scholarly journals Effects of BDNF, T3, and corticosterone on expression of the hypothalamic obesity gene network in vivo and in vitro

2009 ◽  
Vol 296 (4) ◽  
pp. R1180-R1189 ◽  
Author(s):  
Mardi S. Byerly ◽  
Jean Simon ◽  
Elisabeth Lebihan-Duval ◽  
Michel J. Duclos ◽  
Larry A. Cogburn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Composition ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Energy Regulation ◽  
Underlying Mechanisms ◽  
Agouti Related Protein ◽  
Receptor Gene Expression

Hypothalamic neuropeptides, neurotrophins, and systemic hormones modulate food intake and body composition. Although advances toward elucidating these interactions have been made, many aspects of the underlying mechanisms remain vague. Hypothalami from fat and lean chicken lines were assessed for differential expression of anabolic/orexigenic and catabolic/anorexigenic genes. Effects of triiodothyronine (T3), corticosterone (Cort), and brain-derived neurotrophic factor (BDNF) on expression of anabolic/orexigenic and catabolic/anorexigenic genes were tested in cultures of hypothalamic neurons. From this, we found that BDNF increased and T3 decreased gene expression for BDNF, leptin receptor (LEPR), pro-opiomelanocortin (POMC), thyrotropin releasing hormone (TRH), and agouti-related protein (AGRP). Thyroid hormone levels were manipulated during development to show that T3 inhibited BDNF, TRH, and BDNF receptor gene expression. Delivery of T3, Cort, T3 plus Cort, or vehicle in vivo continuously for 72 h indicated that Cort and T3 have overlapping roles in regulating TRH, LEPR, and POMC gene expression and that Cort and T3 regulate BDNF, neuropeptide Y, and AGRP in opposite directions. Collectively, these findings suggest that interactions between the neuropeptide BDNF and the hormones T3 and/or Cort may constitute a homeostatic mechanism that links hypothalamic energy regulation controlling body composition.

scholarly journals Circulating leptin during ovine pregnancy in relation to maternal nutrition, body composition and pregnancy outcome

2001 ◽  
Vol 169 (3) ◽  
pp. 465-476 ◽  
Author(s):  
L Thomas ◽  
JM Wallace ◽  
RP Aitken ◽  
JG Mercer ◽  
P Trayhurn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Composition ◽  
Adipose Tissue ◽  
Dietary Intake ◽  
Leptin Receptor ◽  
Maternal Nutrition ◽  
Receptor Gene ◽  
Mrna Levels ◽  
Tissue Samples ◽  
Receptor Gene Expression

This study examined the pattern of circulating leptin in age-matched sheep during adolescent pregnancy, and its relationship with maternal dietary intake, body composition and tissue expression of the leptin gene. Overfeeding the adolescent pregnant ewe results in rapid maternal growth at the expense of the placenta, leading to growth restriction in the fetus, compared with normal fed controls. Our results demonstrate that, in the adolescent ewe, overfeeding throughout pregnancy was associated with higher maternal leptin concentrations, when compared with moderately fed controls (P<0.05), with no peak in circulating leptin towards the end of pregnancy. There was a close correlation between indices of body composition and circulating leptin levels at day 104 of gestation and at term (P<0.03). Further, when the dietary intake was switched from moderate to high, or high to moderate, at day 50 of gestation, circulating leptin levels changed rapidly, in parallel with the changes in dietary intake. Leptin mRNA levels and leptin protein in perirenal adipose tissue samples, taken at day 128 of gestation, were higher in overfed dams (P<0.04), suggesting that adipose tissue was the source of the increase in circulating leptin in the overnourished ewes. Leptin protein was also detected in placenta but leptin gene expression was negligible. However, leptin receptor gene expression was detected in the ovine placenta, suggesting that the placenta is a target organ for leptin. A negative association existed between maternal circulating leptin and fetal birth weight, placental/cotyledon weight and cotyledon number. In conclusion, in this particular ovine model, hyperleptinaemia was not observed during late pregnancy. Instead, circulating leptin concentrations reflected increased levels of leptin secretion by adipose tissue primarily as a result of the increase in body fat deposition, due to overfeeding. However, there appears to be a direct effect of overfeeding, particularly in the short term. In the nutritional switch-over study, circulating leptin concentrations changed within 48 h of the change in dietary intake. The presence of leptin protein and leptin receptor gene expression in the placenta suggests that leptin could be involved in nutrient partitioning during placental and/or fetal development.

