LTBP-1 blockade in dioxin receptor-null mouse embryo fibroblasts decreases TGF-β activity: Role of extracellular proteases plasmin and elastase

2006 ◽  
Vol 97 (2) ◽  
pp. 380-392 ◽  
Author(s):  
Aurea Gomez-Duran ◽  
Sonia Mulero-Navarro ◽  
Xiaoqing Chang ◽  
Pedro M. Fernandez-Salguero
Keyword(s):  
Mouse Embryo ◽  
Null Mouse ◽  
Extracellular Proteases ◽  
Mouse Embryo Fibroblasts ◽  
Embryo Fibroblasts ◽  
Dioxin Receptor

scholarly journals Rapamycin-independent IGF2 expression in Tsc2-null mouse embryo fibroblasts and human lymphangioleiomyomatosis cells

PLoS ONE ◽  
2018 ◽  
Vol 13 (5) ◽  
pp. e0197105 ◽  
Author(s):  
Blanca E. Himes ◽  
Kseniya Obraztsova ◽  
Lurong Lian ◽  
Maya Shumyatcher ◽  
Ryan Rue ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Null Mouse ◽  
Mouse Embryo Fibroblasts ◽  
Embryo Fibroblasts ◽  
Igf2 Expression

Immortalized mouse embryo fibroblasts are resistant to miR-290-induced senescence regardless of p53 status

2011 ◽  
Vol 43 (20) ◽  
pp. 1153-1159
Author(s):  
Milena Rizzo ◽  
Monica Evangelista ◽  
Laura Mariani ◽  
Marcella Simili ◽  
Giuseppe Rainaldi ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Mouse Embryo ◽  
Nih3t3 Cells ◽  
Mouse Embryo Fibroblasts ◽  
Primary Mouse ◽  
Murine Fibroblasts ◽  
P53 Status ◽  
Embryo Fibroblasts ◽  
Potential Tumor Suppressor

The prosenescence role of miR-290 and nocodazole has been documented in primary mouse embryo fibroblasts (MEF), while it is not clear whether immortal murine fibroblasts are still responsive to these senescence inducing stimuli. To establish this point, immortal murine fibroblasts with functional (NIH3T3) or nonfunctional p53 (I-MEF) and low levels of miR-290 were tested for their capability to undergo senescence after exposure to either nocodazole or miR-290. Our results clearly indicate that nocodazole induces senescence only in NIH3T3 cells with a functional p53 but not in I-MEF lacking a functional p53. miR-290 overexpression is unable to address any of the tested immortalized clones toward senescence, regardless of the p53 status, suggesting that the prosenescence role of miR-290 is specific for primary but not for immortal murine fibroblasts. Moreover our findings suggest that the mere downregulation of a potential tumor suppressor miRNA in a given cell type does not necessarily imply that it behaves as a tumor suppressor.

scholarly journals 5′-AMP-Activated Protein Kinase (AMPK) Is Induced by Low-Oxygen and Glucose Deprivation Conditions Found in Solid-Tumor Microenvironments

2006 ◽  
Vol 26 (14) ◽  
pp. 5336-5347 ◽  
Author(s):  
Keith R. Laderoute ◽  
Khalid Amin ◽  
Joy M. Calaoagan ◽  
Merrill Knapp ◽  
Theresamai Le ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mouse Embryo ◽  
Cellular Response ◽  
Null Mouse ◽  
Low Oxygen ◽  
Tumor Microenvironments ◽  
Mouse Embryo Fibroblasts ◽  
Embryo Fibroblasts ◽  
Amp Activated Protein Kinase

ABSTRACT Low oxygen gradients (hypoxia and anoxia) are important determinants of pathological conditions under which the tissue blood supply is deficient or defective, such as in solid tumors. We have been investigating the relationship between the activation of hypoxia-inducible factor 1 (HIF-1), the primary transcriptional regulator of the mammalian response to hypoxia, and 5′-AMP-activated protein kinase (AMPK), another regulatory system important for controlling cellular energy metabolism. In the present study, we used mouse embryo fibroblasts nullizygous for HIF-1α or AMPK expression to show that AMPK is rapidly activated in vitro by both physiological and pathophysiological low-oxygen conditions, independently of HIF-1 activity. These findings imply that HIF-1 and AMPK are components of a concerted cellular response to maintain energy homeostasis in low-oxygen or ischemic-tissue microenvironments. Finally, we used transformed derivatives of wild-type and HIF-1α- or AMPKα-null mouse embryo fibroblasts to determine whether AMPK is activated in vivo. We obtained evidence that AMPK is activated in authentic hypoxic tumor microenvironments and that this activity overlaps with regions of hypoxia detected by a chemical probe. We also showed that AMPK is important for the growth of this tumor model.

miR-290 acts as a physiological effector of senescence in mouse embryo fibroblasts

2009 ◽  
Vol 39 (3) ◽  
pp. 210-218 ◽  
Author(s):  
Letizia Pitto ◽  
Milena Rizzo ◽  
Marcella Simili ◽  
Daria Colligiani ◽  
Monica Evangelista ◽  
...  
Keyword(s):  
Mouse Embryo ◽  
Expression Profiles ◽  
Embryonic Stem ◽  
Related Factor ◽  
Transcriptional Change ◽  
Differentiated Cells ◽  
Mouse Embryo Fibroblasts ◽  
Mirna Expression Profiles ◽  
Embryo Fibroblasts

The culture-induced senescence of mouse embryo fibroblasts (MEF) correlates with reduction of cell proliferation. In this work we found that the accumulation of cells with 4C DNA content and the transcriptional change of several microRNAs (miRNAs or miRs) are relevant events in culture senescence. By comparing the miRNA expression profiles of physiologically senescent MEF and that of senescent MEF induced by the downregulation of leukemia-related factor, we identified miR-290 as a common upregulated miRNA. When miR-290 was transfected in presenescent MEF, SA-β-gal+ cells and p16, two markers of culture senescence, increased compared with control, indicating that miR-290 is causally involved in senescence. Interestingly, nocodazole (NCZ), which induces G2/M block, increased the percentage of senescent cells as well as the expression of miR-290 and of the tumor suppressor p16, thus mimicking culture senescence. As miR-290 was overexpressed in NCZ-treated cells and it was able to induce senescence in proliferating MEF, we investigated whether miR-290 and NCZ could share common mechanisms of culture senescence. Whereas the induction of SA-β-gal+ by miR-290 was not strengthened by coupling its transfection with NCZ treatment, the transfection of the antagomir 290 (d-290) plus NCZ treatment, while blocking cells at G2/M, suppressed SA-β-gal+ and p16 induction. On the basis of these findings we conclude that miR-290 might act as a physiological effector of NCZ induced as well as culture senescence via p16 regulation expanding the role of this miRNA from embryonic stem to differentiated cells.

Sign in / Sign up

Export Citation Format

Share Document