Immortalization of germ cells and somatic testicular cells using the SV40 large T antigen

Hofmann, Marie‐Claude; Narisawa, Sonoko; Hess, Rex A.; Millán, José Luis

doi:10.1016/0014-4827(92)90291-f

Cited by 243 publications

(255 citation statements)

References 61 publications

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“…36 Similar to freshly isolated cell populations, c-FLIP RNA was found in GC-1spg cell line ( Figure 1a) and the 55 kDa c-FLIP L protein was detected at levels comparable to those found in spermatocytes (Figure 1b). c-FLIP L immunohistochemical localization in adult mouse testis c-FLIP L localization was then examined by immunohistochemistry in mouse testes from young adults (Figure 2a).…”

Section: Results C-flip Expression In Mouse Testissupporting

confidence: 67%

FLIP is expressed in mouse testis and protects germ cells from apoptosis

et al. 2003

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Apoptosis control in adult testis is crucial to achieve normal spermatogenesis. In this study c-FLIP, an apoptosis-modulating protein, was investigated. In Western blot and immunohistochemical analyses, the 55 KDa c-FLIP long isoform (c-FLIP L ) was found to be expressed strongly in spermatocytes and spermatids, at low levels in spermatogonia and at almost undetectable levels in Sertoli cells. This expression pattern was confirmed by Northern blot analyses. Further experiments carried out on GC-1spg germ cell line revealed that reducing c-FLIP L expression increases Fas-dependent apoptosis. Conversely, restoring c-FLIP L expression reduces this response to control levels. Caspase-10 expression was found to match c-FLIP L expression pattern; further, caspase-10 activation upon anti-Fas treatment inversely correlated with c-FLIP L expression. Finally, TUNEL staining of seminiferous tubules incubated with anti-Fas antibody showed that apoptosis occurs mostly in basally located germ cells, indicating that such cells, expressing low levels of c-FLIP L , are sensitive to Fas-mediated apoptosis. These data indicate for the first time that c-FLIP L might control germ cell apoptosis and caspase activity in the adult testis.

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Section: Results C-flip Expression In Mouse Testissupporting

confidence: 67%

FLIP is expressed in mouse testis and protects germ cells from apoptosis

et al. 2003

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“…To test this hypothesis, we generated GC-1 cell lines stably overexpressing Flagtagged PRL2. GC-1 cell was derived from mouse spermatogonia (43), which is physiologically relevant to the present study. As shown in Fig.…”

Section: Prl2 Deficiency Promotes Apoptosis In Germ Cellsmentioning

confidence: 99%

Phosphatase of Regenerating Liver 2 (PRL2) Deficiency Impairs Kit Signaling and Spermatogenesis

Dong

Zhang

Bai

et al. 2014

Journal of Biological Chemistry

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Background:The PRLs are oncogenic when overexpressed but their physiological function is not well defined. Results: PRL2-deficient mice exhibit testis hypotrophy, decreased sperm production, and impaired reproductive potential. Conclusion: PRL2 promotes Kit signaling and germ cell survival by down-regulating PTEN. Significance: The study reveals the biological importance of PRL2 in spermatogenesis and identifies PRL2 as a novel target for cancer and male contraception.

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“…Several experiments have identified physical associations and even cellular junctional attachments between germ cells and Sertoli cells under culture conditions (Smith et al, 1992). Other studies have demonstrated maturation or brief differentiation sequences in vitro (Hofmann et al, 1992(Hofmann et al, , 1994Rassoulzadegan et al, 1993). Often cells remaining in culture retain some morphological characteristics of spermatogonia, such as large nuclear to cytoplasmic ratio, and it seems likely these primitive cells can be maintained in culture for several days or perhaps a few weeks (Kierszenbaum, 1994).…”

Section: Introductionmentioning

confidence: 99%

Culture of mouse spermatogonial stem cells

et al. 1998

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Spermatogenesis occurs within the seminiferous tubules of mammals by a complex process that is highly organized, extremely efficient and very productive. At the foundation of this process is the spermatogonial stem cell that is capable of both self-renewal and production of progeny cells, which undergo differentiation over a period of weeks to months in order to generate mature spermatozoa. It had been thought that germ cells survive only a brief period in culture, generally less than a few weeks. However, an accurate assessment of the presence of spermatogonial stem cells in any cell population has only recently become possible with development of the spermatogonial transplantation technique. Using this technique, we have demonstrated that mouse spermatogonial stem cells can be maintained in culture for approximately 4 months and will generate spermatogenesis following transplantation to the seminiferous tubules of an appropriate recipient. Extensive areas of cultured donor cell-derived spermatogenesis are generated in the host, and production of mature spermatozoa occurs. Cultivation of the testis cells on STO feeders is beneficial to stem cell survival. These results provide the first step in establishing a system that will permit spermatogonial stem cells to be cultivated and their number increased in vitro to allow for genetic modification before transplantation to a recipient testis.

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Immortalization of germ cells and somatic testicular cells using the SV40 large T antigen

Cited by 243 publications

References 61 publications

FLIP is expressed in mouse testis and protects germ cells from apoptosis

FLIP is expressed in mouse testis and protects germ cells from apoptosis

Phosphatase of Regenerating Liver 2 (PRL2) Deficiency Impairs Kit Signaling and Spermatogenesis

Culture of mouse spermatogonial stem cells

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