Primary hepatocytes with glucagon treatment expression profiling
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE68144 | GEO | 2015/06/02
SECONDARY ACCESSION(S): PRJNA282088
REPOSITORIES: GEO
Similar Datasets
Project description:GCGR wt and ko mice Glucagon receptor signaling in GCGR KO mice: fig 2a in Solloway et al.
2015-06-02 | GSE68143 | GEO
Project description:Glucagon receptor deficient liver during postnatal development: fig S5a-S5c in Solloway et al. livers from ko and wt GCGR mice at various developmental stages
2015-06-02 | GSE68141 | GEO
Project description:The transcriptome, enhancer landscape and GR binding profile in primary mouse hepatocytes treated with glucagon and corticosterone
2022-05-09 | GSE189271 | GEO
Project description:The purpose of this experiment was to compared the transcriptome of hepatocyte-like cells (HLCs) generated in vitro and adult primary human hepatocytes (PHHs). HLCs were differentiated from either hESCs or hIPSCs using previously established protocols (Hannah et al 2013; Segeritz et al 2018). Undifferentiated hIPSCs were used as control to confirm differentiation status. PHHs were commercially sourced as well as freshly isolated from donors.
2022-08-11 | E-MTAB-10634 | biostudies-arrayexpress
Project description:The analysis identified 122 genes displaying responses to insulin and/or glucagon administration in the liver of WT male mice. Of 122 genes, 75 genes responded in a insulin-selected manner, 29 genes in a glucagon-selected manner, and 18 genes were regulated by both of insulin and glucagon 60 min after stimulation with each hormone. Insulin upregulated expression of 45 genes including Btg2, Ddit4, and Rasgef1b, downregulated 30 genes such as Arrdc3 Rgs16, and Txnip. Glucagon upregulated expression of 15 genes including Chordc1 and Gck, and downregulated expression of 14 genes such as Mt2 and Lcn2. Seventeen genes showed transcriptional upregulation in response to both insulin and glucagon including Hspa1b, Nr4a1 Trp53inp1, and one gene, Orm2, displayed downregulation after stimulation of insulin or glucagon.
2018-03-06 | GSE111407 | GEO
Project description:To understand in detail the molecular phases that occur during the differentiation of human embryonic stem cells to hepatocyte-like cells we performed an RNA-seq time course of the stages of differentiation across the 21 day differentiation time course. We used a chemically defined (serum-free) protocol, modified from Si-Tayeb et al., 2010 and Song et al., 2009. We describe acquisition of definitive endoderm characteristics at day 3, followed by hepatoblast charcter at day 7-13 and then maturation to hepatocyte-like cells at day 21.
2017-04-28 | GSE70741 | GEO
Project description:To understand in detail the molecular phases that occur during the differentiation of human embryonic stem cells to hepatocyte-like cells we performed an RNA-seq time course of the stages of differentiation across the 21 day differentiation time course. We used a chemically defined (serum-free) protocol, modified from Si-Tayeb et al., 2010 and Song et al., 2009. We describe acquisition of definitive endoderm characteristics at day 3, followed by hepatoblast charcter at day 7-13 and then maturation to hepatocyte-like cells at day 21. Time course of differentiation of human embryoic stem cells to hepatocyte-like cells over 21 days, using an adapted chemically defined protocol of Song et al., 2009; Cell Research
2017-04-28 | E-GEOD-70741 | biostudies-arrayexpress
Project description:Isolated mouse primary hepatocytes were cultured at glucose- and phenol-free DMEM medium, supplemented with 10mM pyruvate sodium and 10mM sodium lactate, and the cells were incubated for 1hr with vehice, recombinant mGP73 (64nM), or glucagon (3μM) ,cells were washed twice with cold PBS and scraped with cold RIPA lysis buffer supplemented with proteases and phosphatases inhibitors. Phosphoproteomics assay was performed by Shanghai luming biological technology co., LTD (Shanghai, China).
2021-11-18 | PXD025381 | iProX
Project description:Appropriate glucagon secretion from pancreatic alpha cells in response to hypoglycemia is an important component of maintaining glucose homeostasis. Dysregulated glucagon secretion leads to the delayed recovery from a hypoglycemic attack in type 1 diabetes patients which can be lethal. Although elucidating the precise mechanism of glucagon secretion in hypoglycemia is warranted, the underlying mechanism remains poorly understood.The present study provides evidence of the role of autophagy in glucagon secretion in hypoglycemia by demonstrating that autophagy regulates adrenergic stimulation of glucagon secretion downstream of beta2 adrenergic receptor. First, from the analyses of T1D human islets and the published database of scRNA-seq of T1D human alpha cells, we described autophagy pathways altered in T1D alpha cells. Second, we generated alpha cell-specific Atg7KO mice (alphaAtg7KO) and clarified that the lack of autophagy in alpha cells impairs the reactive glucagon secretion in acute hypoglycemia. Third, to interrogate the molecular mechanism of autophagy-mediated glucagon regulation, we analyzed top genes downregulated inT1D and T2D alpha cells and found the expression of beta2 adrenergic receptor showed significant down-regulation in T1D alpha cells. We confirmed the decreased expression of beta2 adrenergic receptor in alpha cells of the T1D pancreas section, the islets of alphaAtg7KO mice, and a murine alpha cell line with stable knockdown of Atg7. Furthermore, in vivo and ex vivo studies of alphaAtg7KO mice exhibited that lack of autophagy led to the loss of stimulatory effect of beta2-adrenergic signaling on glucagon secretion. Finally, we established the Atg7 knockdown model in sorted human alpha cells and confirmed the effect of autophagy on the expression of the beta2 adrenergic receptor. Together, our study provides novel insights into the regulatory role of autophagy in glucagon secretion in response to hypoglycemia and provides therapeutic options to achieve stable glycemic control in T1D patients.
2024-03-31 | GSE171352 | GEO
Project description:Liver mitochondria play a central role in metabolic adaptations to changing nutritional states, yet their dynamic regulation upon anticipated changes in the energy state has remained unaddressed. Here, we show that sensory food perception rapidly induces mitochondrial fission in the liver via protein kinase B/AKT-dependent phosphorylation of serine 131 of the Mitochondrial fission factor (MFFS131), a response mediated via activation of hypothalamic Pro-opiomelanocortin (POMC)-expressing neurons. A non-phosphorylatable MFFS131G knock-in mutation abrogates AKT-induced mitochondrial fragmentation in vitro. In vivo, MFFS131G knock-in mice display altered liver mitochondrial dynamics upon refeeding and impaired insulin stimulated suppression of gluconeogenesis. Collectively, we reveal a critical role for rapid activation of a hypothalamic/liver axis to adapt mitochondrial function to anticipated changes of nutritional state in control of hepatic glucose metabolism. R26-fl-Akt-C mice Mice carrying a conditional myristoylation tagged Akt-C transgene in the ROSA26 locus were used to activate AKT in the liver with a liver specific Cre-dependent virus. The generation of this line has been described previously (V. Kohlhaas et al, 2021) For AAV mediated liver-specific delivery of Cre, R26-fl-Akt-C or control mice were injected with a AAV8-TBG-iCre virus (VB1724, Vector Biolabs). This repository contains two experiments a) Liver of liver active Akt-CA and b) Insulin stimulation of primary heptocytes. Please note that replicate one of the hepatocyte dataset have been removed from the analysis due to the limited number of posphosites compared to others.
2024-03-28 | PXD049957 | Pride