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Expression data fom human capillary network-derived cells before and after adipogenic differentation, and after chronic adenylate cyclase activation of differentiated cells

ABSTRACT: Progenitors in human vasculature expanded in-vitro were differentiated with adipogenic cocktail for 12 days, following which they were stimulated with forskolin for 7 days Microarrays were used to detail the program of differentiation of thermogenic human adipose cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE73385 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA296865

REPOSITORIES: GEO

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Expression data fom human capillary network-derived cells before and after adipogenic differentation, and after chronic adenylate cyclase activation of differentiated cells

Project description:Progenitors in human vasculature expanded in-vitro were differentiated with adipogenic cocktail for 12 days, following which they were stimulated with forskolin for 7 days Microarrays were used to detail the program of differentiation of thermogenic human adipose cells Adipose tissue from three individuals was cultured in hydrogel under pro-angiogenic conditions. Capillary networks emerging from the explants were subcultured on plastic, grown to confluence, subjected to adipogenic differentiation and after 12 days treated with vehicle or forskolin for 7 days

2016-07-03 | E-GEOD-73385 | biostudies-arrayexpress

Expression data from human adipocytes after adenylate cyclase activation

2018-01-22 | GSE65190 | GEO

PTHRP/Adenylate cyclase promotes parietal whereas Wnt/β-catenin signaling promotes visceral endoderm differentiation of rat XEN cells.

Project description:In this study we showed that rat XEN cells grown in the presence of a GSK3 inhibitor exhibited enhanced formation of cell contacts and decreased motility. In contrast, treatment with forskolin induced the PE formation and epithelial-mesenchymal transition (EMT) in rat XEN cells. Using microarray and real-time PCR assays, we found that VE versus PE formation of rat XEN cells was correlated with change in expression levels of VE or PE marker genes. Similar to forskolin, EMT was prompted upon treatment of rat XEN cells with recombinant parathyroid hormone related peptide (PTHRP), an activator of the cAMP pathway in vivo. Taken together, our data suggest that rat XEN cells are PrE-like cells. The activation of Wnt pathway in rat XEN cells leads to the acquisition of VE characteristics, whereas the activation of the PTHRP/cAMP pathway leads to EMT and the formation of PE. Rat XEN cells were cultured in four different conditions with 3 parallels for each condition: (1-3) without treatments control, (4-6) 2 days treated with CHIR alone, (7-9) 1 day treated with CHIR and 1 day with both CHIR and forskolin, and (10-12) 1 day treated with forskolin alone. In all samples on DAY1 cells were plated, at DAY2 cells were cultured in usual conditions (DMEM F12 medium and 10% Fetal Bovine Serum, both from Sigma) and inhibitor of GSK3 kinase 3 μM CHIR99021 (Axon Medchem) was added in samples 4-9. On DAY3 all cells were cultured in medium with 0.1% serum to exclude the influence of serum and in CONTROL (1-3) cells were cultured without experimental treatments, in CHIR (4-6) cells were further cultured with 3 μM CHIR99021, in CHIR plus FORSKOLIN cells were cultured with 3 μM CHIR99021 and 10μM Forskolin (Sigma), in FORSKOLIN cells were cultured for 1 day with 10 μM Forskolin. On DAY4 RNA was isolated.

2013-02-01 | E-GEOD-42438 | biostudies-arrayexpress

PTHRP/Adenylate cyclase promotes parietal whereas Wnt/β-catenin signaling promotes visceral endoderm differentiation of rat XEN cells.

2013-02-01 | GSE42438 | GEO

Phospholipase A activity of adenylate cyclase toxin?

Project description: Not available

| S-EPMC5856560 | biostudies-literature

Adenylate cyclase 10 promotes brown adipose tissue thermogenesis.

Project description:Brown adipose tissue (BAT) thermogenesis dissipates energy through heat production and thereby it opposes metabolic disease. It is mediated by mitochondrial membrane uncoupling, yet the mechanisms sustaining the mitochondrial membrane potential (ΔΨm) in brown adipocytes are poorly understood. Here we show that isocitrate dehydrogenase (IDH) activity and the expression of the soluble adenylate cyclase 10 (ADCY10), a CO2/bicarbonate sensor residing in mitochondria, are upregulated in BAT of cold-exposed mice. IDH inhibition or ADCY10 deficiency reduces cold resistance of mice. Mechanistically, IDH increases the ΔΨm in brown adipocytes via ADCY10. ADCY10 sustains complex I activity and the ΔΨm via exchange protein activated by cAMP1 (EPAC1). However, neither IDH nor ADCY10 inhibition affect uncoupling protein 1 (UCP1) expression. Hence, we suggest that ADCY10, acting as a CO2/bicarbonate sensor, mediates the effect of IDH on complex I activity through cAMP-EPAC1 signaling, thereby maintaining the ΔΨm and enabling thermogenesis in brown adipocytes.

| S-EPMC11821413 | biostudies-literature

Adenylate cyclase regulates elongation of mammalian primary cilia.

