scholarly journals Induction of apoptotic cell death in the seminiferous tubule of the adult rat testis: assessment of the germ cell types that exhibit the ability to enter apoptosis after hormone suppression by oestradiol treatment

1996 ◽  
Vol 19 (4) ◽  
pp. 237-247 ◽  
Author(s):  
J. BLANCO-RODRÍGUEZ ◽  
C. MARTÍNEZ-GARCÍA
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Seminiferous Tubule ◽  
Apoptotic Cell ◽  
Cell Types ◽  
Apoptotic Cell Death ◽  
Rat Testis ◽  
Adult Rat ◽  
Oestradiol Treatment

scholarly journals Alteration of Transforming Growth Factor-β Signaling System Expression in Adult Rat Germ Cells with a Chronic Apoptotic Cell Death Process after Fetal Androgen Disruption

Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5135-5143 ◽  
Author(s):  
Magali Maire ◽  
Anne Florin ◽  
Krisztian Kaszas ◽  
Daniel Regnier ◽  
Pierre Contard ◽  
...  
Keyword(s):  
Cell Death ◽  
Germ Cell ◽  
Germ Cells ◽  
Apoptotic Cell ◽  
In Utero ◽  
Apoptotic Cell Death ◽  
Death Process ◽  
Rat Testis ◽  
Adult Rat ◽  
Cell Death Process

In utero exposure to chemicals with antiandrogen activity induces undescended testis, hypospadias, and sub- or infertility. The hypospermatogenesis observed in the adult rat testis exposed in utero to the antiandrogen flutamide has been reported to be a result of a long-term apoptotic cell death process in mature germ cells. However, little if anything is known about the upstream signaling mechanisms controlling this apoptosis. In the present study, we have investigated the possibility that the TGF-β signaling pathway may be at play in this control of the apoptotic germ cell death process. By using a model of adult rat exposed in utero to 0, 0.4, 2, or 10 mg/kg·d flutamide, we observed that pro-TGF-β signaling members, such as the three isoforms of TGF-β ligands (TGF-β1–3), the two TGF-β receptors (TGF-βRI and -RII) and the R-Smads Smad 1, Smad 2, Smad 3, and Smad 5 were inhibited at the mRNA and protein levels, whereas the anti-TGF-β signaling member Smad 7 was overexpressed. Furthermore, we report that the overexpression of Smad 7 mRNA could induce an activation of c-Jun N-terminal kinase, because of the observed c-Jun overexpression, activation, and nuclear translocation leading to an increase in the transcription of the proapoptotic factor Fas-L. Together, the alterations of TGF-β signaling may represent upstream mechanisms underlying the adult germ cell apoptotic process evidenced in adult rat testis exposed in utero to antiandrogenic compounds such as flutamide.

234. Hedgehog signalling components in adult rat testis spermatogonial cells

2008 ◽  
Vol 20 (9) ◽  
pp. 34
Author(s):  
Z. Sahin ◽  
M. Meistrich ◽  
A. Szczepny ◽  
K. Loveland
Keyword(s):  
Stem Cells ◽  
Germ Cell ◽  
In Situ Hybridisation ◽  
Cell Types ◽  
Spermatogonial Stem Cells ◽  
Male Rats ◽  
Brown Norway ◽  
Hedgehog Signalling ◽  
Rat Testis ◽  
Adult Rat