scholarly journals Up-regulation of interleukin (IL)-6 receptor gene expression in vitro and in vivo in IL-6 deprived myeloma cells

FEBS Letters ◽  
1992 ◽  
Vol 302 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Marielle Portier ◽  
Delphine Lees ◽  
Emmanuelle Caron ◽  
Michel Jourdan ◽  
Jean-Michel Boiron ◽  
...  
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Myeloma Cells ◽  
Receptor Gene Expression

scholarly journals Induction of VEGF and VEGF receptor gene expression by hypoxia: Divergent regulation in vivo and in vitro

1997 ◽  
Vol 51 (2) ◽  
pp. 448-453 ◽  
Author(s):  
Peter Sandner ◽  
Konrad Wolf ◽  
Ulrike Bergmaier ◽  
Bernhard Gess ◽  
Armin Kurtz
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Vegf Receptor ◽  
Receptor Gene Expression

scholarly journals Effects of ANG II on bradykinin receptor gene expression in cardiomyocytes and vascular smooth muscle cells

2001 ◽  
Vol 281 (4) ◽  
pp. H1778-H1783 ◽  
Author(s):  
Ekaterina Kintsurashvili ◽  
Irena Duka ◽  
Irene Gavras ◽  
Conrado Johns ◽  
Dimitrios Farmakiotis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Knockout ◽  
Receptor Gene ◽  
Ang Ii ◽  
Wild Type ◽  
Receptor Mrna ◽  
Gene Knockout Mice ◽  
Receptor Gene Expression

Bradykinin has vasodilatory and tissue-protective effects exerted via its B2 type receptor, whereas the B1 receptor is constitutively absent but inducible by inflammation and toxins. In previous studies, we found that B2 receptor gene knockout mice exhibit overexpression of the B1 receptor, which assumes a vasodilatory function and is further upgraded in renovascular hypertension. The present study was designed to explore the effects of excess angiotensin II (ANG II) on B1 receptor and B2 receptor gene expression in mouse cardiomyocytes and rat vascular smooth muscle cells (VSMC) in vivo (after a 3-day infusion of 30 ng/min ANG II in 11 wild-type and in 13 genetically engineered mice with deleted B2 receptor gene) and in vitro (ANG II added in rat VSMC culture in the presence or absence of AT1 or AT2 receptor antagonist). Expression of B1 and B2 receptor mRNA was assessed by reverse transcriptase-polymerase chain reaction. ANG II infusion caused upregulation by 30% of the already significantly overexpressed B1 receptors in cardiomyocytes of the B2receptor gene knockout mice, but in the wild-type mice it upregulated only the B2 receptor mRNA by 47%. The addition of ANG II in VSMC culture produced a time-dependent induction of B1and upregulation of B2 receptor gene expression, maximal at 3 h (by fivefold), declining almost to baseline by 24 h. The addition of losartan completely blocked this effect, whereas the AT2 blocker PD-123319 made no difference, indicating that this is an AT1-mediated effect of ANG II. The data indicate that excess ANG II in subpressor doses in vivo upregulates expression of the B2 receptor, but in its absence, the already overexpressed B1 receptor is further upregulated, evidently assuming a counterregulatory response; in vitro, it transiently upregulates both bradykinin receptors.

