Track topics on Twitter Track topics that are important to you
Methamphetamine (METH) is a commonly abused psychostimulant that can induce severe neurotoxicity. Cardiovascular injury caused by METH has recently gained increasing attention; however, the underlying mechanisms remain unclear. As autophagy has been shown to be associated with cell injury, the association between autophagy and METH-mediated cell apoptosis was investigated in the present study. METH treatment significantly increased the expression of two key autophagy proteins, i.e., Beclin-1 and LC3-II, in the cardiomyocyte cell line H9C2. Furthermore, according to western blot and flow cytometry analyses, METH contributed to cell injury and markedly enhanced cleaved-caspase 3 and PARP expression. In addition, the corresponding AKT-mTOR survival pathway axis was appeared deactivated. The autophagic activity was closely associated with METH-mediated cell injury because rapamycin, which is an autophagy inducer, markedly attenuated METH-induced cell injury, while 3-Methyladenine (3-MA), which is an autophagy inhibitor, and bafilomycinA1 (Baf-A1), which is a blocker of autophagosome-lysosome fusion, markedly exacerbated METH-induced cell injury. Notably, defective autophagosome-lysosome fusion might be partially involved in the METH-induced enhancement of LC3-II expression and cell injury. However, the underlying mechanisms require further investigation.
This article was published in the following journal.
Name: Toxicology letters
Cadmium (Cd) is a highly ubiquitous detrimental metal in the environment. It is a well-known inducer of tumorigenesis, but the mechanism is not clear. In our previous study, we found that ROS-dependen...
Autophagy is a lysosomal degradation process that maintains cellular homeostasis by removing dysfunctional organelles and unfolded proteins. Increasing evidence has shown that autophagy proteins are i...
The balance between cell survival and cell death is often lost in human pathologies such as inflammation and cancer. Autophagy plays a critical role in cell survival: essential nutrients are generated...
Glucocorticoid-induced endothelial injury has been reported in several diseases. Although there are several theories, the exact mechanism underlying the role of glucocorticoids in this process remains...
Cadmium (Cd) is a toxic heavy metal and its toxic mechanism is not entirely clear. The goal of the present study was to investigate the toxic mechanism of Cd on rPT cells, and to elucidate the role of...
In recent years, evidence has shown that mitochondrial dysfunction plays an important role in the development of age-related muscle decline that may lead to frailty. During aging, there i...
The intent of this study is to see if the rate that the body breaks down l-methamphetamine (l-MA) could be used as an accurate estimate for the rate that the body breaks down d-methampheta...
This is the first study of pomaglumetad in humans using methamphetamine. The goal of the study is to determine if pomaglumetad is safe when administered with methamphetamine. If shown to b...
The purpose of this study is to find out if GVG can reduce drug use and determine safety and effects of GVG when used together with methamphetamine. This study involves staying in the hosp...
The purpose of the study is to determine if cytidine 5'diphosphocholine (CDP-choline, a naturally occurring chemical in your body) has efficacy in reducing the methamphetamine craving of t...
A CARD signaling adaptor protein that plays a role in the mitochondria-stimulated apoptosis (APOPTOSIS, INTRINSIC PATHWAY). It binds to CYTOCHROME C in the CYTOSOL to form an APOPTOSOMAL PROTEIN COMPLEX and activates INITIATOR CASPASES such as CASPASE 9.
A tumor necrosis factor receptor family member that is specific for RANK LIGAND and plays a role in bone homeostasis by regulating osteoclastogenesis. It also expressed on DENDRITIC CELLS where is plays a role in regulating dendritic cell survival. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
An autophagy related protein that is similar to UBIQUITIN-ACTIVATING ENZYME E1. It functions in CYTOPLASM to VACUOLE transport (Cvt) and AUTOPHAGY by activating ATG12 PROTEIN for its conjugation with ATG5 PROTEIN, as well as the conjugation of ATG8 FAMILY PROTEINS with phosphatidylethanolamine for ATG8 association to Cvt vesicles and AUTOPHAGOSOME membranes. It is also required for the nitrogen starvation response in yeast, MITOPHAGY; and autophagic cell death induced by CASPASE 8 inhibition.
A secreted tumor necrosis factor receptor family member that has specificity for TNF-RELATED APOPTOSIS-INDUCING LIGAND. It plays a modulating role in activation of APOPTOSIS signaling.
A member of the TNF receptor family that was initially identified as a DEXAMETHASONE-induced protein from a T-CELL line. It may play a role in regulating APOPTOSIS and modulating immune response by T-lymphocytes. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.