Project description:The primary cilium is a non-motile microtubule-based structure that shares many similarities with the structures of flagella and motile cilia. It is well known that the length of flagella is under stringent control, but it is not known whether this is true for primary cilia. In this study, we found that the length of primary cilia in fibroblast-like synoviocytes, either in log phase culture or in quiescent state, was confined within a range. However, when lithium was added to the culture to a final concentration of 100 mM, primary cilia of synoviocytes grew beyond this range, elongating to a length that was on average approximately 3 times the length of untreated cilia. Lithium is a drug approved for treating bipolar disorder. We dissected the molecular targets of this drug, and observed that inhibition of adenylate cyclase III (ACIII) by specific inhibitors mimicked the effects of lithium on primary cilium elongation. Inhibition of GSK-3beta by four different inhibitors did not induce primary cilia elongation. ACIII was found in primary cilia of a variety of cell types, and lithium treatment of these cell types led to their cilium elongation. Further, we demonstrate that different cell types displayed distinct sensitivities to the lithium treatment. However, in all cases examined primary cilia elongated as a result of lithium treatment. In particular, two neuronal cell types, rat PC-12 adrenal medulla cells and human astrocytes, developed long primary cilia when lithium was used at or close to the therapeutic relevant concentration (1-2 mM). These results suggest that the length of primary cilia is controlled, at least in part, by the ACIII-cAMP signaling pathway.

| S-EPMC3161028 | biostudies-literature

Adenylate cyclase-deficient mutant of Corynebacterium glutamicum

Project description:Corynebacterium glutamicum GlxR suppressor mutant of adenylate cyclase (cyaB) deletion strain

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Targeted Pituitary Adenylate Cyclase-Activating Peptide Therapies for Migraine.

Project description:Here, we review the role of pituitary adenylate cyclase-activating peptide-38 (PACAP38) in migraine pathophysiology and data implicating PAC1 receptor as a future drug target in migraine. Much remains to be fully elucidated about migraine pathophysiology, but recent attention has focused on signaling molecule PACAP38, a vasodilator able to induce migraine attacks in patients who experience migraine without aura. PACAP38, with marked and sustained effect, dilates extracerebral arteries but not the middle cerebral artery. The selective affinity of PACAP38 to the PAC1 receptor makes this receptor a highly interesting and potential novel target for migraine treatment. Efficacy of antagonism of this receptor should be investigated in randomized clinical trials.

| S-EPMC5935633 | biostudies-literature

Adenylate Cyclase Toxin promotes bacterial internalisation into non phagocytic cells.

Project description:Bordetella pertussis causes whooping cough, a respiratory infectious disease that is the fifth largest cause of vaccine-preventable death in infants. Though historically considered an extracellular pathogen, this bacterium has been detected both in vitro and in vivo inside phagocytic and non-phagocytic cells. However the precise mechanism used by B. pertussis for cell entry, or the putative bacterial factors involved, are not fully elucidated. Here we find that adenylate cyclase toxin (ACT), one of the important toxins of B. pertussis, is sufficient to promote bacterial internalisation into non-phagocytic cells. After characterization of the entry route we show that uptake of "toxin-coated bacteria" proceeds via a clathrin-independent, caveolae-dependent entry pathway, allowing the internalised bacteria to survive within the cells. Intracellular bacteria were found inside non-acidic endosomes with high sphingomyelin and cholesterol content, or "free" in the cytosol of the invaded cells, suggesting that the ACT-induced bacterial uptake may not proceed through formation of late endolysosomes. Activation of Tyr kinases and toxin-induced Ca(2+)-influx are essential for the entry process. We hypothesize that B. pertussis might use ACT to activate the endocytic machinery of non-phagocytic cells and gain entry into these cells, in this way evading the host immune system.

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