Gene expression profile regulated by leptin
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Chun-Ju (Alice) Chang
PROVIDER: E-GEOD-58059 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Osteoarthritis (OA) is the most prevalent chronic joint disease and the precise genetic mechanisms are yet to be fully elucidated. The aim of this study is to evaluate, for the first time, the differences in gene expression profiles of healthy and leptin-induced cartilage in rat. To investigate the underlying pathogenic factors in OA, alterations in gene expression between leptin-induced articular cartilage rat models and healthy control rat models were investigated using the Whole Rat Genome Oligo Microarray. In the present study, 1857 differentially expressed genes (DEGs; 1197 up-regulated and 660 down-regulated) were identified. Expression of some OA-related known genes is known to be associated with leptin induction, including matrix metalloproteinase (MMP), inflammatory factors, growth factors and genes involved in cell death, apoptosis and osteoclast differentiation. However, some new candidate genes that had never been reported to be related with OA, such as BCL2L11, were consistently observed to be up-regulated, suggesting they might be involved in OA progression. Our findings indicate that leptin plays an important role in the progression of OA by mediating expression change in multiple genes, although the molecular mechanisms need to be further clarified. Further study of these leptin-induced genes may provide new insights into understanding the molecular mechanisms underlying OA. To identify genes with changed expression in response to leptin, genome wide expression profiles were generated for leptin-affected cartilage (L group) and healthy controls (H group) in rats. 24 rats were divided into two groups: control animals (H group, n = 12) and leptin-induced animals (L group, n = 12). H group included two replicates, sample1 and sample2. L group also included two replicates, sample3 and sample4.
2016-08-19 | E-GEOD-85785 | biostudies-arrayexpress
Project description:Gallstone disease is a major contributor to health care costs in the United States. Approximately 12 % of the U.S. population has gallstones. As a result, more than 700,000 cholecystectomies are performed in this country each year. Many of these patients are obese and have a positive family history; but surprisingly, little is known about the link between obesity, genetics and gallstone formation. Obese individuals have been shown to have supersaturated bile, larger gallbladder fasting volumes and impaired gallbladder emptying. We have recently demonstrated that leptin plays a role in gallbladder motility. In an effort to understand the genetic basis for these observations, we tested the hypothesis that leptin would alter gallbladder gene expression. Methods: Affymetrix oligonucleotide microarrays 430 2.0 were used to compare gallbladder gene expression profiles from 12 week old control saline-treated leptin-deficient (Lep ob) and from leptin-treated Lep ob female mice. Analyses were performed on pooled RNA (n=4) from the gallbladders of 12 saline-treated Lep ob mice and from 12 Lep ob mice which were administered daily IP 5 ug/g of recombinant murine leptin for 4 weeks. Resulting data were analyzed utilizing Gene Chip Operating Software or MAS 5.0. Results: Of the genes analyzed 314 were upregulated and 108 were downregulated by leptin administration. Numerous genes related to gallstone pathogenesis, gallbladder absorption/secretion, inflammatory cytokines, and insulin resistance were altered by leptin. Experiment Overall Design: Female B6.V-lepob obese mice (n=24) aged 7 weeks were obtained from The Jackson Laboratory (Bar Harbor, ME). Upon arrival, mice were placed on a standard chow diet and were allowed to acclimate for 1 week before starting the experiment. For leptin treatments, mice received daily intraperitoneal injections of either recombinant mouse leptin (R&D Systems, Minneapolis, MN) (n=12) at a dose of 5 µg/g body weight or with saline as a control (n=12) for 4 weeks. At 12 weeks of age, mice were fasted overnight with free access to water. The following morning the mice underwent cholecystectomy. Three gallbladders were pooled to create 4 pools in each treatment and total RNA was isolated. Affymetrix murine 430 2.0 arrays were utilized to examine altered gallbladder gene expression as a result of leptin administration. The resulting data was analyzed utlizing Gene Chip Operating Software or MAS 5.0.
