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Effect of Leptin on Mouse Trophoblast Giant Cells

ABSTRACT: 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 TGFß 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

ORGANISM(S): Mus musculus

PROVIDER: GSE10297 | GEO | 2008/12/22

SECONDARY ACCESSION(S): PRJNA108511

REPOSITORIES: GEO

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Effect of Leptin on Mouse Trophoblast Giant Cells

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

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Project description:HepG2-MEK Inhibition with PD98059

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HepG2-MEK Inhibition with PD98059

Project description:Transcripts (mRNA) during amino acid limitation after MEK was inhibited were analyzed. HepG2 cells were pretreated with MEK inhibitor, PD98059 for 1 hour, then incubated in complete medium and a medium depleted for Histidine for 8 hours. For Inhibitor treated cells, PD98059 was included in the medium during the following 8 hours-incubation.

2014-09-02 | E-GEOD-58869 | biostudies-arrayexpress

Antidyskinetic effects of MEK inhibitor are associated with multiple neurochemical alterations in the striatum of hemiparkinsonian rats

Project description:L-DOPA-induced dyskinesia (LID) represents one of the major problems of the long-term therapy of patients with Parkinson's disease (PD). Although the pathophysiologic mechanisms underlying LID are not completely understood, activation of the extracellular signal regulated kinase (ERK) is recognized to play a key role. ERK is phosphorylated by mitogen-activated protein kinase kinase (MEK), and thus MEK inhibitor can prevent ERK activation. Here the effect of the MEK inhibitor PD98059 on LID and the associated molecular changes were examined. Rats with unilateral 6-OHDA lesions of the nigrostriatal pathway received daily L-DOPA treatment for three weeks, and abnormal involuntary movements (AIMs) were assessed every other day. PD98059 was injected in the lateral ventricle daily for 12 days starting from day 10 of L-DOPA treatment. Striatal molecular markers of LID were analyzed together with gene regulation using microarray. The administration of PD98059 significantly reduced AIMs. In addition, ERK activation and other associated molecular changes including ΔFosB were reversed in rats treated with the MEK inhibitor. PD98059 induced significant up-regulation of 418 transcripts and down-regulation of 378 transcripts in the striatum. Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Analysis of protein levels showed that PD98059 reduced the striatal TH. These results support the association of p-ERK1/2, ΔFosB, p-H3 to the regulation of TH and ARNT in the mechanisms of LID, and pinpoint other gene regulatory changes, thus providing clues for identifying new targets for LID therapy.

2017-01-18 | GSE93695 | GEO

Leptin-Mediated Gene Expression Profiling Exhibits New Candidate Genes Associated with Osteoarthritis in Rat

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

Leptin is Implicated in Aromatase Inhibitor Resistance in Breast Cancer Cells

Project description:Obesity represents a risk factor for breast cancer development and therapy resistance, but the molecular players underling these links are unclear. Here, we identify a role for the obesity-cytokine leptin in sustaining aromatase inhibitor (AI) resistant growth and progression in breast cancer. Using as a cellular model MCF-7 breast cancer cells surviving long-term to the AI treatment Anastrozole (AnaR) and Ana-sensitive counterparts, we found that AnaR cells expressed higher levels of leptin and its receptors (ObR) along with a constitutive activation of downstream effectors. Accordingly, leptin signaling inhibition reduced only AnaR cell growth and motility, highlighting the existence of an autocrine loop in mechanisms governing drug-resistant phenotype. In agreement with ObR overexpression, increasing doses of leptin were able to stimulate at a greater extent growth and migration in AnaR than sensitive cells. Moreover, leptin contributed to an enhanced crosstalk between AnaR cells and macrophages within tumor microenvironment. Indeed, AnaR through leptin secretion modulated macrophage profiles and increased macrophage motility through CXCR4 signaling, as evidenced by RNA-sequencing, realtime-PCR and immunoblotting. Reciprocally, activated macrophages increased AnaR cell growth and motility in coculture systems.

2022-03-04 | E-MTAB-8843 | biostudies-arrayexpress

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Project description:Effect of Leptin on Mouse Trophoblast Giant Cells

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ANGPTL4 binds to leptin receptor to regulate ectopic bone formation and fat metabolism

Project description:Leptin protein was thought to be unique to leptin receptor (LepR), but the phenotypes of mice with mutation in LepR (db/db) and leptin (ob/ob) are not identical, and the cause remains unclear. Here, we show that db/db, but not ob/ob mice had defect in tenotomy-induced heterotopic ossification (HO), implicating alternative ligand(s) for LepR might be involved. Ligand screening revealed that ANGPTL4, a stress and fasting-induced factor, was elicited from brown adipose tissue after tenotomy, bound to LepR on PRRX1+ mesenchymal cells at the HO cite, thus promotes chondrogenesis and HO development. Disruption of LepR in PRRX1+ cells, or lineage ablation of LepR+ cells, or deletion of ANGPTL4 impeded chondrogenesis and HO in mice. Surprisingly, exogenous ANGPTL4 treatment not only promoted HO, but facilitated the transformation from white to brown adipose tissue in mice. These findings identify ANGPTL4 as a novel ligand for LepR to stimulate HO and regulate fat metabolism.

2024-07-03 | PXD043087 | Pride

Effect of STMN1 knockdown on prostate cancer cell lines

Project description:STMN1 is is a highly conserved 18 KDa cytosolic phosphoprotein, involved in the control of cell proliferation, differentiation, motility, clonogenicity and survival. Over-expression of STMN1 has been shown to be a marker of poor outcome in nasopharyngeal, ovarian, estrogen receptor positive tamoxifen treated early breast and oral squamous cell carcinomas. Limited studies have shown overexpression of STMN1 in higher grade localized prostate cancers; however its association with outcome and metastatic disease is unclear. Here, we investigate role and regulation of STMN1 during prostate cancer progression.

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