8 research outputs found
Mechanisms of mitochondrial cell death
Mitochondria are double-membrane bound organelles that not only provide energy for intracellular metabolism, but also play a key role in the regulation of cell death. Mitochondrial outer membrane permeabilization (MOMP), allowing the release of inter-membrane space proteins like cytochrome c, is considered a point of no return in apoptosis. MOMP is controlled by the proteins of the B-cell lymphoma 2 (BCL-2) family, including pro-and anti-apoptotic members, whose balance determines the decision between cell death and survival. Other factors such as membrane lipid environment, membrane dynamics, and inter-organelle communications are also known to influence this process. MOMP and apoptosis have been acknowledged as immunologically silent. Remarkably, a growing body of evidence indicates that MOMP can engage in various pro-inflammatory signaling functions. In this mini-review, we discuss about our current knowledge on the mechanisms of mitochondrial apoptosis, as well as the involvement of mitochondria in other kinds of programmed cell death pathways
A Classification Method for Workers’ Physical Risk
In Industry 4.0 scenarios, wearable sensing allows the development of monitoring solutions for workers’ risk prevention. Current approaches aim to identify the presence of a risky event, such as falls, when it has already occurred. However, there is a need to develop methods capable of identifying the presence of a risk condition in order to prevent the occurrence of the damage itself. The measurement of vital and non-vital physiological parameters enables the worker’s complex state estimation to identify risk conditions preventing falls, slips and fainting, as a result of physical overexertion and heat stress exposure. This paper aims at investigating classification approaches to identify risk conditions with respect to normal physical activity by exploiting physiological measurements in different conditions of physical exertion and heat stress. Moreover, the role played in the risk identification by specific sensors and features was investigated. The obtained results evidenced that k-Nearest Neighbors is the best performing algorithm in all the experimental conditions exploiting only information coming from cardiorespiratory monitoring (mean accuracy 88.7±7.3% for the model trained with max(HR), std(RR) and std(HR))
NOX2-Dependent Reactive Oxygen Species Regulate Formyl-Peptide Receptor 1-Mediated TrkA Transactivation in SH-SY5Y Cells
Wound healing activity and phytochemical screening of purified fractions of Sempervivum tectorum L. leaves on HCT 116
Sempervivum tectorumL. (Crassulaceae), is a succulent perennial plantwidespread in Mediterranean countries and commonly used in traditional medicinefor ear inflammation, ulcers and skin rashes as a refrigerant and astringent. To demonstrate the therapeutic effects of the plant, various fractionswere purified and characterised. The potential wound healing activity, proliferationrate and intracellular signalling cascades were investigated by using human epithelialcolorectal carcinoma (HCT 116) cells
DRP1 interacts directly with BAX to induce its activation and apoptosis
The apoptotic executioner protein BAX and the dynamin-like protein DRP1 co-localize at mitochondria during apoptosis to mediate mitochondrial permeabilization and fragmentation. However, the molecular basis and functional consequences of this interplay remain unknown. Here, we show that BAX and DRP1 physically interact, and that this interaction is enhanced during apoptosis. Complex formation between BAX and DRP1 occurs exclusively in the membrane environment and requires the BAX N-terminal region, but also involves several other BAX surfaces. Furthermore, the association between BAX and DRP1 enhances the membrane activity of both proteins. Forced dimerization of BAX and DRP1 triggers their activation and translocation to mitochondria, where they induce mitochondrial remodeling and permeabilization to cause apoptosis even in the absence of apoptotic triggers. Based on this, we propose that DRP1 can promote apoptosis by acting as noncanonical direct activator of BAX through physical contacts with its N-terminal region