Induction of Early Growth Response-1 Mediates Microglia Activation In Vitro But is Dispensable In Vivo

2009 ◽  
Vol 11 (2) ◽  
pp. 87-96 ◽  
Author(s):  
Thomas Langmann ◽  
Stefanie Ebert ◽  
Yana Walczak ◽  
Karin Weigelt ◽  
Markus U. Ehrengruber ◽  
...  
Keyword(s):  
Growth Response ◽  
Early Growth ◽  
Microglia Activation ◽  
Early Growth Response ◽  
Early Growth Response 1

scholarly journals Early Growth Response 1 Acts as a Tumor Suppressor In vivo and In vitro via Regulation of p53

2005 ◽  
Vol 65 (12) ◽  
pp. 5133-5143 ◽  
Author(s):  
Anja Krones-Herzig ◽  
Shalu Mittal ◽  
Kelly Yule ◽  
Hongyan Liang ◽  
Chris English ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Growth Response ◽  
Early Growth ◽  
Early Growth Response ◽  
Early Growth Response 1

scholarly journals Early Growth Response Protein 1 Binds to the Luteinizing Hormone-β Promoter and Mediates Gonadotropin-Releasing Hormone-Stimulated Gene Expression

1999 ◽  
Vol 13 (5) ◽  
pp. 752-763 ◽  
Author(s):  
Michael W. Wolfe ◽  
Gerald B. Call
Keyword(s):  
Growth Response ◽  
Early Growth ◽  
Steroidogenic Factor 1 ◽  
Response Elements ◽  
Cis Acting ◽  
Early Growth Response ◽  
Endogenous Expression ◽  
Synergistic Activation

Abstract The hypothalamic neuropeptide, GnRH, regulates the synthesis and secretion of LH from pituitary gonadotropes. Furthermore, it has been shown that the LH β-subunit gene is regulated by the transcription factors steroidogenic factor-1 (SF-1) and early growth response protein 1 (Egr1) in vitro and in vivo. The present study investigated the roles played by Egr1 and SF-1 in regulating activity of the equine LHβ-subunit promoter in the gonadotrope cell line, αT3–1, and the importance of these factors and cis-acting elements in regulation of the promoter by GnRH. All four members of the Egr family were found to induce activity of the equine promoter. The region responsible for induction by Egr was localized to the proximal 185 bp of the promoter, which contained two Egr response elements. Coexpression of Egr1 and SF-1 led to a synergistic activation of the equine (e)LHβ promoter. Mutation of any of the Egr or SF-1 response elements attenuated this synergism. Endogenous expression of Egr1 in αT3–1 cells was not detectable under basal conditions, but was rapidly induced after GnRH stimulation. Reexamination of the promoter constructs harboring mutant Egr or SF-1 sites indicated that these sites were required for GnRH induction. In fact, mutation of both Egr sites within the eLHβ promoter completely attenuated its induction by GnRH. Thus, GnRH induces expression of Egr1, which subsequently activates the eLHβ promoter. Finally, GnRH not only induced expression of Egr1, but also its corepressor, NGFI-A (Egr1) binding protein (Nab1), which can repress Egr1- induced transcription of the eLHβ promoter.

scholarly journals Helicobacter pylori Activates the Early Growth Response 1 Protein in Gastric Epithelial Cells

2004 ◽  
Vol 72 (6) ◽  
pp. 3549-3560 ◽  
Author(s):  
M. M. M. Abdel-Latif ◽  
H. J. Windle ◽  
K. A. Fitzgerald ◽  
Y. S. Ang ◽  
D. Ní Eidhin ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Growth Response ◽  
Early Growth ◽  
Dependent Manner ◽  
Mobility Shift ◽  
Ags Cells ◽  
Early Growth Response ◽  
H Pylori ◽  
Early Growth Response 1

ABSTRACT The early growth response 1 (Egr-1) transcription factor is rapidly induced by various stimuli and is implicated in the regulation of cell growth, differentiation, and gene expression. The aim of this study was to examine the effect of Helicobacter pylori on the expression of Egr-1 and Egr-1-regulated genes in gastric epithelial AGS cells. Egr-1 expression was assayed by immunoblotting and electrophoretic mobility shift assays using H. pylori-stimulated AGS cells. Transient transfection experiments with promoter-reporter constructs of CD44, ICAM-1, and CD95L were used for expression studies. H. pylori induced the expression of Egr-1 in gastric epithelial cell lines in a dose-dependent manner, with the rapid kinetics that are typical of this class of transcription factors. Immunohistochemical studies of biopsies revealed that Egr-1 expression is more abundant in H. pylori-positive patients than in uninfected individuals. Reporter-promoter transfection studies indicated that Egr-1 binding is required for the H. pylori-induced transcriptional promoter activity of the CD44, ICAM-1, and CD95L (APO-1/Fas) constructs. The blocking of egr-1 with an antisense sequence prevented H. pylori-induced Egr-1 and CD44 protein expression. The MEK1/2 signaling cascade participates in H. pylori-mediated Egr-1 expression, but the p38 pathway does not. The data indicate that H. pylori induces Egr-1 expression in AGS cells in vitro and that the Egr-1 protein is readily detectable in biopsies from H. pylori-positive subjects. These observations suggest that H. pylori-associated Egr-1 expression may play a role, in part, in H. pylori-induced pathology.