2007-09-07 | E-GEOD-3293 | biostudies-arrayexpress
Project description:The effects of leptin-A morpholino oligonucleotides and recombinant leptin-A on embryonic zebrafish transcriptome content were evaluated using Affymetrix 1.1 ST gene array strips.
2018-04-02 | E-MTAB-6548 | biostudies-arrayexpress
Project description:Concentrations of leptin decline during food restriction. This study was designed to test the hypothesis that some of the effects of maternal food restriction on placental development are mediated by the loss of leptin. Mice were randomized to 3 treatment groups on day 1.5 of pregnancy: (1) ad libitum fed (control) (2) 50% food restriction (restricted) (3) 50% food restriction with leptin replacement (1µg/g body weight/day) (leptin). On day 11.5 placentas were collected, and two placentas from each mother were pooled for microarray analysis.
2012-12-07 | E-GEOD-38095 | biostudies-arrayexpress
Project description:Breast cancer stem cells (BCSCs) play crucial roles in tumor initiation, metastasis and resistance to anticancer therapies. These cells rely for their properties on complex interactions with the tumor microenvironment through networks of cytokines and growth factors. In this study, we investigated how leptin, as a mediator of tumor-stromal interactions, may affect BCSC activity using breast cancer cell lines and patient-derived samples. Microarray analyses revealed a similar expression profile of genes involved in stem cell biology in mammosphere cells treated with stromal cell-CM and leptin.
2015-12-17 | E-MTAB-3641 | biostudies-arrayexpress
Project description:The effect of recombinant leptin (100 ng/ml) on gene expression in two human myeloma cell lines (RPMI 8226 and ANBL-6) were studied in cells incubated with and without leptin for 24 h.
2006-11-27 | E-MEXP-921 | biostudies-arrayexpress
Project description:Caloric Restriction in Leptin Deficiency Worsens Myocardial Steatosis: Failure to Upregulate PPAR gamma and Thermogenic Glyecrolipid/Fatty Acid Cycling Growing evidence supports an anti-lipotoxic role for leptin in preventing inappropriate peripheral tissue lipid deposition. Obese, leptin deficient ob/ob mice develop left ventricular (LV) hypertrophy and myocardial steatosis with increased apoptosis and decreased longevity. Here we investigated the cardiac effects of caloric restriction in leptin deficiency. Echocardiography was performed on C57Bl/6 wild-type mice (WT) and 7-month-old ob/ob mice fed ad lib, leptin-repleted (LR-ob/ob), or calorie-restricted (CR-ob/ob) for four weeks. Ventricular tissue was examined by electron microscopy (EM), mitochondrial coupling assay, and microarray expression profiling. LR and CR-ob/ob mice showed decreased body weight, heart weight, and LV wall thickness compared to ad lib ob/ob mice. LV fractional shortening was decreased in ad lib ob/ob mice, but restored to WT levels in LR and CR groups. However, EM revealed severe cardiac steatosis in the CR-ob/ob group compared to only moderate steatosis in ad lib ob/ob . Despite marked cardiac steatosis, CR (like LR) restored mitochondrial coupling to WT levels. CR up-regulated genes associated with oxidative stress and cell death, changes suggestive of cardiac lipotoxicity. LR, but not CR was shown to induce core genes involved in glycerolipid/free fatty acid cycling, a highly thermogenic pathway that can reduce intracellular lipid stores. LR, but not CR up-regulated and restored PGC1 and PPARto wild type levels; CR paradoxically further suppressed cardiac PPAR. Thus, leptin is essential in protecting the heart from lipotoxicity, and the inability to up-regulate the thermogenic glycerolipid/free fatty acid cycling pathway may impair the response of leptin deficient animals to the lipotoxic stress of calorie restriction. 6 month aged ob/ob mice were either leptin repleted with osmotic mini-pumps, calorie restricted to match the caloric intake of the leptin repleted mice, or fed ad lib for one month. 6-8 month C57Bl/6J mice were aged to serve as controls.
