scholarly journals Effects of H3 and H4 Histones Acetylation and Bindings of CREB Binding Protein and p300 at the Promoter on Hepatic Expression of γ-glutamyltransferase Gene in a Streptozotocin-Induced Moderate Hypoinsulinemic Rat Model

2021 ◽  
pp. 475-480
Author(s):  
T TANAKA ◽  
T MIZUNO ◽  
T NAKAGAWA ◽  
T HAYAKAWA ◽  
M SHIMADA
Keyword(s):  
Insulin Secretion ◽  
Rat Model ◽  
Binding Protein ◽  
Histone Acetyltransferases ◽  
Creb Binding Protein ◽  
Concerted Effort ◽  
Promoter Regions ◽  
Gamma Glutamyltransferase ◽  
Hepatic Expression ◽  
Increased Risk

Gamma-glutamyltransferase (GGT), a marker of liver disease, has been shown to be associated with increased risk of diabetes and relative insulin secretion deficiency. However, the mechanism of hepatic Ggt regulation has not been explored fully. In this study, we made a concerted effort to understand the mechanism by investigating the effects of acetylation of histones H3 and H4, and bindings of histone acetyltransferases, CREB binding protein (CBP) and p300, at the Ggt promoter on the regulation of the expression of Ggt gene in the livers of streptozotocin (STZ)-induced moderate hypoinsulinemia rat model. The rats treated with STZ showed remarkably higher serum GGT level and hepatic Ggt/GGT expression than the untreated control rats. Furthermore, the acetylation of histones H3 and H4, and the binding of CBP not p300 at the Ggt promoter regions were significantly higher in the livers of STZ rats than those of the control rats. These results suggest that an enhanced hepatic expression of Ggt is associated with increased acetylation of histones H3 and H4 and CBP binding at the Ggt promoter in STZ-induced moderate hypoinsulinemic rats.

PPARδ-mediated p21/p27 induction via increased CREB-binding protein nuclear translocation in beraprost-induced antiproliferation of murine aortic smooth muscle cells

2009 ◽  
Vol 297 (2) ◽  
pp. C321-C329 ◽  
Author(s):  
Yuh-Mou Sue ◽  
Chih-Peng Chung ◽  
Heng Lin ◽  
Ying Chou ◽  
Chih-Yu Jen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transcriptional Activation ◽  
Nuclear Translocation ◽  
Binding Protein ◽  
Peroxisome Proliferator ◽  
Creb Binding Protein ◽  
Promoter Regions ◽  
Peroxisome Proliferator Activated Receptor ◽  
Aortic Smooth Muscle ◽  
Responsive Element

We previously showed that an increase in the peroxisome proliferator-activated receptor-δ (PPARδ), together with subsequent induction of inducible nitric oxide synthase (iNOS) by beraprost (BPS), inhibits aortic smooth muscle cell proliferation. Herein, we delineated the mechanisms of the antiproliferative effects of BPS through the induction of p21/p27. BPS concentration dependently induced the p21/p27 promoter- and consensus cAMP-responsive element (CRE)-driven luciferase activities, which were significantly suppressed by blocking PPARδ activation. Surprisingly, other than altering the CRE-binding protein (CREB), BPS-mediated PPARδ activation increased nuclear localization of the CREB-binding protein (CBP), a coactivator, which was further confirmed by chromatin immunoprecipitation. Furthermore, novel functional PPAR-responsive elements (PPREs) next to CREs in the rat p21/p27 promoter regions were identified, where PPARδ interacted with CREB through CBP recruitment. BPS-mediated suppression of restenosis in mice with angioplasty was associated with p21/p27 induction. Herein, we demonstrate for the first time that BPS-mediated PPARδ activation enhances transcriptional activation of p21/p27 by increasing CBP nuclear translocation, which contributes to the vasoprotective action of BPS.

Recovery of glucose-induced insulin secretion in a rat model of NIDDM is not accompanied by return of the B-cell GLUT2 glucose transporter

Diabetes ◽  
1992 ◽  
Vol 41 (10) ◽  
pp. 1320-1327 ◽  
Author(s):  
C. Chen ◽  
B. Thorens ◽  
S. Bonner-Weir ◽  
G. C. Weir ◽  
J. L. Leahy
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Rat Model ◽  
Glucose Transporter ◽  
Glut2 Glucose Transporter

CREB-binding protein (CREBBP) and preeclampsia: a new promising target gene

2021 ◽  
Vol 48 (3) ◽  
pp. 2117-2122
Author(s):  
Hossein Sadeghi ◽  
Sahra Esmkhani ◽  
Reihaneh Pirjani ◽  
Mona Amin-Beidokhti ◽  
Milad Gholami ◽  
...  
Keyword(s):  
Target Gene ◽  
Binding Protein ◽  
Creb Binding Protein ◽  
Promising Target

scholarly journals Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

2021 ◽  
Vol 22 (7) ◽  
pp. 3762
Author(s):  
Sarah M. Kedziora ◽  
Kristin Kräker ◽  
Lajos Markó ◽  
Julia Binder ◽  
Meryam Sugulle ◽  
...  
Keyword(s):  
Rat Model ◽  
Renal Damage ◽  
Kidney Injury ◽  
Tissue Growth ◽  
Female Rats ◽  
Male Rats ◽  
Renal Diseases ◽  
Transgenic Rat ◽  
Increased Risk ◽  
Before And After

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.

Sign in / Sign up

Export Citation Format

Share Document