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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE214598 | GEO | 2022/10/08

REPOSITORIES: GEO

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Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on gene expression in a new immortalized mouse adipocyte progenitor (MAP) cell line (RNA-Seq).

Project description:To characterize biphasic adipocyte browning induced by chronic FSK treatment and compare this process to Rosi-induced browning, We performed gene expression profiling using MAP cells treated with vehicle or with FSK for mulitple time durations (4h, 1D, and 3D) or with Rosi for 3D.

2022-10-08 | GSE214596 | GEO

Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line (ATAC-Seq).

Project description:To investigate how the chromatin accessibility landscape is altered during biphasic FSK-induced browning in comparison with single-phase Rosi-induced browning, We performed chromatin lanscape profiling using the nuclei sorted from MAP cells treated with vehicle (Control) or with FSK for mulitple time durations (4 hours, 1 day, or 3 days) or with Rosi for 3 days.

2022-10-08 | GSE214597 | GEO

Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line

Project description:Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on the chromatin accessibility landscape in a new immortalized mouse adipocyte progenitor (MAP) cell line

| PRJNA886071 | ENA

Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on gene expression in a new immortalized mouse adipocyte progenitor (MAP) cell line (RNA-Seq).

Project description:Effect of time-course forskolin (FSK) treatment versus rosiglitazone (Rosi) treatment on gene expression in a new immortalized mouse adipocyte progenitor (MAP) cell line (RNA-Seq).

| PRJNA886072 | ENA

| PRJNA886073 | ENA

In vitro skin diffusion study of pure forskolin versus a forskolin-containing Plectranthus barbatus root extract.

Project description:An in vitro skin diffusion study of pure forskolin (1) versus a 1-containing Plectranthus barbatus root extract (P. barbatus extract) in hairless guinea pig skin and human skin in a flow-through diffusion cell system was conducted and is being reported for the first time. Both topical agents were formulated in a solution of 70% ethanol and 30% propylene glycol (v/v). The results showed that forskolin can be delivered through the stratum corneum and that the flux of this compound was enhanced when 1 was delivered as a constituent of the P. barbatus extract as compared to an equivalent amount in pure form. These results suggest that the P. barbatus extract used contains permeation enhancement activity from other compound(s) contained in the crude root extract. It is possible that P. barbatus root extract may be used as an economical source of 1 to perform topical chemical manipulation of pigmentation in high-risk populations.

| S-EPMC5082746 | biostudies-literature

Differentiation of human monocytes to macrophages in the presence of GM-CSF +/- forskolin (FSK)

Project description:Macrophages are central mediators of the innate immune system that can be differentiated from monocytes upon exposure to cytokines. While increased cyclic adenosine monophosphate (cAMP) levels inhibit many lipopolysaccharide (LPS) -elicited macrophage inflammatory responses, the effects of elevated cAMP on macrophage differentiation are not well understood. We have differentiated monocytes to macrophages in the presence of GM-CSF or GM-CSF + FSK to elevate cAMP levels and determine its effects on differentiation.

2009-10-22 | GSE18654 | GEO

Differentiation of human monocytes to macrophages in the presence of GM-CSF +/- forskolin (FSK)

2010-06-20 | E-GEOD-18654 | biostudies-arrayexpress

Transcriptional profiling of immortalized and K-ras-transformed mouse fibroblasts upon PKA stimulation by forskolin in low glucose availability.

Project description:Forskolin (FSK) induces activation of protein kinase A (PKA). This activation protects specifically some cancer cells from death induced by glucose starvation. Cell effects upon FSK treatment prompted us to investigate in detail the physiological role of PKA in the activation of pro-survival mechanisms in glucose starvation. In this regard we performed a microarray analysis of normal NIH3T3 and transformed NIH3T3-K-ras mouse fibroblasts cultured at 1 mM glucose and daily treated or not with 10 μM FSK until 72 h of growth, when the samples were collected. The microarray is deposited into Gene Expression Omnibus under Series GSE68266. The microarray data revealed that the activation of PKA regulates the expression of genes involved in metabolic, stress-response and pro-survival processes, like glutamine metabolism, autophagy and unfolded protein response, preventing cancer cell death in glucose starvation. Altogether these findings suggest that PKA activation, by inducing a complex transcriptional program, leads to cancer survival in nutrient stress, a typical feature of developing tumor. These transcriptional data, identifying this important role of PKA, will be useful to identify novel target in cancer therapy.

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Anti-Inflammatory Effects of Rosiglitazone in Obesity-Impaired Wound Healing Depend on Adipocyte Differentiation.

Project description:Combined diabetes-obesity syndromes severely impair regeneration of acute skin wounds in mouse models. This study assessed the contribution of subcutaneous adipose tissue to exacerbated wound inflammatory conditions. Genetically obese (ob/ob) mice showed an increased expression of positive transcriptional effectors of adipocyte differentiation such as Krüppel-like factor (KLF)-5 and peroxisome proliferator-activated receptor (PPAR)-? and an associated expression of leptin and fatty acid-binding protein (FABP)-4, but also CXCL2 in isolated subcutaneous fat. This observation in obese mice is in keeping with differentially elevated levels of KLF-5, PPAR-?, leptin, FABP-4 and CXCL2 in in vitro-differentiated 3T3-L1 adipocytes. Notably, CXCL2 expression restrictively appeared upon cytokine (IL-1?/TNF-?) stimulation only in mature, but not immature 3T3-L1 adipocytes. Of importance, the critical regulator of adipocyte maturation, PPAR-?, was merely expressed in the final phase of in-vitro induced adipocyte differentiation from 3T3-L1 pre-adipocytes. Consistently, the PPAR-? agonist rosiglitazone suppressed cytokine-induced CXCL2 release from mature adipocytes, but not from early 3T3-L1 adipocyte stages. The inhibitory effect of PPAR-? activation on CXCL2 release appeared to be a general anti-inflammatory effect in mature adipocytes, as cytokine-induced cyclooxygenase (Cox)-2 was simultaneously repressed by rosiglitazone. In accordance with these findings, oral administration of rosiglitazone to wounded obese mice significantly changed subcutaneous adipocyte morphology, reduced wound CXCL2 and Cox-2 expression and improved tissue regeneration. Thus, our data suggest that PPAR-? might provide a target to suppress inflammatory signals from mature adipocytes, which add to the prolonged wound inflammation observed in diabetes-obesity conditions.

| S-EPMC5167406 | biostudies-literature

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