muscle, cartilage and blood vessels. However, nothing is known for the role of Kindlin-2 in mesoderm-derived reproductive organs. Here, we report that loss of Kindlin-2 in Sertoli cells caused severe testis hypoplasia, abnormal germ cell development and complete infertility in male mice. Functionally, loss of Kindlin-2 inhibits proliferation, increases apoptosis, impairs phagocytosis in Sertoli cells and destroyed the integration of blood-testis barrier structure in testes. Mechanistically, Kindlin-2 interacts with LATS1 and YAP, the key components of Hippo pathway. Kindlin-2 impedes LATS1 interaction with YAP, and depletion of Kindlin-2 enhances LATS1 interaction with YAP, increases YAP phosphorylation and decreases its nuclear translocation. For clinical relevance, lower Kindlin-2 expression and decreased nucleus localization of YAP was found in SCOS patients. Collectively, we demonstrated that Kindlin-2 in Sertoli cells is essential for sperm development and male reproduction.

scholarly journals Sertoli Cell Is a Potential Target for Perfluorooctane Sulfonate–Induced Reproductive Dysfunction in Male Mice

2013 ◽  
Vol 135 (1) ◽  
pp. 229-240 ◽  
Author(s):  
Lianglin Qiu ◽  
Xuhui Zhang ◽  
Xiaoming Zhang ◽  
Yudong Zhang ◽  
Jun Gu ◽  
...  
Keyword(s):  
Sertoli Cell ◽  
Perfluorooctane Sulfonate ◽  
Male Mice ◽  
Reproductive Dysfunction ◽  
Potential Target

Nesfatin-1 ameliorates type-2 diabetes-associated reproductive dysfunction in male mice

2019 ◽  
Vol 43 (4) ◽  
pp. 515-528 ◽  
Author(s):  
A. Ranjan ◽  
M. Choubey ◽  
T. Yada ◽  
A. Krishna
Keyword(s):  
Type 2 Diabetes ◽  
Male Mice ◽  
Reproductive Dysfunction

Oleanolic acid causes reversible contraception in male mice by increasing the permeability of the germinal epithelium

2019 ◽  
Vol 31 (10) ◽  
pp. 1589 ◽  
Author(s):  
David Fisher ◽  
Faizel Mosaval ◽  
Darla L. Tharp ◽  
Doug K. Bowles ◽  
Ralf Henkel
Keyword(s):  
Oleanolic Acid ◽  
Sertoli Cells ◽  
Electrical Resistance ◽  
Experimental Models ◽  
Ethanol Solution ◽  
Germinal Epithelium ◽  
Control Group ◽  
Male Mice ◽  
Rt Pcr ◽  
Daily Dose

The effects of oleanolic acid (OA) on the fertility of male mice were investigated using both invivo and invitro experimental models. The experimental group (n=12) was treated with a daily dose of 30mgOAkg−1 bodyweight (i.p.), while the control group (n=6) received a daily dose of 10% ethanol solution (1mLkg−1 bodyweight). The effect of OA on the permeability status of TM4 Sertoli monolayers was investigated by measuring the transepithelial electrical resistance (TER), intracellular electrical resistance and semiquantitative RT–PCR. After 45 days, OA-treated males produced no pregnancies but in the control group, all 12 females were impregnated (69 offspring). Male mice, which demonstrated sterility when exposed to OA, recovered their fertility after 30 days (78 offspring). Testicular histological observations of OA-treated mice showed detachment of adjacent Sertoli–Sertoli cells. A control monolayer developed TER of 300–400 Ω.cm2, but OA (50, 100, 200µgL−1) treated monolayers developed TER of approximately 100Ω.cm2. Intracellular electrophysiological and RT–PCR data supported the premise that OA compromised tight junctional permeability. The study demonstrated reversible contraception in male mice by increasing the permeability of the germinal epithelium and further postulates that contraceptive reversibility is brought about by the reconstitution of the paracellular junctions between adjacent Sertoli cells.

scholarly journals Basigin null mutant male mice are sterile and exhibit impaired interactions between germ cells and Sertoli cells

2013 ◽  
Vol 380 (2) ◽  
pp. 145-156 ◽  
Author(s):  
Jiajia Bi ◽  
Yanfen Li ◽  
Fengyun Sun ◽  
Anja Saalbach ◽  
Claudia Klein ◽  
...  
Keyword(s):  
Germ Cells ◽  
Sertoli Cells ◽  
Null Mutant ◽  
Male Mice ◽  
Mutant Male

scholarly journals Importin α7 deficiency causes infertility in male mice by disrupting spermatogenesis

Development ◽  
2021 ◽  
Author(s):  
Na Liu ◽  
Fatimunnisa Qadri ◽  
Hauke Busch ◽  
Stefanie Huegel ◽  
Gabin Sihn ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Male Fertility ◽  
Target Genes ◽  
Cell Function ◽  
Expression Patterns ◽  
Male Mice ◽  
Loss Of Function ◽  
Altered Expression ◽  
Importin Α

Spermatogenesis is driven by an ordered series of events, which rely on trafficking of specific proteins between nucleus and cytoplasm. The importin α family of proteins mediates movement of specific cargo proteins when bound to importin β. Importin α genes have distinct expression patterns in mouse testis, implying they may have unique roles during mammalian spermatogenesis. Here we use a loss-of-function approach to specifically determine the role of importin α7 in spermatogenesis and male fertility. We show that ablation of importin α7 in male mice leads to infertility and has multiple cumulative effects on both germ cells and Sertoli cells. Importin α7-deficient mice exhibit an impaired Sertoli cell function, including loss of Sertoli cells and a compromised nuclear localization of the androgen receptor. Furthermore, our data demonstrate devastating defects in spermiogenesis including incomplete sperm maturation and massive loss of sperms that are accompanied by disturbed histone-protamine-exchange, differential localization of the transcriptional regulator Brwd1 and altered expression of Rfx2 target genes. Our work uncovers the essential role of importin α7 in spermatogenesis and hence in male fertility.

scholarly journals Importin α7 deficiency causes infertility in male mice by disrupting spermatogenesis

2020 ◽  
Author(s):  
Na Liu ◽  
Fatimunnisa Qadri ◽  
Hauke Busch ◽  
Stefanie Huegel ◽  
Gabin Sihn ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Male Fertility ◽  
Target Genes ◽  
Cell Function ◽  
Expression Patterns ◽  
Male Mice ◽  
Loss Of Function ◽  
Altered Expression ◽  
Importin Α

AbstractSpermatogenesis is driven by an ordered series of events, which rely on trafficking of specific proteins between nucleus and cytoplasm. The importin α family of proteins mediates movement of specific cargo proteins when bound to importin β. Importin α genes have distinct expression patterns in mouse testis, implying they may have unique roles during mammalian spermatogenesis. Here we use a loss-of-function approach to specifically determine the role of importin α7 in spermatogenesis and male fertility. We show that ablation of importin α7 in male mice leads to infertility and has multiple cumulative effects on both germ cells and Sertoli cells. Importin α7-deficient mice exhibit an impaired Sertoli cell function, including loss of Sertoli cells and a compromised nuclear transport of the androgen receptor. Furthermore, our data demonstrate devastating defects in spermiogenesis that are accompanied by disturbed histone-protamine-exchange, absence of the transcriptional regulator Brwd1 and altered expression of Rfx2 target genes, resulting in incomplete sperm maturation and massive loss of sperms. Our work uncovers the essential role of importin α7 in spermatogenesis and hence in male fertility.

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