In normal tissues, Hedgehog-induced progenitor cell proliferation is transient and tightly regulated, preventing continuous regeneration. However, activation of constitutive Hedgehog signalling results in unregulated self-renewal of progenitor cells in association with several human cancers. Although the contribution of Hedgehog signalling to cancers is widely accepted, its impact on spermatogonial stem cells and impact on male fertility are unknown. In this study, we aimed to clarify the possible role of Hh signalling on normal spermatogenesis in the adult rat and in adult testicular stem cells in the irradiated model {1}. Adult male rats were obtained from Monash University Central Animal Service and killed by cervical dislocation before tissue removal and fixation in Bouins for routine histochemical procedures. For studies on irradiated testes, adult LBNF1 male rats (hybrids between Lewis and Brown–Norway) were purchased from Harlan Sprague–Dawley, Inc. (Indianapolis, IN, USA). Testes were irradiated with 6 Gy to deplete all maturing germ cell types. At 15 weeks after irradiation the animals were injected simultaneously with 1.5 mg each of Cetrorelix pamoate and Cetrorelix acetate. Testes were collected 1, 2 or 4 weeks after injection. In situ hybridisation combined with immunohistochemistry was performed using DIG-labelled cRNA probes to identify the cells in which Hedgehog signalling components are made {2}. Signals for mRNAs encoding t he transmembrane receptors Ptc2 and Smo are most intensely detected in spermatogonia and spermatocytes and are much less intense in the round spermatids. The mRNA for the cytoplamic regulator, Fused, is restricted to the earliest germ cell types, whereas expression of the negative cytoplasmic regulator, SuFu, only begins in the round spermatids and persists in elongating spermatids. Gli1 and Gli3 are expressed from spermatogonia through to round spermatids, whereas Gli2 is restricted to spermatogonia and spermatocytes. This pattern mimics what was reported for mouse {2}. Examination of the irradiated rat testis model revealed that Hedgehog signalling machinery is produced by resting spermatogonial stem cells but is turned off when they differentiate in response to hormones. This matches the emerging understanding of Hedgehog signals in cancer stem cells and provides the first demonstration that Hedgehog signalling may influence stem cells in the adult testis. (1) Shuttlesworth G.A. et al. 2000. Endocrinology. 141: 37–49 (2) Szczepny A. et al. 2006. Dev Dyn. 235:3063–3070.

Erdosteine protects rat testis tissue from hypoxic injury by reducing apoptotic cell death

Andrologia ◽  
2012 ◽  
Vol 46 (1) ◽  
pp. 50-58 ◽  
Author(s):  
A. Guven ◽  
M. Ickin ◽  
O. Uzun ◽  
C. Bakar ◽  
E. Gulec Balbay ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Hypoxic Injury ◽  
Rat Testis ◽  
Testis Tissue

scholarly journals Long-Term Apoptotic Cell Death Process with Increased Expression and Activation of Caspase-3 and -6 in Adult Rat Germ Cells Exposedin Uteroto Flutamide

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 648-661 ◽  
Author(s):  
Asma Omezzine ◽  
Sonia Chater ◽  
Claire Mauduit ◽  
Anne Florin ◽  
Eric Tabone ◽  
...  
Keyword(s):  
Cell Death ◽  
Germ Cells ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Death Process ◽  
Adult Rat ◽  
Cell Death Process

Apoptotic cell death kinetics in vitro depend on the cell types and the inducers used

APOPTOSIS ◽  
2004 ◽  
Vol 9 (3) ◽  
pp. 385-392 ◽  
Author(s):  
F. Wolbers ◽  
P. Buijtenhuijs ◽  
C. Haanen ◽  
I. Vermes
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Cell Types ◽  
Apoptotic Cell Death ◽  
Death Kinetics

scholarly journals PDE2A2 regulates mitochondria morphology and apoptotic cell death via local modulation of cAMP/PKA signalling

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Stefania Monterisi ◽  
Miguel J Lobo ◽  
Craig Livie ◽  
John C Castle ◽  
Michael Weinberger ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Signal Propagation ◽  
Cell Types ◽  
Apoptotic Cell Death ◽  
Mitochondria Dynamics ◽  
Subcellular Domains ◽  
Camp Levels ◽  
Rat Cardiac Myocytes ◽  
High Resolution Microscopy

cAMP/PKA signalling is compartmentalised with tight spatial and temporal control of signal propagation underpinning specificity of response. The cAMP-degrading enzymes, phosphodiesterases (PDEs), localise to specific subcellular domains within which they control local cAMP levels and are key regulators of signal compartmentalisation. Several components of the cAMP/PKA cascade are located to different mitochondrial sub-compartments, suggesting the presence of multiple cAMP/PKA signalling domains within the organelle. The function and regulation of these domains remain largely unknown. Here, we describe a novel cAMP/PKA signalling domain localised at mitochondrial membranes and regulated by PDE2A2. Using pharmacological and genetic approaches combined with real-time FRET imaging and high resolution microscopy, we demonstrate that in rat cardiac myocytes and other cell types mitochondrial PDE2A2 regulates local cAMP levels and PKA-dependent phosphorylation of Drp1. We further demonstrate that inhibition of PDE2A, by enhancing the hormone-dependent cAMP response locally, affects mitochondria dynamics and protects from apoptotic cell death.

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