Chlamydia trachomatis enhances the expression of matrix metalloproteinases in an in vitro model of the human fallopian tube infection

2002 ◽  
Vol 187 (5) ◽  
pp. 1377-1383 ◽  
Author(s):  
Kevin A. Ault ◽  
Kathleen A. Kelly ◽  
Paul E. Ruther ◽  
Angelo A. Izzo ◽  
Linda S. Izzo ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Matrix Metalloproteinases ◽  
Fallopian Tube ◽  
In Vitro Model ◽  
Human Fallopian Tube ◽  
Vitro Model

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 An in vitro model of azithromycin-induced persistent Chlamydia trachomatis infection

2017 ◽  
Vol 364 (14) ◽  
Author(s):  
Yaohua Xue ◽  
Heping Zheng ◽  
Zhida Mai ◽  
Xiaolin Qin ◽  
Wentao Chen ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
In Vitro Model ◽  
Chlamydia Trachomatis Infection ◽  
Vitro Model

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 An in vitro Model of Chlamydia trachomatis Infection in the Regenerative Phase of the Human Endometrial Cycle

Microbiology ◽  
1988 ◽  
Vol 134 (7) ◽  
pp. 2077-2087 ◽  
Author(s):  
S. Campbell ◽  
S. J. Richmond ◽  
P. Haynes ◽  
D. Gump ◽  
P. Yates ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
In Vitro Model ◽  
Chlamydia Trachomatis Infection ◽  
Vitro Model ◽  
Regenerative Phase

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.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

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