scholarly journals Effect of dehydroepiandroesterone and triamcinolone acetonide on 3T3-L1 cell line

2017 ◽  
Author(s):  
◽  
G. Gutiérrez-Iglesias
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Triamcinolone Acetonide ◽  
Biological Effects ◽  
Fibroblast Cell ◽  
Cell Protection ◽  
Molecular Alterations ◽  
Recommended Treatment ◽  
Keloid Scars ◽  
Anti Oxidant

The skin in the human is the largest organ, his integrity represents protection against various chemical, biological and mechanical agents. The injuries in this tissue are solved by forming a scar, however, different molecular alterations may overstimulate this process, leading to the formation of aberrant scars (hypertrophic or keloid). The most recommended treatment for such injuries is the intralesional application of triamcinolone acetonide (TA) and on the other hand, dehydroepiandrosterone (DHEA) is a pro-hormone that has a wide variety of biological effects such as regulation of the synthesis of collagen fibers, cell protection, anti-tumor properties, anti-inflammatory and anti-oxidant. In this paper, the combination of AT-DHEA on proliferation and cell death in fibroblast cell line 3T3-L1 was studied. The results showed that the AT 100 and 1000 M DHEA to inhibit proliferation by 50 and 40% respectively. The combination of AT-DHEA (10000-10 M) inhibits cell proliferation and induce programmed cell death, so this combination could be used in hypertrophic or keloid scars for disposal.

scholarly journals Effect of dehydroepiandroesterone and triamcinolone acetonide on 3T3-L1 cell line

2017 ◽  
Author(s):  
◽  
G. Gutiérrez-Iglesias
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Triamcinolone Acetonide ◽  
Biological Effects ◽  
Fibroblast Cell ◽  
Cell Protection ◽  
Molecular Alterations ◽  
Recommended Treatment ◽  
Keloid Scars ◽  
Anti Oxidant

The skin in the human is the largest organ, his integrity represents protection against various chemical, biological and mechanical agents. The injuries in this tissue are solved by forming a scar, however, different molecular alterations may overstimulate this process, leading to the formation of aberrant scars (hypertrophic or keloid). The most recommended treatment for such injuries is the intralesional application of triamcinolone acetonide (TA) and on the other hand, dehydroepiandrosterone (DHEA) is a pro-hormone that has a wide variety of biological effects such as regulation of the synthesis of collagen fibers, cell protection, anti-tumor properties, anti-inflammatory and anti-oxidant. In this paper, the combination of AT-DHEA on proliferation and cell death in fibroblast cell line 3T3-L1 was studied. The results showed that the AT 100 and 1000 M DHEA to inhibit proliferation by 50 and 40% respectively. The combination of AT-DHEA (10000-10 M) inhibits cell proliferation and induce programmed cell death, so this combination could be used in hypertrophic or keloid scars for disposal.

scholarly journals The DF-1 Chicken Fibroblast Cell Line: Transformation Induced by Diverse Oncogenes and Cell Death Resulting from Infection by Avian Leukosis Viruses

Virology ◽  
1998 ◽  
Vol 248 (2) ◽  
pp. 295-304 ◽  
Author(s):  
Martin Himly ◽  
Douglas N. Foster ◽  
Ivan Bottoli ◽  
Jason S. Iacovoni ◽  
Peter K. Vogt
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Avian Leukosis Viruses ◽  
Chicken Fibroblast

Synergy with combination of AKT inhibitor (MK-2206) and paclitaxel in head and neck squamous cell carcinoma.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e13532-e13532 ◽  
Author(s):  
Omar Ahmed ◽  
Wen-Liang Kuo ◽  
Madhavi Nagilla ◽  
Jeannette S. Messer ◽  
David L. Boone ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Cell Lines ◽  
Protein Localization ◽  
Competent Cell ◽  
Akt Inhibitor ◽  
Tissue Samples ◽  
Molecular Alterations ◽  
Protein Levels ◽  
Effective Combination

