scholarly journals Triticum vulgare Extract Modulates Protein-Kinase B and Matrix Metalloproteinases 9 Protein Expression in BV-2 Cells: Bioactivity on Inflammatory Pathway Associated with Molecular Mechanism Wound Healing

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Niccola Funel ◽  
Valentina Dini ◽  
Agata Janowska ◽  
Barbara Loggini ◽  
Massimiliano Minale ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Matrix Metalloproteinases ◽  
Inflammatory Process ◽  
In Vitro Model ◽  
Protein Kinase B ◽  
Inflammatory Marker ◽  
Triticum Vulgare ◽  
Inflammatory Processes ◽  
Vitro Model

Matrix metalloproteinases (MMPs) are a large family of ubiquitously expressed zinc-dependent enzymes with proteolitic activities. They are expressed in physiological situations and pathological conditions involving inflammatory processes including epithelial to mesenchymal transition (EMT), neuronal injury, and cancer. There is also evidence that MMPs regulate inflammation in tumor microenvironment, which plays an important role in healing tissue processes. Looking at both inflammatory and neuronal damages, MMP9 is involved in both processes and their modulation seems to be regulated by two proteins: tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6). However other important genes are involved in molecular regulation of transcription factors, protein-kinase B (AKT), and p65. In addition, Triticum vulgare extract (TVE) modulated the biological markers associated with inflammatory processes, including p65 protein. While there are no evidence that TVE might be involved in the biological modulation of other inflammatory marker as AKT, we would like to assess whether TVE is able to (1) modulate phosphorylation of AKT (pAKT) as an early marker of inflammatory process in vitro and (2) affect MMP9 protein expression in an in vitro model. The BV-2 cells (microglial of mouse) have been used as an in vitro model to simulate both inflammatory and neuronal injury pathologies. Here, MMP9 seems to be involved in cellular migration through inflammatory marker activation. We simulate an inflammatory preclinical model treating BV-2 cells with lipopolysaccharide (LPS) to induce proinflammatory activation affecting pAKT and p65 proteins. TVE is revealed to restore the native expression of AKT and p65. Additionally, TVE extract modulates also the protein concentration of MMP9. Nevertheless, immunofluorescence confocal analyses revealed that both AKT and MMP9 are regulated together, synchronously. This work seems to demonstrate that two important genes can be used to monitor the beginning of an inflammatory process, AKT and MMP9, in which TVE seems able to modulate their expression of inflammation-associated molecules.

scholarly journals P1658microRNA 146a modulates activity of matrix-metalloproteinases in an in vitro model of arterial stiffness

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
A Dannert ◽  
I N Schellinger ◽  
J Jakubiczka-Smorag ◽  
K Mattern ◽  
G Hasenfuss ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Arterial Stiffness ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Mycoplasma fermentansand TNF-β interact to amplify immune-modulating cytokines in human lung fibroblasts

2006 ◽  
Vol 291 (4) ◽  
pp. L781-L793 ◽  
Author(s):  
James P. Fabisiak ◽  
Fei Gao ◽  
Robyn G. Thomson ◽  
Robert M. Strieter ◽  
Simon C. Watkins ◽  
...  
Keyword(s):  
Protein Kinase ◽  
In Vitro Model ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Mycoplasma Fermentans ◽  
Human Lung Fibroblasts ◽  
Toll Like Receptor 2 ◽  
Vitro Model ◽  
Specific Ligand

