Ghrelin modulates gene and protein expression of digestive enzymes in the intestine and hepatopancreas of goldfish (Carassius auratus) via the GHS-R1a: Possible roles of PLC/PKC and AC/PKA intracellular signaling pathways

2017 ◽  
Vol 442 ◽  
pp. 165-181 ◽  
Author(s):  
Ayelén Melisa Blanco ◽  
Juan Ignacio Bertucci ◽  
Aída Sánchez-Bretaño ◽  
María Jesús Delgado ◽  
Ana Isabel Valenciano ◽  
...  
Keyword(s):  
Protein Expression ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Digestive Enzymes ◽  
Carassius Auratus ◽  
Intracellular Signaling Pathways ◽  
Goldfish Carassius Auratus ◽  
Gene And Protein Expression

Modulation of proinflammatory bacteria- and lipid–coupled intracellular signaling pathways in a transwell triple co-culture model by commensal Bifidobacterium animalis R101-8

2020 ◽  
Vol 19 ◽  
Author(s):  
Darab Ghadimi ◽  
Annegret Nielsen ◽  
Mohamed Farghaly Yoness Hassan ◽  
Regina Fölster-Holst ◽  
Michael Ebsen ◽  
...  
Keyword(s):  
Protein Expression ◽  
Palmitic Acid ◽  
Signaling Pathways ◽  
Cell Line ◽  
Intracellular Signaling ◽  
Expression Levels ◽  
Bifidobacterium Animalis ◽  
Intracellular Signaling Pathways ◽  
Culture Model ◽  
Tnf Α

Background and aims: Following a fat-rich diet, alterations in gut microbiota contribute to enhanced gut permeability, metabolic endotoxemia, and low grade inflammation–associated metabolic disorders. To better understand whether commensal bifidobacteria influence the expression of key metaflammation-related biomarkers (chemerin, MCP-1, PEDF) and modulate the pro-inflammatory bacteria- and lipid–coupled intracellular signaling pathways, we aimed at i) investigating the influence of the establishment of microbial signaling molecules- based cell-cell contacts on the involved intercellular communication between enterocytes, immune cells, and adipocytes, and ii) assessing their inflammatory mediators’ expression profiles within an inflamed adipose tissue model. Material and Methods: Bifidobacterium animalis R101-8 and Escherichia coli TG1, respectively, were added to the apical side of a triple co-culture model consisting of intestinal epithelial HT-29/B6 cell line, human monocyte-derived macrophage cells, and adipose-derived stem cell line in the absence or presence of LPS or palmitic acid. mRNA expression levels of key lipid metabolism genes HILPDA, MCP- 1/CCL2, RARRES2, SCD, SFRP2 and of TLR4 were determined using TaqMan qRT-PCR. Protein expression levels of cytokines (IL-1β, IL-6, and TNF-α), key metaflammation-related biomarkers including adipokines (chemerin and PEDF), chemokine (MCP-1) as well as cellular triglycerides were assessed by cell-based ELISA, while those of p-ERK, p-JNK, p-p38, NF-κB, p-IκBα, pc-Fos, pc-Jun, and TLR4 were assessed by Western blotting. Results: B. animalis R101-8 inhibited LPS- and palmitic acid-induced protein expression of inflammatory cytokines IL-1β, IL-6, TNF-α concomitant with decreases in chemerin, MCP-1, PEDF, and cellular triglycerides, and blocked NF-kB and AP-1 activation pathway through inhibition of p-IκBα, pc-Jun, and pc-Fos phosphorylation. B. animalis R101-8 downregulated mRNA and protein levels of HILPDA, MCP-1/CCL2, RARRES2, SCD and SFRP2 and TLR4 following exposure to LPS and palmitic acid. Conclusion: B. animalis R101-8 improves biomarkers of metaflammation through at least two molecular/signaling mechanisms that are triggered by pro-inflammatory bacteria/lipids. First, B. animalis R101-8 modulates the coupled intracellular signaling pathways via metabolizing saturated fatty acids and reducing available bioactive palmitic acid. Second, it inhibits NF-kB’s and AP-1’s transcriptional activities, resulting in reduction of pro-inflammatory markers. Thus, the molecular basis may be formed by which commensal bifidobacteria improve intrinsic cellular tolerance against excess pro-inflammatory lipids, and participate in homeostatic regulation of metabolic processes in vivo.

p38 and EGF receptor kinase-mediated activation of the phosphatidylinositol 3-kinase/Akt pathway is required for Zn2+-induced cyclooxygenase-2 expression

2005 ◽  
Vol 289 (5) ◽  
pp. L883-L889 ◽  
Author(s):  
Weidong Wu ◽  
Robert A. Silbajoris ◽  
Young E. Whang ◽  
Lee M. Graves ◽  
Philip A. Bromberg ◽  
...  
Keyword(s):  
Protein Expression ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Egf Receptor ◽  
Cyclooxygenase 2 ◽  
Dominant Negative ◽  
Phosphatidylinositol 3 Kinase ◽  
Akt Phosphorylation ◽  
Intracellular Signaling Pathways ◽  
Cox 2

Cyclooxygenase 2 (COX-2) expression is induced by physiological and inflammatory stimuli. Regulation of COX-2 expression is stimulus and cell type specific. Exposure to Zn2+ has been associated with activation of multiple intracellular signaling pathways as well as the induction of COX-2 expression. This study aims to elucidate the role of intracellular signaling pathways in Zn2+-induced COX-2 expression in human bronchial epithelial cells. Inhibitors of the phosphatidylinositol 3-kinase (PI3K) potently block Zn2+-induced COX-2 mRNA and protein expression. Overexpression of adenoviral constructs encoding dominant-negative Akt kinase downstream of PI3K or wild-type phosphatase and tensin homolog deleted on chromosome 10, an important PI3K phosphatase, suppresses COX-2 mRNA expression induced by Zn2+. Zn2+ exposure induces phosphorylation of the tyrosine kinases, including Src and EGF receptor (EGFR), and the p38 mitogen-activated protein kinase. Blockage of these kinases results in inhibition of Zn2+-induced Akt phosphorylation as well as COX-2 protein expression. Overexpression of dominant negative p38 constructs suppresses Zn2+-induced increase in COX-2 promoter activity. In contrast, the c-Jun NH2-terminal kinase and the extracellular signal-regulated kinases have minimal effect on Akt phosphorylation and COX-2 expression. Inhibition of p38, Src, and EGFR kinases with pharmacological inhibitors markedly reduces Akt phosphorylation induced by Zn2+. However, the PI3K inhibitors do not show inhibitory effects on p38, Src, and EGFR. These data suggest that p38 and EGFR kinase-mediated Akt activation is required for Zn2+-induced COX-2 expression and that the PI3K/Akt signaling pathway plays a central role in this event.

scholarly journals Interaction of dual intracellular signaling pathways activated by the melanocortin-3 receptor.

1994 ◽  
Vol 269 (18) ◽  
pp. 13162-13166
Author(s):  
Y. Konda ◽  
I. Gantz ◽  
J. DelValle ◽  
Y. Shimoto ◽  
H. Miwa ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Intracellular Signaling Pathways
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