e13532 Background: Though there have been many advances in the treatment of HNSCC, the 5-year survival rate remains at 50%. This is partly due to molecular alterations such as the activation of the PI3k-AKT pathway in HNSCC, which has been associated with treatment failure. We stained human tissue samples and saw increased expression of p-AKT and pS6 in HNSCC compared to normal and dysplasia. This led us to investigate the role of the AKT inhibitor MK-2206 in combination with an already established chemotherapeutic agent, paclitaxel. Methods: Cell viability and Combination index were used to determine synergy in 4 HNSCC cell lines. PI exclusion and Annexin/PI staining were used to determine cell death and apoptosis, respectively. Autophagy was measured through changes in LC3BII protein levels using western blot analysis and a stably transfected GFP-LC3BII cell line was used to detect changes in protein localization under confocal microscopy. Results: All cell lines were sensitive to paclitaxel while only some were sensitive to MK-2206. However, there was effective synergy to the combination treatment in all cell lines. Apoptotic synergy was observed in some cell lines indicating that the combination stimulates cell death in the appropriate context. In one autophagy competent cell line, MK-2206 induced robust autophagy while paclitaxel blocked a latter step in the pathway leading to an accumulation of autophagosomes prior to induction of apoptosis. Conclusions: Paclitaxel and MK-2206 appears to be an effective combination in HNSCC possibly through their effect on autophagy trafficking, leading to an accumulation of autophagosomes and eventual apoptosis. Clinical trials examining this combination are warranted.

Use of EPR and FTIR to detect biological effects of ultrasound and microbubbles on a fibroblast cell line

2011 ◽  
Vol 40 (10) ◽  
pp. 1115-1120 ◽  
Author(s):  
D. Pozzi ◽  
P. Fattibene ◽  
D. Viscomi ◽  
L. Di Giambattista ◽  
P. Grimaldi ◽  
...  
Keyword(s):  
Cell Line ◽  
Biological Effects ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line

scholarly journals Lysosome-dependent cell death and deregulated autophagy induced by amine-modified polystyrene nanoparticles

Open Biology ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 170271 ◽  
Author(s):  
Fengjuan Wang ◽  
Anna Salvati ◽  
Patricia Boya
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Fibroblast Cell ◽  
Mouse Embryonic Fibroblast ◽  
Autophagic Flux ◽  
Polystyrene Nanoparticles ◽  
Dependent Cell ◽  
Modified Polystyrene ◽  
Embryonic Fibroblast ◽  
1321N1 Cell

Nanoparticles (NPs) typically accumulate in lysosomes. However, their impact on lysosomal function, as well as autophagy, a lysosomal degradative pathway, is still not well known. We have previously reported in the 1321N1 cell line that amine-modified polystyrene (NH 2 -PS) NPs induce apoptosis through damage initiated in the lysosomes leading ultimately to release of lysosomal content in the cytosol, followed by apoptosis. Here, by using a combination of biochemical and cell biological approaches, we have characterized in a mouse embryonic fibroblast cell line that the lysosomal alterations induced by NH 2 -PS NPs is progressive, initiating from mild lysosomal membrane permeabilization (LMP), to expansion of lysosomal volume and intensive LMP before the summit of cell death. Though the cells initially seem to induce autophagy as a surviving mechanism, the damage of NH 2 -PS NPs to lysosomes probably results in lysosomal dysfunctions, leading to blockage of autophagic flux at the level of lysosomes and the eventual cell death.

scholarly journals A Comparison of p53 Isoform Profiles and Apoptosis Induced by Camptothecin or a Herbal Khat Extract (Catha Edulis (Vahl) Forssk. ex Endl.) in Leukemic Cell Lines: Exploring Cellular Responses in Therapy Development

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3596
Author(s):  
Therese Bredholt Onyango ◽  
Sigrun M. Hjelle ◽  
Ingvild Haaland ◽  
Olav K. Vintermyr ◽  
Anne Christine Johannessen ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Bone Marrow Cells ◽  
Biological Effects ◽  
P53 Protein ◽  
Cancer Therapeutics ◽  
P38 Map Kinase ◽  
Catha Edulis ◽  
Knock Out

Khat (Catha edulis (Vahl) Forssk. ex Endl.) is habitually used as a natural stimulant by millions of people, but is associated with adverse effects on gastrointestinal, cardiovascular and central neural systems. At the cellular level khat toxicity involves p53 induction and cell cycle arrest, decreased mitochondrial function and activation of receptor- and mitochondria-mediated cell death pathways. In this study we have examined an extract of khat for induction of p53 post-translational modifications (PTMs) and the functional role of p53 in khat-mediated cell death. Khat was shown to induce phosphorylation and acetylation of p53 in both the khat-sensitive MOLM-13 and the khat-resistant MV-4-11 cell line, but accumulation of the full-length p53 isoform was only observed in the khat sensitive cell line. Small molecule inhibitors of p38 MAP kinase sensitized MV-4-11 cells for khat-treatment without concomitant stabilization of p53. Experiments using a p53 knock-down cell line and murine p53 knock-out bone marrow cells indicated that p53 was redundant in khat-mediated cell death in vitro. We suggest that analysis of isoform patterns and p53 PTMs are useful for elucidation of biological effects of complex plant extracts, and that p53 protein analysis is particularly useful in the search for new chemical probes and experimental cancer therapeutics.

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