Sertoli Cell Lines

Roberts, Kenneth P.

doi:10.1016/b978-012647751-1/50020-9

Cited by 6 publications

(4 citation statements)

References 112 publications

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“…Differences on cell type employed could account for these different results. Even though TM4 cell line retains major characteristics of primary Sertoli cells, they do not completely replicate primary Sertoli cells 42 …”

Section: Discussionmentioning

confidence: 99%

TNF‐α inhibits GDNF levels in Sertoli cells, through a NF‐κB‐dependent, HES1‐dependent mechanism

et al. 2021

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Background Glial cell line‐derived neurotrophic factor (GDNF) is a soluble molecule crucial for the regulation of the spermatogonial stem cells (SSC) of the testis. The effects of GDNF on target cells have been extensively described, but mechanisms underlying GDNF regulation are currently under investigation. In the nervous system, GDNF expression is regulated by pro‐inflammatory cytokines including lipopolysaccharide (LPS), interleukin 1 beta (IL‐1β), and tumor necrosis factor alpha (TNF‐α) but the effect of these cytokines on GDNF expression in the testis is unclear. Objectives The aim of the present study was to investigate the impact of TNF‐α on GDNF expression levels using primary murine Sertoli cells as experimental model. Material and methods The expression of TNF‐α‐regulated genes including Gdnf in different culture conditions was determined by real‐time PCR. GDNF protein levels were determined by ELISA. The activation of the NF‐κb pathway and HES1 levels were assessed by Western Blot analysis and immunofluorescence. HES1 expression was downregulated by RNAi. Results In primary Sertoli cells, TNF‐α downregulates GDNF levels through a nuclear factor‐κB (NF‐κB)‐dependent mechanism. Mechanistically, TNF‐α induces the transcriptional repressor HES1 by a NF‐Κb‐dependent mechanism, which in turn downregulates GDNF. Discussion Under physiological conditions, TNF‐α is secreted by germ cells suggesting that this cytokine plays a role in the paracrine control of SSC niche by modulating GDNF levels. HES1, a well‐known target of the Notch pathway, is implicated in the regulation of GDNF expression. In Sertoli cells, TNF‐α and Notch signaling may converge at molecular level, to regulate the expression of HES1 and HES1‐ target genes, including GDNF. Conclusions Because of the importance of GDNF for spermatogonial stem cell self‐renewal and proliferation, this data may give important insights on how cytokine signals in the testis modulate the expression of niche‐derived factors.

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Section: Discussionmentioning

confidence: 99%

TNF‐α inhibits GDNF levels in Sertoli cells, through a NF‐κB‐dependent, HES1‐dependent mechanism

et al. 2021

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“…It has been reported that TM4 cells secrete multiple factor as primary SCs (Roberts 2005) and are able to create a proper environment for the proliferation and differentiation of other co-cultured cells via PI3K/ AKT and MAPK pathway [e.g., BM-MSCs (Tian et al 2014), ESCs (Miryounesi et al 2013) and SSCs (Simon et al 2007)]. However, previous studies showed that some of these factors (such as EGF, TGFbs) could enhance the ADSCs proliferation, stemness, differentiation, survival and migration.…”

Section: Discussionmentioning

confidence: 99%

Co-culture with TM4 cells enhances the proliferation and migration of rat adipose-derived mesenchymal stem cells with high stemness

Luo

Mohsin

et al. 2018

Cytotechnology

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The proliferation and migration of mesenchymal stem cells (MSCs) are the efficiency determinants in MSCs transplant therapy. Sertoli cells considered as "nurse cell" possesses the ability to enhance the proliferation and migration of umbilical cord mesenchymal stem cells (UCMSCs). However, no reports about TM4 cells' effect on the proliferation and migration of adipose tissue-derived mesenchymal stem cells (ADSCs) have been found until at present research work. Therefore, this study investigates the effect of TM4 cells on the proliferation and migration of ADSCs. We found that the performance of proliferation and migration of ADSCs were improved significantly while maintaining their stemness and reducing their apoptosis rate. After co-culturing with TM4 cells, the co-cultured ADSCs demonstrated higher proportion of synthetic phase (S) cells and colony-forming units-fibroblastic (CFU-F) number, lower proportion of sub-G1 phase cells and enhanced osteogenic and adipogenic differentiation ability. Moreover, results confirmed the higher multiple proteins involved in cell proliferation and migration including expression of the phospho-Akt, mdm2, pho-CDC2, cyclin D1 CXCR4, MMP-2, as well as phospho-p44 MAPK and phospho-p38 MAPK in co-cultured ADSCs. Furthermore, the process of TM4 cells promoting the proliferation of ADSCs was significantly inhibited by the administration of the PI3K/AKT inhibitor LY294002. Obtained results indicated that TM4 cells through MAPK/ERK1/2, MAPK/p-38 and PI3K/Akt pathways influence the proliferation and migration of ADSCs. These findings indicated that TM4 cells were found effective in promoting stemness and migration of ADSCs, that proves adopted co-culturing technique as an efficient approach to obtain ADSCs in transplantation therapy.

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“…There are several Sertoli cell lines, some of which were created to retain properties from the parent cell type required for specific studies (Robert, 2004;Guttenbach et al, 2001). For example, TM4 cells are an established cell line of Sertoli cell origin, derived from the normal testes of a prepubertal 11 -13 day old BALB/c mouse (Mather et al, 1982;Mather, 1980).…”

Section: Introductionmentioning

confidence: 99%

Sub-lethal concentrations of CdCl2 disrupt cell migration and cytoskeletal proteins in cultured mouse TM4 Sertoli cells

Egbowon

Harris

Arnott

et al. 2016

Toxicology in Vitro

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The aims of this study were to examine the effects of CdCl2 on the viability, migration and cytoskeleton of cultured mouse TM4 Sertoli cells. Time-and concentration-dependent changes were exhibited by the cells but 1 µM CdCl2 was sub-cytotoxic at all time-points. Exposure to 1 and 12 µM CdCl2 for 4 h resulted in disruption of the leading edge, as determined by chemical staining. Cell migration was inhibited by both 1 and 12 µM CdCl2 in a scratch assay monitored by live cell imaging, although exposure to the higher concentration was associated with cell death. Western blotting and immunofluorescence staining indicated that CdCl2 caused a concentration dependent reduction in actin and tubulin levels. Exposure to Cd 2+ also resulted in significant changes in the levels and/or phosphorylation status of the microtubule and microfilament destabilising proteins cofilin and stathmin, suggesting disruption of cytoskeletal dynamics. Given that 1-12 µM Cd 2+ is attainable in vivo, our findings are consistent with the possibility that Cd 2+ induced impairment of testicular development and reproductive health may involve a combination of reduced Sertoli cell migration and impaired Sertoli cell viability depending on the timing, level and duration of exposure.

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Sertoli Cell Lines

Cited by 6 publications

References 112 publications

TNF‐α inhibits GDNF levels in Sertoli cells, through a NF‐κB‐dependent, HES1‐dependent mechanism

TNF‐α inhibits GDNF levels in Sertoli cells, through a NF‐κB‐dependent, HES1‐dependent mechanism

Co-culture with TM4 cells enhances the proliferation and migration of rat adipose-derived mesenchymal stem cells with high stemness

Sub-lethal concentrations of CdCl2 disrupt cell migration and cytoskeletal proteins in cultured mouse TM4 Sertoli cells

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