Role of early growth response 1 in arteriogenesis: Impact on vascular cell proliferation and leukocyte recruitment in vivo

2012 ◽  
Vol 107 (03) ◽  
pp. 562-574 ◽  
Author(s):  
Tibor Ziegelhoeffer ◽  
Matthias Heil ◽  
Silvia Fischer ◽  
Borja Fernández ◽  
Wolfgang Schaper ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Femoral Artery ◽  
Growth Response ◽  
Early Growth ◽  
Leukocyte Recruitment ◽  
Artery Ligation ◽  
Vascular Cell ◽  
Early Growth Response ◽  
Early Growth Response 1

SummaryBased on previous findings that early growth response 1 (Egr-1) participates in leukocyte recruitment and cell proliferation in vitro, this study was designed to investigate its mode of action during arteriogenesis in vivo. In a model of peripheral arteriogenesis, Egr-1 was significantly upregulated in growing collaterals of wild-type (WT) mice, both on mRNA and protein level. Egr-1−/− mice demonstrated delayed arteriogenesis after femoral artery ligation. They further showed increased levels of monocytes and granulocytes in the circulation, but reduced levels in adductor muscles under baseline conditions. After femoral artery ligation, elevated numbers of macrophages were detected in the perivascular zone of collaterals in Egr-1−/− mice and mRNA of leukocyte recruitment mediators was upregulated. Other Egr family members (Egr-2 to -4) were significantly upregulated only in Egr-1−/− mice, suggesting a mechanism of counterbalancing Egr-1 deficiency. Moreover, splicing factor-1, downregulated in WT mice after femoral artery ligation in the process of increased vascular cell proliferation, was upregulated in Egr-1−/− mice. αSM-actin on the other hand, significantly downregulated in WT mice, showed no differential expression in Egr-1−/− mice. While cell cycle regulator cyclin E and cdc20 were upregulated in Egr-1−/− mice, cyclin D1 expression decreased below the detection limit in collaterals, and the proliferation marker ki67 was not differentially expressed. In conclusion, compensation for deficiency in Egr-1 function in leukocyte recruitment can presumably be mediated by other transcription factors; however, Egr-1 is indispensable for effective vascular cell cycle progression in arteriogenesis.

Abstract 133: Transcription Factor Early Growth Response 1 Promotes T-Type Calcium Channel Cav3.2 in Response to Hypertrophic Stimulation Through Evolutionary Conserved Promoter

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Shao-Chun Hsu ◽  
Chien-Chang Chen
Keyword(s):  
Transcription Factor ◽  
Cardiac Hypertrophy ◽  
Calcium Channel ◽  
Reporter Gene ◽  
Growth Response ◽  
Regulatory Elements ◽  
Early Growth ◽  
Early Growth Response ◽  
Early Growth Response 1

Introduction: Although it is known that the Ca v 3.2 T-type calcium channel is predominantly expressed in the embryonic stage and re-expressed in adult hearts during the cardiac hypertrophy. What does regulate the reexpression of Ca v 3.2 in hearts? Hypothesis: Because the mRNA re-expression is mainly through the transcriptional regulation in the promoter or enhancer conserved in different species, we assessed to the hypothesis that the evolutionary conserved promoter (ECP) of Ca v 3.2 carries important binding sites for transcription factors that regulate its re-expression in the hypertrophic hearts. Methods and Results: In this study, the ECP is gotten by aligning Ca v 3.2 genes from different species. By fusing mouse ECP with the reporter gene firefly luciferase, we showed that the ECP drove high luciferase activity in the cells expressing endogenous Ca v 3.2 but not in the one without Ca v 3.2. To further validate ECP in vivo, Ca v 3.2 reporter mice were generated by fusing the Ca v 3.2 promoter with the reporter gene luciferase. ECP confers the reporter expressing as the endogenous Ca v 3.2 in the tissue distribution, development of hearts, and most importantly, the inducibility of hypertrophic stimuli. By injecting reporters driven by different truncated promoters followed with the trans-aortic banding (TAB) surgery, the hypertrophic regulatory elements are identified_ -41 to -81 relative to the transcription start site (TSS) of Ca v 3.2. At the end, we found the early growth response 1 (Egr1) is the important transcription factor to enhance Ca v 3.2 gene expression. Our EMSA data suggested that Egr1 can bind to three regions of the hypertrophic regulatory elements. Conclusion: In conclusion, transcription factor early growth response 1 (Egr1) regulates the reexpression of Ca v 3.2 T-type Calcium Channel in the cardiac hypertrophy.

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