Some of the deregulated proteins such as thioredoxin 2, glutathione S transferase, T complex protein 1 subunit β (tcbp1), heat shock protein 90 and E3 ubiquitin ligase were previously reported to be associated with either diabetes or insulin resistance.
These results provided the first expression profile of thiol-related genes in a model of diabetes and demonstrated a novel role for endogenous thioredoxin 2 in protecting cells against high ambient glucose.
These results provided the first expression profile of thiol-related genes in a model of diabetes and demonstrated a novel role for endogenous thioredoxin 2 in protecting cells against high ambient glucose.
Some of the deregulated proteins such as thioredoxin 2, glutathione S transferase, T complex protein 1 subunit β (tcbp1), heat shock protein 90 and E3 ubiquitin ligase were previously reported to be associated with either diabetes or insulin resistance.
The aim of our study was to investigate the relationship between genetic polymorphisms in the mitochondrial thioredoxin reductase 2 (TrxR2) and myocardial infarction (MI) in subjects with type 2 diabetes mellitus (T2DM) of Slovenian origin.
Single nucleotide polymorphisms in the Trx2/TXNIP and TrxR2 genes of the mitochondrial thioredoxin antioxidant system and the risk of diabetic retinopathy in patients with Type 2 diabetes mellitus.
Interestingly, the overexpression of mitochondrial thioredoxin 2 or mitochondrial superoxide dismutase attenuates AngII-induced hypertension, which demonstrates the importance of mitochondrial ROS in AngII-mediated cardiovascular diseases.
These results indicate that miR-27a and -b suppress SNAP25 and TXN2 expression via posttranscriptional gene silencing, leading to efficient suppression of Ad infection.<b>IMPORTANCE</b> Adenovirus (Ad) is widely used as a platform for replication-incompetent Ad vectors (Adv) and replication-competent oncolytic Ad (OAd) in gene therapy and virotherapy.
Interestingly, the overexpression of mitochondrial thioredoxin 2 or mitochondrial superoxide dismutase attenuates AngII-induced hypertension, which demonstrates the importance of mitochondrial ROS in AngII-mediated cardiovascular diseases.
In brief, this study shows that IPC conferred neuroprotection against ischemic injury by maintaining Trx2 and suggests that the maintenance or enhancement of Trx2 expression by IPC may be a legitimate strategy for therapeutic intervention of cerebral ischemia.
Here, we had focused on the role of Trx2 in ischemic preconditioning (IPC)-mediated neuroprotection against oxidative stress followed by a subsequent lethal transient cerebral ischemia.
Single nucleotide polymorphisms in the Trx2/TXNIP and TrxR2 genes of the mitochondrial thioredoxin antioxidant system and the risk of diabetic retinopathy in patients with Type 2 diabetes mellitus.
Here, we show in wild-type (WT) experimental autoimmune encephalomyelitis (EAE) mice that PGC-1α is decreased 13 d after EAE induction followed by a steady decline up to 20 d. These changes were accompanied by parallel alterations in levels of superoxide dismutase 2, peroxiredoxin 3, thioredoxin 2, UCP4, and UCP5.
In this study, we explored the distribution and role of the mitochondrial antioxidants peroxiredoxin-3 and thioredoxin-2 as well as their regulator peroxisome proliferator-activated receptor gamma coactivator1-alpha (PGC-1α) in MS pathogenesis.
The aim of our study was to investigate the relationship between genetic polymorphisms in the mitochondrial thioredoxin reductase 2 (TrxR2) and myocardial infarction (MI) in subjects with type 2 diabetes mellitus (T2DM) of Slovenian origin.
In HCC, Trx1 correlated significantly with cell proliferation, and with a trend towards increased levels with micro-vascular invasion, while expression of Trx2 decreased with tumor size.