Genes involved in nonpermissive temperature-induced cell differentiation in Sertoli TTE3 cells bearing temperature-sensitive simian virus 40 large T-antigen

Tabuchi, Yoshiaki; Kondo, Takashi; Suzuki, Yuzuru; Obinata, Masuo

doi:10.1016/j.bbrc.2005.02.065

Cited by 11 publications

(26 citation statements)

References 39 publications

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“…Now, novel transcript profiling technology, including cDNA microarray and real-time qPCR, allows the accurate measurement of changes in gene expression [13]. Therefore, we examined the time course of gene expression changes using it.…”

Section: Introductionmentioning

confidence: 99%

Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase

et al. 2008

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Under mechanical ventilation with high-inspired oxygen concentration, diffuse alveolar damage was found to take place in some patients. To clarify the molecular pathophysiology of this condition, we investigated the time course of gene expression changes induced by hyperoxia exposure in mouse lung using real-time quantitative polymerase chain reaction (qPCR). Our results normalized by glyceraldehyde 3-phosphate dehydrogenase showed that mRNA levels of cysteine rich protein 61 (CYR61) and connective tissue growth factor (CTGF) were significantly upregulated, while those of surfactant-associated protein C (SFTPC), cytochrome P450, 2F2 (CYP2F2), Claudin 1, (CLDN1), membrane-associated zonula occludens protein-1 (ZO-1), lysozyme (LYZS), and P lysozyme structural (LZP-S) were significantly downregulated. Increasing level of mRNAs, each encoding CYR61 and CTGF, suggests a serious risk of fibrosing alveolitis. Decrease in levels of mRNAs for SFTPC, CYP2F2, CLDN1, ZO-1, LYZS, and LZP-S suggests alveolar dysfunction and disruption of the immune system. Moreover, we confirmed apoptotic conditions, such as significant upregulations of mRNA levels in Myc and Galectin-3. Hyperoxic condition probably yielded reactive oxygen species (ROS), which resulted in a malignant cycle of ROS production by Myc overexpression.

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Section: Introductionmentioning

confidence: 99%

Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase

et al. 2008

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“…] cells immortalized by the tsSV40 large T-antigen is associated with growth arrest, apoptosis, and differentiation, and leads to the activation of p53 and the induction of p21 waf1 [Guenal and Mignotte, 1995]. As expected, the RCG-12 cells showed temperature-sensitive growth characteristics, as do other tsSV40 large T-antigen-expressed cell lines such as GSM06 [Sugiyama et al, 1993], TTE3 [Tabuchi et al, 2005a], and MEPC5 [Tabuchi et al, 2005b]. Although high expression level of large T-antigen was observed at 338C in the RCG-12 cells, the level was gradually decreased at 398C.…”

Section: Discussionmentioning

confidence: 65%

Identification of genetic networks involved in the cell growth arrest and differentiation of a rat astrocyte cell line RCG‐12

Takasaki

Takarada

Yasuda

et al. 2007

J of Cellular Biochemistry

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The purpose of the present study is to establish and characterize a conditionally immortalized astrocyte cell line and to clarify the genetic networks responsible for the cell growth arrest and differentiation. A conditionally immortalized astrocyte cell line, RCG-12, was established by infecting primary cultured rat cortical glia cells with a temperature-sensitive simian virus 40 large T-antigen. At a permissive temperature of 33 degrees C, the large T-antigen was expressed and cells grew continuously. On the other hand, the down-regulation of T-antigen at a non-permissive temperature of 39 degrees C led to growth arrest and differentiation. The cells expressed astrocyte-expressed genes such as glial fibrillary acidic protein. Interestingly, the differentiated condition induced by the non-permissive temperature significantly elevated the expression levels of several astrocyte-expressed genes. To identify the detailed mechanisms by which non-permissive temperature-induced cell growth arrest and differentiation, we performed high-density oligonucleotide microarray analysis and found that 556 out of 15,923 probe sets were differentially expressed 2.0-fold. A computational gene network analysis revealed that a genetic network containing up-regulated genes such as RB, NOTCH1, and CDKN1A was associated with the cellular growth and proliferation, and that a genetic network containing down-regulated genes such as MYC, CCNB1, and IGF1 was associated with the cell cycle. The established cell line RCG-12 retains some characteristics of astrocytes and should provide an excellent model for studies of astrocyte biology. The present results will also provide a basis for understanding the detailed molecular mechanisms of the growth arrest and differentiation of astrocytes.

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“…At a permissive temperature (33°C), the tsSV40LT-antigen induces immortalization by inactivating the functions of several tumor suppressor molecules, such as p53 and pRB, but at a nonpermissive temperature it is rapidly inactivated and degraded, and releases pRB or p53 from the complexes (DeCaprio et al, 1988;Hsieh et al, 2000;Jat and Sharp, 1989;Yanai and Obinata, 1994). Previous findings suggest that the tsSV40LT antigen gene is useful for establishing conditionallyimmortalized cell lines that have proved difficult to culture in vitro (Ebihara et al, 2004;Tabuchi et al, 2005). However, in this study, the use of temperature-sensitive UCSMCs was mainly an attempt to improve the cell survival and differentiation rate after hypothermic transplantation.…”

Section: Discussionmentioning

confidence: 98%

Combination of Temperature-Sensitive Stem Cells and Mild Hypothermia: A New Potential Therapy for Severe Traumatic Brain Injury

Chen

Sun

et al. 2012

Journal of Neurotrauma

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Stem cell transplantation holds great potential for the treatment of traumatic brain injury (TBI). However, the micro-environment of reduced oxygen and accumulated toxins leads to low survival rates of grafted cells, which dramatically limits their clinical application. Mild hypothermia has been demonstrated to improve the micro-environment after severe TBI. Thus, we speculate that combinational therapy of mild hypothermia may promote survival of grafted cells, especially temperature-sensitive stem cells, which show the most activity in mild temperatures. In this study, we first isolated mesenchymal stem cells from umbilical cord (UCSMCs) and generated the temperature-sensitive UCSMCs (tsUCSMCs) by infection with a retrovirus carrying the temperature-sensitive tsA58 SV40 LT antigen gene. We demonstrated that tsUCSMCs grew and proliferated with more activity at 33°C than at 37°C by counting cell numbers with a hematocytometer, measuring the cell cycle with flow cytometry, and detecting proliferating cell nuclear antigen (PCNA) with immunofluorescence staining. Thereafter, we established the rat severe TBI model by fluid percussion, and injected PBS, UCSMCs, or tsUCSMCs into the injured region, and subject the animals to normothermia or mild hypothermia (33°C). We found that, compared with UCSMC or tsUCSMC treatment alone, their combination with hypothermia could significantly improve motor and cognitive function with more survival of the grafted cells. Furthermore, we observed that combined therapy with hypothermia and tsUCSMCs exerted the most protective effect on the recovery of neurological function of all the tested treatments, with the highest survival and proliferation rates, and the lowest apoptosis rate. Thus this may represent a new therapeutic strategy for the treatment of severe TBI.

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Genes involved in nonpermissive temperature-induced cell differentiation in Sertoli TTE3 cells bearing temperature-sensitive simian virus 40 large T-antigen

Cited by 11 publications

References 39 publications

Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase

Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase

Identification of genetic networks involved in the cell growth arrest and differentiation of a rat astrocyte cell line RCG‐12

Combination of Temperature-Sensitive Stem Cells and Mild Hypothermia: A New Potential Therapy for Severe Traumatic Brain Injury

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