Transient disruption of spermatogenesis by deregulated expression of neurturin in testis

Meng, Xiaojuan; Pata, Illar; Pedrono, Eric; Popsueva, Anna; Rooij, Dirk G. de; Jänne, Marja; Rauvala, Heikki; Sariola, Hannu

doi:10.1016/s0303-7207(01)00649-9

Cited by 19 publications

(17 citation statements)

References 19 publications

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“…The binding of Gdnf triggers the activation of multiple signaling pathways in responsive cells (Airaksinen and Saarma, 2002). As mentioned previously, Gdnf in the testis is produced by Sertoli cells, which establish the niche in which the SSCs reside (Viglietto et al, 2000;Meng et al, 2000;Meng et al, 2001a), and this activity extends throughout life (Chen et al, 2005). In Sertoli cells, the production of Gdnf is mainly under the influence of FSH, growth factors and cytokines (Tadokoro et al, 2002;Simon et al, 2007).…”

Section: Role Of Gdnf In the Mammalian Testismentioning

confidence: 96%

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Hofmann

2008

Molecular and Cellular Endocrinology

203

178

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SummaryMammalian spermatogenesis is a complex process in which male germ-line stem cells develop to ultimately form spermatozoa. Spermatogonial stem cells, or SSCs, are found in the basal compartment of the seminiferous epithelium. They self-renew to maintain the pool of stem cells throughout life, or they differentiate to generate a large number of germ cells. A balance between SSC self-renewal and differentiation in the adult testis is therefore essential to maintain normal spermatogenesis and fertility. Maintenance and self-renewal are tightly regulated by extrinsic signals from the surrounding microenvironment, called the spermatogonial stem cell niche. By physically supporting the SSCs and providing them with growth factors, the Sertoli cell is the main component of the niche. In addition, adhesion molecules that connect the SSCs to the basement membrane and cellular components of the interstitium between the seminiferous tubules are important regulators of the niche function. This review mainly focuses on glial cell line-derived neurotrophic factor (Gdnf), which is produced by Sertoli cells to maintain SSCs self-renewal, and the downstream signaling pathways induced by this crucial growth factor. Interactions between Gdnf and other signaling pathways that maintain self-renewal, as well as the role of novel SSC-and Sertoli cell-specific transcription factors, are also discussed.

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Section: Role Of Gdnf In the Mammalian Testismentioning

confidence: 96%

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Hofmann

2008

Molecular and Cellular Endocrinology

203

178

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“…For example, GDNF can also bind to GFRa2 and GFRa3 and artemin to GFRa1 (Bespalov and Saarma, 2007). Apart from the GFRa-RET signaling mechanism, RET-independent signaling pathways have also been described (Poteryaev et al, 1999;Trupp et al, 1999;Meng et al, 2001b;Paratcha et al, 2003;Popsueva et al, 2003;Sariola and Saarma, 2003;Enomoto et al, 2004). GDNF, for example, has been shown to activate cytoplasmic Src family tyrosine kinases through GFRa1 in RET-deficient cells (Poteryaev et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Artemin is oncogenic for human mammary carcinoma cells

et al. 2009

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We report that artemin, a member of the glial cell linederived neurotrophic factor family of ligands, is oncogenic for human mammary carcinoma. Artemin is expressed in numerous human mammary carcinoma cell lines. Forced expression of artemin in mammary carcinoma cells results in increased anchorage-independent growth, increased colony formation in soft agar and in three-dimensional Matrigel, and also promotes a scattered cell phenotype with enhanced migration and invasion. Moreover, forced expression of artemin increases tumor size in xenograft models and leads to highly proliferative, poorly differentiated and invasive tumors. Expression data in Oncomine indicate that high artemin expression is significantly associated with residual disease after chemotherapy, metastasis, relapse and death. Artemin protein is detectable in 65% of mammary carcinoma and its expression correlates to decreased overall survival in the cohort of patients. Depletion of endogenous artemin with small interfering RNA, or antibody inhibition of artemin, decreases the oncogenicity and invasiveness of mammary carcinoma cells. Artemin is therefore oncogenic for human mammary carcinoma, and targeted therapeutic approaches to inhibit artemin function in mammary carcinoma warrant consideration.

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“…For example, an isochromosome 12p and de®ciencies in the short arms of chromosomes 1, 3, and 11 are concurrent with TGCTs (reviewed in Looijenga et al, 1999a;Looijenga and Oosterhuis, 1999b), implicating the presence of potential TGCT suppressor genes in these de®ciency regions. Recently, seminomas have also been correlated to the altered activities of speci®c genes such as glial cell line-derived neurotrophic factor (GDNF), members of placental alkaline phosphatase family, Zinc ®nger genes on chromosome 19, eukaryotic initiation factor 3 p110 mRNA, and Testis Speci®c Protein Y Encoded (TSPY; Ogawa et al, 1998;Rothe et al, 2000;Lau et al, 2000;Meng et al, 2001;Shigenari et al, 1998). Despite these progresses, the genetic mechanism that leads to the pathenogenesis of seminomas remains elusive.…”

Section: Introductionmentioning

confidence: 99%