2011-04-29 | E-GEOD-16790 | biostudies-arrayexpress
Project description:We hypothesize that gene expression in the lungs of these differentially-treated mice are divergent thus contributing to the disparity in their phenotypes. More specifically, (1) Effects of Leptin-treatment of ob/ob postnatal mice lungs are known to be volume-dependent from 2 to 10 wks of age, and are independent of the hypometabolism associated with leptin deficiency. ; (2) Leptin is critical to postnatal lung remodeling, particularly related to enlarged alveolar surface area. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between lungs of leptin or saline-treated ob/ob postnatal mice. Experiment Overall Design: This study utilizes microarray analysis to test these hypotheses. Three sets of lungs were harvested from both treatments (Leptin or Saline) at around 1 mo. postnatal. RNA was isolated and used for global gene expression profiling (Affymetrix Mouse 430A array). Statistically significant gene expression was determined as a minimum 6 counts of 9 pairwise comparisons, minimum 1.5-fold change, and p < 0.05.
2008-06-18 | E-GEOD-10915 | biostudies-arrayexpress
Project description:Leptin, a hormone produced primarily by adipose tissue, plays a role in both energy homeostasis and reproduction, and is required in early pregnancy. Leptin stimulates metalloproteinase activity in cultured human trophoblast and stimulates invasiveness of cultured mouse trophoblast. The goal of the present study was to examine molecular mechanisms of this function in primary cultures of mouse trophoblast. Leptin was found to stimulate the phosphorylation of MEK, but not STAT3.. It also increased levels of the protein SOCS3. The ability of leptin to stimulate metalloproteinase activity was blocked by the MEK inhibitor PD98059, but also by the vehicle inhibitor DMSO. Microarray analysis revealed that leptin stimulated some genes associated with cell motility, such as Stmn1. In addition, leptin appeared to inhibit changes in gene expression associated with terminal differentiation of trophoblast giant cells, including inhibition of members of the TGFÃ signaling pathway and of genes associated with endoreduplication. However, feulgen staining revealed a loss of cells with low ploidy. We conclude that leptin may be promoting trophoblast invasion by maintaining cells in an intermediate stage of differentiation. Keywords: time course, response to hormone treatment, primary cell culture The experiments were performed on primary cultures of mouse trophoblast cells which were isolated from placentas on day 10 of pregnancy. There were two treatments: control (serum-free medium) and recombinant mouse leptin (50 ng/mL). RNA was collected at two time points, 1 hour and 24 hours, for the controls. RNA was collected at three time points after leptin treatment: 1 hour, 6 hours, and 24 hours. Thus, there were 5 samples for each experiment. The experiment was repeated four times, for a total of 20 arrays.
2010-10-08 | E-GEOD-10297 | biostudies-arrayexpress
Project description:Leptin monotherapy (i.e. without the use of administered insulin and/or any other molecule) corrects ID-induced metabolic aberrancies and promotes survival of insulin deficient rodents. These results generated great interest in the possibility of treating insulin deficient patients with leptin and/or molecule(s) underlying its beneficial effects. Hence, with the goal of identifying circulating molecule(s) underlying the advantageous effect of leptin we performed quantitative proteomic analysis of plasma and identified S100A9 as a putative peripheral mediator of leptin action. Here, to identify circulating molecule(s) underlying the advantageous effect of leptin we compared the results obtained by quantitative proteomic analysis of plasma between 2 groups of mice: streptozotocin (STZ)-treated mice that underwent intracerebroventricular (icv) leptin treatment for 12 days (STZ-Leptin) and ii) STZ-treated mice that underwent icv leptin treatment for 10 days and were withdrawn from leptin treatment for the following two days (STZ-Leptin-STOP). STZ treatment led to a massive loss of pancreatic insulin-producing β-cells, diminished pancreatic Proinsulin mRNA level, and caused severe insulinopenia, and hyperglycemia. icv leptin administration normalized hyperglycemia. However, two days after leptin delivery was halted hyperglycemia reappeared. We hypothesized that change in plasmatic protein(s) content could underlie re-emergence of hyperglycemia following decrease of leptin action.
2019-07-12 | PXD013466 | Pride