scholarly journals Trehalose Modulates Autophagy Process to Counteract Gliadin Cytotoxicity in an In Vitro Celiac Disease Model

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 348 ◽  
Author(s):  
Federico Manai ◽  
Alberto Azzalin ◽  
Martina Morandi ◽  
Veronica Riccardi ◽  
Lisa Zanoletti ◽  
...  
Keyword(s):  
Celiac Disease ◽  
In Vitro Model ◽  
Wheat Gluten ◽  
Disease Model ◽  
Autoimmune Disorder ◽  
Beneficial Effects ◽  
Gliadin Peptides ◽  
Autophagy Pathway ◽  
Vitro Model

Celiac disease (CD) is a chronic systemic autoimmune disorder that is triggered by the ingestion of gliadin peptides, the alcohol-soluble fraction of wheat gluten. These peptides, which play a key role in the immune response that underlies CD, spontaneously form aggregates and exert a direct toxic action on cells due to the increase in the reactive oxygen species (ROS) levels. Furthermore, peptic-tryptic digested gliadin peptides (PT-gliadin) lead to an impairment in the autophagy pathway in an in vitro model based on Caco-2 cells. Considering these premises, in this study we have analyzed different mTOR-independent inducers, reporting that the disaccharide trehalose, a mTOR-independent autophagy activator, rescued the autophagy flux in Caco-2 cells treated with digested gliadin, as well as improved cell viability. Moreover, trehalose administration to Caco-2 cells in presence of digested gliadin reduced the intracellular levels of these toxic peptides. Altogether, these results showed the beneficial effects of trehalose in a CD in vitro model as well as underlining autophagy as a molecular pathway whose modulation might be promising in counteracting PT-gliadin cytotoxicity.

The Coexistence of Cystic Fibrosis and Celiac Disease

PEDIATRICS ◽  
1976 ◽  
Vol 57 (5) ◽  
pp. 715-721
Author(s):  
Aubrey J. Katz ◽  
Z. Myron Falchuk ◽  
Harry Shwachman
Keyword(s):  
Cystic Fibrosis ◽  
Celiac Disease ◽  
Organ Culture ◽  
Intestinal Mucosa ◽  
In Vitro Model ◽  
Duodenal Mucosa ◽  
Common Type ◽  
The Other ◽  
Vitro Model

Two patients with cystic fibrosis (CF) who subsequently developed celiac disease (CD) are described. Since organ culture of intestinal mucosa has been used to establish an in vitro model for the study of CD, we utilized this opportunity to determine whether duodenal mucosa obtained from each of these two patients and their immediate families differed in its organ culture behavior from mucosa obtained from patients with CD alone. Additionally, as specific HL-A types are associated with CD, we used HL-A typing to determine whether the two patients with CF-CD differed genetically from patients with CD alone. One of our patients was HL-A8, the most common type associated with CD; the other was HL-A12, as are many of the non-HL-A8 celiac patients. The response in organ culture of the mucosa of these two patients was the same as the response in organ culture of the mucosa from patients with CD alone. These and other data suggest that CD occurring in patients with CF is no different than CD occurring alone.

Beneficial effects of curcumin on GFAP filament organization and down-regulation of GFAP expression in an in vitro model of Alexander disease

2012 ◽  
Vol 318 (15) ◽  
pp. 1844-1854 ◽  
Author(s):  
Tiziana Bachetti ◽  
Eleonora Di Zanni ◽  
Pietro Balbi ◽  
Roberto Ravazzolo ◽  
GianPietro Sechi ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Alexander Disease ◽  
Down Regulation ◽  
Beneficial Effects ◽  
Gfap Expression ◽  
Vitro Model

In vitro Model of the Pathogenesis of Celiac Disease

1998 ◽  
Vol 16 (6) ◽  
pp. 341-344 ◽  
Author(s):  
Georg Oberhuber ◽  
Maria Schwarzenhofer ◽  
Harald Vogelsang
Keyword(s):  
Celiac Disease ◽  
In Vitro Model ◽  
Vitro Model

Transport of wheat gluten exorphins A5 and C5 through an in vitro model of intestinal epithelium

2016 ◽  
Vol 88 ◽  
pp. 319-326 ◽  
Author(s):  
Margherita Maggioni ◽  
Milda Stuknytė ◽  
Paola De Luca ◽  
Stefano Cattaneo ◽  
Amelia Fiorilli ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
In Vitro Model ◽  
Wheat Gluten ◽  
Vitro Model

scholarly journals Silybin Modulates Collagen Turnover in an In Vitro Model of NASH