Mycoplasma can establish latent infections and are associated with arthritis, leukemia, and chronic lung disease. We developed an experimental model in which lung cells are deliberately infected with Mycoplasma fermentans. Human lung fibroblasts (HLF) were exposed to live M. fermentans and immune-modulating cytokine release was assessed with and without known inducers of cytokine production. M. fermentans increased IL-6, IL-8/CXCL8, MCP-1/CCL2, and Gro-α/CXCL1 production. M. fermentans interacted with TNF-β to release more IL-6, CXCL8, and CXCL1 than predicted by the responses to either stimulus alone. The effects of live infection were recapitulated by exposure to M. fermentans-derived macrophage-activating lipopeptide-2 (MALP-2), a Toll-like receptor-2- and receptor-6-specific ligand. The synergistic effect of combined stimuli was more pronounced with prolonged incubations. Preexposure to TNF-β sensitized the cells to subsequent MALP-2 challenge, but preexposure to MALP-2 did not alter the IL-6 response to TNF-β. Exposure to M. fermentans or MALP-2 did not enhance nuclear localization, DNA binding, or transcriptional activity of NF-κB and did not modulate early NF-κB activation in response to TNF-β. Application of specific inhibitors of various MAPKs suggested that p38 and JNK/stress-activated protein kinase were involved in early IL-6 release after exposure to TNF-β and M. fermentans, respectively. The combined response to M. fermentans and TNF-β, however, was uniquely sensitive to delayed application of SP-600125, suggesting that JNK/stress-activated protein kinase contributes to the amplification of IL-6 release. Thus M. fermentans interacts with stimuli such as TNF-β to amplify lung cell production of immune-modulating cytokines. The mechanisms accounting for this interaction can now be dissected with the use of this in vitro model.

scholarly journals Inhibition of MLKL Attenuates Necroptotic Cell Death in a Murine Cell Model of Ischaemia Injury

2021 ◽  
Vol 10 (2) ◽  
pp. 212
Author(s):  
Raji Baidya ◽  
Jérémie Gautheron ◽  
Darrell H. G. Crawford ◽  
Haolu Wang ◽  
Kim R. Bridle
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
In Vitro Model ◽  
Cell Model ◽  
Glucose Deprivation ◽  
Insoluble Fraction ◽  
Ischaemic Injury ◽  
Interacting Protein ◽  
Vitro Model

Background: Steatosis in donor livers poses a major risk of organ dysfunction due to their susceptibility to ischaemia-reperfusion (I/R) injury during transplant. Necroptosis, a novel form of programmed cell death, is orchestrated by receptor-interacting protein kinase 1 (RIPK1), receptor-interacting protein kinase 3 (RIPK3) and mixed-lineage kinase domain-like pseudokinase (MLKL), has been implicated in I/R injury. Here we investigated the mechanisms of cell death pathways in an in vitro model of hepato-steatotic ischaemia. Methods: Free fatty acid (FFA) treated alpha mouse liver 12 (AML-12) cells were incubated in oxygen-glucose-deprivation (OGD) conditions as seen during ischaemia. Results: We found that OGD triggered upregulation of insoluble fraction of RIPK3 and MLKL in FFA + OGD cells compared to FFA control cells. We report that intervention with small interfering (si) MLKL and siRIPK3 significantly attenuated cell death in FFA + OGD cells. Absence of activated CASPASE8 and cleaved-CASPASE3, no change in the expression of CASPASE1 and prostaglandin-endoperoxide synthase 2 (Ptgs2) in FFA + OGD treated cells compared to FFA control cells indicated that apoptosis, pyroptosis and ferroptosis, respectively, are unlikely to be active in this model. Conclusion: Our findings indicate that RIPK3-MLKL dependent necroptosis contributed to cell death in our in vitro model. Both MLKL and RIPK3 are promising therapeutic targets to inhibit necroptosis during ischaemic injury in fatty liver.

The Role of Matrix Metalloproteinases in an in Vitro Model of Bladder Tumor Invasion

1999 ◽  
pp. 413-417 ◽  
Author(s):  
Catherine Booth ◽  
Patricia Harnden ◽  
Peter J. Selby ◽  
Ludwik K. Trejdosiewicz ◽  
Jennifer Southgate
Keyword(s):  
Matrix Metalloproteinases ◽  
Tumor Invasion ◽  
Bladder Tumor ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Nubebe Gambi tablets suppresses adiposity by regulating adenosine monophosphate-activated protein kinase in vivo and in vitro model

2020 ◽  
Vol 9 ◽  
pp. 100600
Author(s):  
Yea-Jin Park ◽  
Divina Cominguez ◽  
Hyo-Jung Kim ◽  
Duck-jae Koh ◽  
Seo-Young Kim ◽  
...  
Keyword(s):  
Protein Kinase ◽  
In Vitro Model ◽  
Adenosine Monophosphate ◽  
Vitro Model
Sign in / Sign up

Export Citation Format

Share Document