scholarly journals 191 TRANSGLUTAMINASE 2 INDUCED BY RETINOIC ACID DECREASE HUMAN CHONDROCYTE APOPTOSIS INDUCED BY HYDROGEN PEROXIDE

2010 ◽  
Vol 18 ◽  
pp. S91-S92
Author(s):  
M. Lee ◽  
H. Park ◽  
S. Lee ◽  
I. Han ◽  
J. Jang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Retinoic Acid ◽  
Transglutaminase 2 ◽  
Chondrocyte Apoptosis ◽  
Human Chondrocyte

scholarly journals Benefits of Combined All-Trans Retinoic Acid and Arsenic Trioxide Treatment of Acute Promyelocytic Leukemia Cells and Further Enhancement by Inhibition of Atypically Expressed Transglutaminase 2

Cancers ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 648 ◽  
Author(s):  
Károly Jambrovics ◽  
Iván P. Uray ◽  
Jeffrey W. Keillor ◽  
László Fésüs ◽  
Zoltán Balajthy
Keyword(s):  
Retinoic Acid ◽  
Arsenic Trioxide ◽  
Acute Promyelocytic Leukemia ◽  
Transglutaminase 2 ◽  
Promyelocytic Leukemia ◽  
Dependent Manner ◽  
Wild Type ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Tnf Α

Randomized trials in acute promyelocytic leukemia patients have shown that treatment with a combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) is superior in efficacy to monotherapy, with significantly decreased mortality. So far, there are little data available to explain the success of the ATRA and ATO combination treatment in molecular terms. We showed that ATRA- and ATO-treated cells had the same capacity for superoxide production, which was reduced by two-thirds in the combined treatment. Secreted inflammatory biomarkers (monocyte chemoattractant protein-1 [MCP-1], interleukin-1 beta [IL-1β] and tumor necrosis factor-α [TNF-α]) were significantly decreased and were further reduced in a transglutaminase 2 (TG2) expression-dependent manner. The amount of secreted TNF-α in the supernatant of NB4 TG2 knockout cells was close to 50 times lower than in ATRA-treated differentiated wild-type NB4 cells. The irreversible inhibitor of TG2 NC9 not only decreased reactive oxygen species production 28-fold, but decreased the concentration of MCP-1, IL-1β and TNF-α 8-, 15- and 61-fold, respectively in the combined ATRA + ATO-treated wild-type NB4 cell culture. We propose that atypical expression of TG2 leads to the generation of inflammation, which thereby serves as a potential target for the prevention of differentiation syndrome.

Role of transglutaminase 2 in apoptosis induced by hydrogen peroxide in human chondrocytes

2010 ◽  
Vol 29 (2) ◽  
pp. 252-257 ◽  
Author(s):  
Ilkyu Han ◽  
Hee Jung Park ◽  
Sang Cheol Seong ◽  
Sahnghoon Lee ◽  
In-Gyu Kim ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Transglutaminase 2 ◽  
Human Chondrocytes

scholarly journals Role of miR-146a in human chondrocyte apoptosis in response to mechanical pressure injury in vitro

2014 ◽  
Vol 34 (2) ◽  
pp. 451-463 ◽  
Author(s):  
LEI JIN ◽  
JIAN ZHAO ◽  
WENSEN JING ◽  
SHIJU YAN ◽  
XIN WANG ◽  
...  
Keyword(s):  
Chondrocyte Apoptosis ◽  
Mechanical Pressure ◽  
Human Chondrocyte ◽  
Pressure Injury

scholarly journals Induction of Transglutaminase 2 by a Liver X Receptor/Retinoic Acid Receptor α Pathway Increases the Clearance of Apoptotic Cells by Human Macrophages

2009 ◽  
Vol 105 (4) ◽  
pp. 393-401 ◽  
Author(s):  
Cédric Rébé ◽  
Magalie Raveneau ◽  
Angélique Chevriaux ◽  
Daniela Lakomy ◽  
Anne-Laure Sberna ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Transglutaminase 2 ◽  
Liver X Receptor ◽  
Apoptotic Cells ◽  
Human Macrophages ◽  
Acid Receptor ◽  
Retinoic Acid Receptor Α

scholarly journals Retinoic acid attenuates oxidative injury in bovine mammary epithelial cells induced by hydrogen peroxide

2017 ◽  
Vol 62 (No. 12) ◽  
pp. 539-548
Author(s):  
L. Jin ◽  
S. Yan ◽  
B. Shi ◽  
H. Shi ◽  
X. Guo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hydrogen Peroxide ◽  
Arachidonic Acid ◽  
Retinoic Acid ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Oxidative Injury ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Pre Treatment

The objective of this study was to explore how retinoic acid (RA) attenuates oxidative injury induced by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) in bovine mammary epithelial cells (BMEC). Subconfluence BMEC were randomly divided into four groups with six replicates: the control group (incubated in serum-free medium without RA or H<sub>2</sub>O<sub>2 </sub>for 30 h), H<sub>2</sub>O<sub>2</sub> group (pre-incubated for 24 h without RA, then for another 6 h with 600 μM H<sub>2</sub>O<sub>2</sub>), RA group (incubated with 1 mg/ml RA for 30 h without H<sub>2</sub>O<sub>2</sub>), and RA + H<sub>2</sub>O<sub>2</sub> group (RA prevention group, pre-incubated with 1 mg/ml RA for 24 h and then for another 6 h with 600 mM H<sub>2</sub>O<sub>2</sub>). The results showed that the H<sub>2</sub>O<sub>2</sub> treatment significantly decreased several measured traits, including the cell viability, glutathione peroxidase (GPX) and thioredoxin reductase (TRXR) activities, selenoprotein P (SELP) content, catalase and superoxide dismutase activities, total antioxidant capacity, and GPX1, TRXR1, and SELP gene expression, as well as GPX1 and TRXR1 protein expression. H<sub>2</sub>O<sub>2</sub> treatment also increased the malondialdehyde and reactive oxygen species contents and induced a marked increase of several measured traits, including the arachidonic acid (ARA) concentration, cytosolic phospholipase A2 and 5-lipoxygenase gene expression and activity, and 15-hydroxy twenty-four arachidonic acid and hydroxy peroxide tetracosenic arachidonic acid contents. RA pre-treatment prevented corresponding increases in parameters related to ARA metabolism and increased the activity of TRXR. Moreover, RA pre-treatment attenuated the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase and effectively decreased the ARA content. These results suggest that RA protected BMEC from oxidative stress by elevating TRXR activity, which inhibited the MAPK signaling pathway and led to a decreased concentration of ARA.

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