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1280 ◽  
Author(s):  
Beatrice Anfuso ◽  
Pablo Giraudi ◽  
Claudio Tiribelli ◽  
Natalia Rosso
Keyword(s):  
Cell Viability ◽  
In Vitro Model ◽  
Early Stage ◽  
Antioxidant Properties ◽  
Ros Generation ◽  
Driving Mechanism ◽  
Beneficial Effects ◽  
Huh7 Cells ◽  
Vitro Model

Silybin has been proposed as a treatment for nonalcoholic steatohepatitis (NASH). In this study, we assessed the effect of Silybin in a well-established in vitro coculture model of early-stage NASH. LX2 and Huh7 cells were exposed to free fatty acid (FFA) and Silybin as mono- or coculture (SCC). Cell viability, LX2 activation, collagen deposition, metalloproteinase 2 and 9 (MMP2-9) activity, and ROS generation were determined at 24, 96, and 144 h. Exposure to FFA induced the activation of LX2 as shown by the increase in cell viability and upregulation of collagen biosynthesis. Interestingly, while cotreatment with Silybin did not affect collagen production in LX2, a significant reduction was observed in SCC. MMP2-9 activity was reduced in FFA-treated Huh7 and SCC and cotreatment with Silybin induced a dose-dependent increase, while no effect was observed in LX2. Silybin also showed antioxidant properties by reducing the FFA-induced production of ROS in all the cell systems. Based on these data, Silybin exerts its beneficial effects by reducing LX2 proliferation and ROS generation. Moreover, MMP2-9 modulation in hepatocytes represents the driving mechanism for the net reduction of collagen in this NASH in vitro model, highlighting the importance of hepatic cells interplay in NASH development and resolution.

Cosilencing Intestinal Transglutaminase-2 and Interleukin-15 Using Gelatin-Based Nanoparticles in an in Vitro Model of Celiac Disease

2017 ◽  
Vol 14 (9) ◽  
pp. 3036-3044 ◽  
Author(s):  
Husain Attarwala ◽  
Valerie Clausen ◽  
Prasoon Chaturvedi ◽  
Mansoor M. Amiji
Keyword(s):  
Celiac Disease ◽  
In Vitro Model ◽  
Transglutaminase 2 ◽  
Interleukin 15 ◽  
Vitro Model

Beneficial Effects of Choline Alphoscerate on Amyloid-β Neurotoxicity in an In vitro Model of Alzheimer’s Disease

2021 ◽  
Vol 18 ◽  
Author(s):  
Chiara Burgaletto ◽  
Giulia Di Benedetto ◽  
Antonio Munafò ◽  
Renato Bernardini ◽  
Giuseppina Cantarella
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Vitro Model ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Health Concern ◽  
Noic Acid ◽  
Beneficial Effects ◽  
Vitro Model

Background: Alzheimer’s disease (AD) is the most common form of neurodegenerative disorder characterized by cognitive impairment, which represents an urgent public health concern. Given the worldwide impact of AD, there is a compelling need for effective therapies to slow down or halt this disorder. Objective: Choline alphoscerate (α-GPC) represents a potentially effective cholinergic neurotrans- mission enhancing agent with an interesting clinical profile in cognitive dysfunctions improve- ment, although only scanty data are available about the mechanisms underlying such beneficial ef- fects. Method: The SH-SY5Y neuronal cell line, differentiated for 1 week with 10 μm of all-trans-reti- noic acid (RA), to achieve a switch towards a cholinergic phenotype, was used as an in vitro model of AD. SH-SY5Y cells were pre-treated for 1h with α-GPC (100nM) and treated for 72 h with Aβ25-35 (10μM). Results: α-GPC was able to antagonize Aβ25-35 mediated neurotoxicity and attenuate the Aβ-in- duced phosphorylation of the Tau protein. Moreover, α-GPC exerted its beneficial effects by em- ploying the NGF/TrkA system, knocked down in AD and, consequently, by sustaining the expres- sion level of synaptic vesicle proteins, such as synaptophysin. Conclusion: Taken together, our data suggest that α-GPC can have a role in neuroprotection in the course of toxic challenges with Aβ. Thus, a deeper understanding of the mechanism underlying its beneficial effect, could provide new insights into potential future pharmacological applications of its functional cholinergic enhancement, with the aim to mitigate AD and could represent the basis for innovative therapy.

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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