Molecular biology of nickel carcinogenesis: Identification of differentially expressed genes in morphologically transformed C3H10T1/2 Cl 8 mouse embryo fibroblast cell lines induced by pecific insoluble nickel compounds

2004 ◽  
Vol 255 (1/2) ◽  
pp. 203-216 ◽  
Author(s):  
Rini Verma ◽  
Jamuna Ramnath ◽  
Farrah Clemens ◽  
Lisa C. Kaspin ◽  
Joseph R. Landolph
Author(s):  
И.Н. Рыболовлев ◽  
И.Н. Власов ◽  
А.Х. Алиева ◽  
П.А. Сломинский ◽  
М.И. Шадрина

Болезнь Паркинсона (БП) является многофакторным гетерогенным нейродегенеративным заболеванием. Поскольку этиопатогенез БП недостаточно изучен, кроме поиска и анализа изменений на уровне ДНК, необходимо распространить фокус исследований на другие уровни: транскриптом и метилом. Изменения на уровне эпигенома можно исследовать у лиц с идентичной генетической конституцией, такой «моделью» являются дискордантные по этому заболеванию монозиготные близнецы. В исследовании приняло участие 3 пары фенотипически и генотипически монозиготных близнецов русского происхождения; В исследовании приняло участие 3 пары фенотипически и генотипически монозиготных близнецов русского происхождения. БП была уточнена у одного из каждой пары близнецов; длительность течения болезни у близнеца с БП составило по меньшей мере 7 лет.; длительность течения болезни у близнеца с БП составила по меньшей мере 7 лет. Были проанализированы метиломы крови и отобраны точки варьирующегося метилирования. Нами было найдено 8 дифференциально экспрессирующихся генов, которые могут быть дифференциально метилированы. Были выявлены различия между здоровым близнецом и близнецом с БП по уровню метилирования ДНК для ряда этих генов в клеточных линиях фибробластов. Полученные нами данные могут указывать на участие процесса ДНК-метилирования в регуляции транскрипции кандидатных генов-участников патогенеза БП. In recent years it has been convincingly demonstrated that genetic factors play an important role in progression of Parkinson’s disease (PD). Since the etiology of PD has not been elucidated completely yet, it is crucial to shift focus of the research to the broader areas - to dive into investigations of methylome and transcriptome. Epigenetic regulation of gene expression may take part in pathogenesis of PD. Changes in epigenome can be conveniently investigated in case of individuals with almost identical genetic makeup, and monozygotic twins discordant for PD may be such “model”. 3 pairs phenotypically and genotypically monozygous twins of Russian ancestry were enrolled in the study. PD was diagnosed in one of each pair. The disease duration was at least 7 years. Data on blood methylomes was analyzed. Points of variable methylation in blood methylomes were selected. With this approach, 8 differentially expressed genes were found that also may be differentially methylated. Changes in methylation level for some of this genes were found in monozygotic twins discordant for PD fibroblasts cell-lines between healthy and afflicted siblings. Acquired data might suggest participation of DNA-methylation in transcription regulation of PD pathogenesis-related candidate genes.


Blood ◽  
1989 ◽  
Vol 74 (5) ◽  
pp. 1557-1562 ◽  
Author(s):  
H Onoue ◽  
Y Ebi ◽  
H Nakayama ◽  
XM Ru ◽  
Y Kitamura ◽  
...  

Abstract Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3T3 cells did not affect the growth factor-dependent proliferation of CMC, but WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells significantly suppressed the proliferation. Close cell-to-cell contact was necessary for the suppression. The NWS1 fibroblast cell line was established from the spleen cells of an adult WBB6F1-+/+ mouse. Although the NWS1 cell line had no supporting effect on the proliferation of CMC in the absence of diffusible growth factors, it did not suppress the proliferation of CMC induced by the growth factors. The present result suggests that a product of mutant Sl genes may be involved in the suppressive activity of WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells.


1986 ◽  
Vol 33 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Alan E. Levine ◽  
Craig A. Crandall ◽  
Diane Brattain ◽  
Subhas Chakrabarty ◽  
Michael G. Brattain

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1058
Author(s):  
Juan Manuel Velázquez-Enríquez ◽  
Jovito Cesar Santos-Álvarez ◽  
Alma Aurora Ramírez-Hernández ◽  
Edilburga Reyes-Jiménez ◽  
Armando López-Martínez ◽  
...  

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible, and highly fatal disease. It is characterized by the increased activation of both fibroblast and myofibroblast that results in excessive extracellular matrix (ECM) deposition. Extracellular vesicles (EVs) have been described as key mediators of intercellular communication in various pathologies. However, the role of EVs in the development of IPF remains poorly understood. This study aimed to characterize the differentially expressed proteins contained within EVs cargo derived from the fibroblast cell lines LL97A (IPF-1) and LL29 (IPF-2) isolated from lungs bearing IPF as compared to those derived from the fibroblast cell lines CCD8Lu (NL-1) and CCD19Lu (NL-2) isolated from healthy donors. Isolated EVs were subjected to label-free quantitative proteomic analysis by LC-MS/MS, and as a result, 331 proteins were identified. Differentially expressed proteins were obtained after the pairwise comparison, including all experimental groups. A total of 86 differentially expressed proteins were identified in either one or more comparison groups. Of note, proteins involved in fibrogenic processes, such as tenascin-c (TNC), insulin-like-growth-factor-binding protein 7 (IGFBP7), fibrillin-1 (FBN1), alpha-2 collagen chain (I) (COL1A2), alpha-1 collagen chain (I) (COL1A1), and lysyl oxidase homolog 1 (LOXL1), were identified in EVs cargo isolated from IPF cell lines. Additionally, KEGG pathway enrichment analysis revealed that differentially expressed proteins participate in focal adhesion, PI3K-Akt, and ECM–receptor interaction signaling pathways. In conclusion, our findings reveal that proteins contained within EVs cargo might play key roles during IPF pathogenesis.


Blood ◽  
1989 ◽  
Vol 74 (5) ◽  
pp. 1557-1562
Author(s):  
H Onoue ◽  
Y Ebi ◽  
H Nakayama ◽  
XM Ru ◽  
Y Kitamura ◽  
...  

Two modes of mast cell growth are present, one dependent on diffusible growth factors (interleukins [IL] 3 and 4) and another dependent on contact with fibroblasts. The 3T3 fibroblast cell lines derived from WCB6F1-+/+ mouse embryos supported the proliferation of cultured mast cells (CMC), whereas the 3T3 fibroblast cell lines from WCB6F1-Sl/Sld mouse embryos did not. To investigate the relationship between growth factor-dependent and fibroblast-dependent growths of mast cells, we cocultured CMC and 3T3 fibroblasts in the presence of diffusible growth factors. WCB6F1-+/+ mouse embryo-derived 3T3 cells did not affect the growth factor-dependent proliferation of CMC, but WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells significantly suppressed the proliferation. Close cell-to-cell contact was necessary for the suppression. The NWS1 fibroblast cell line was established from the spleen cells of an adult WBB6F1-+/+ mouse. Although the NWS1 cell line had no supporting effect on the proliferation of CMC in the absence of diffusible growth factors, it did not suppress the proliferation of CMC induced by the growth factors. The present result suggests that a product of mutant Sl genes may be involved in the suppressive activity of WCB6F1-Sl/Sld mouse embryo-derived 3T3 cells.


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