scholarly journals CircFAM13B promotes the proliferation of hepatocellular carcinoma by sponging miR-212, upregulating E2F5 expression and activating the P53 pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Xie ◽  
Xiaofeng Hang ◽  
Wensheng Xu ◽  
Jing Gu ◽  
Yuanjing Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Gene Expression Omnibus ◽  
Differentially Expressed ◽  
In Vivo Studies ◽  
Circular Rnas ◽  
Novel Target ◽  
Underlying Mechanisms

Abstract Background Most of the biological functions of circular RNAs (circRNAs) and the potential underlying mechanisms in hepatocellular carcinoma (HCC) have not yet been discovered. Methods In this study, using circRNA expression data from HCC tumor tissues and adjacent tissues from the Gene Expression Omnibus database, we identified out differentially expressed circRNAs and verified them by qRT-PCT. Functional experiments were performed to evaluate the effects of circFAM13B in HCC in vitro and in vivo. Results We found that circFAM13B was the most significantly differentially expressed circRNA in HCC tissue. Subsequently, in vitro and in vivo studies also demonstrated that circFAM13B promoted the proliferation of HCC. Further studies revealed that circFAM13B, a sponge of miR-212, is involved in the regulation of E2F5 gene expression by competitively binding to miR-212, inhibits the activation of the P53 signalling pathway, and promotes the proliferation of HCC cells. Conclusions Our findings revealed the mechanism underlying the regulatory role played by circFAM13B, miR-212 and E2F5 in HCC. This study provides a new theoretical basis and novel target for the clinical prevention and treatment of HCC.

scholarly journals c-Jun N-Terminal Kinase Activation of Activator Protein-1 Underlies Homologous Regulation of the Gonadotropin-Releasing Hormone Receptor Gene in αT3-1 Cells

Endocrinology ◽  
2003 ◽  
Vol 144 (3) ◽  
pp. 839-849 ◽  
Author(s):  
Buffy S. Ellsworth ◽  
Brett R. White ◽  
Ann T. Burns ◽  
Brian D. Cherrington ◽  
Annette M. Otis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Cell Model ◽  
Receptor Gene ◽  
Critical Role ◽  
Dominant Negative ◽  
Activator Protein 1 ◽  
Activator Protein

Reproductive function is dependent on the interaction between GnRH and its cognate receptor found on gonadotrope cells of the anterior pituitary gland. GnRH activation of the GnRH receptor (GnRHR) is a potent stimulus for increased expression of multiple genes including the gene encoding the GnRHR itself. Thus, homologous regulation of the GnRHR is an important mechanism underlying gonadotrope sensitivity to GnRH. Previously, we have found that GnRH induction of GnRHR gene expression in αT3-1 cells is partially mediated by protein kinase C activation of a canonical activator protein-1 (AP-1) element. In contrast, protein kinase A and a cAMP response element-like element have been implicated in mediating the GnRH response of the GnRHR gene using a heterologous cell model (GGH3). Herein we find that selective removal of the canonical AP-1 site leads to a loss of GnRH regulation of the GnRHR promoter in transgenic mice. Thus, an intact AP-1 element is necessary for GnRH responsiveness of the GnRHR gene both in vitro and in vivo. Based on in vitro analyses, GnRH appeared to enhance the interaction of JunD, FosB, and c-Fos at the GnRHR AP-1 element. Although enhanced binding of cFos reflected an increase in gene expression, GnRH appeared to regulate both FosB and JunD at a posttranslational level. Neither overexpression of a constitutively active Raf-kinase nor pharmacological blockade of GnRH-induced ERK activation eliminated the GnRH response of the GnRHR promoter. GnRH responsiveness was, however, lost in αT3-1 cells that stably express a dominant-negative c-Jun N-terminal kinase (JNK) kinase, suggesting a critical role for JNK in mediating GnRH regulation of the GnRHR gene. Consistent with this possibility, we find that the ability of forskolin and membrane-permeable forms of cAMP to inhibit the GnRH response of the GnRHR promoter is associated with a loss of both JNK activation and GnRH-mediated recruitment of the primary AP-1-binding components.

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