Unsaturated fatty acids with special structural features have been shown to activate serine/threonine protein phosphatase type 2C (PP2C) isoforms alpha and beta at physiological Mg(2+)-concentrations in vitro. These compounds also induce apoptosis in neuronal and endothelial cells. In this study we further analysed this striking correlation and tried to elucidate whether or not there is a causative relationship between activation of PP2C and induction of apoptosis. We employed RNA interference to simultaneously knock down PP2Calpha and PP2Cbeta in SH-SY5Y cells or HUVECs, respectively. This downregulation was transient. Treatment of SH-SY5Y cells or HUVECs with oleic acid (18:1,cis-Delta(9)) caused apoptosis in a time- and concentration-dependent manner. In both cases, cells with reduced PP2C-levels were less susceptible to oleic acid-induced cell damage. In conclusion, our results demonstrate that PP2C activation by unsaturated fatty acids actually causes apoptosis in neuronal and endothelial cells.
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http://dx.doi.org/10.1007/s10495-006-6982-1 | DOI Listing |
Exp Eye Res
January 2025
Department of Biochemistry and Molecular Biology, Pondicherry University, Puducherry, 605 014, India. Electronic address:
Diabetic Retinopathy (DR), a leading complication of diabetes mellitus, has long been considered as a microvascular disease of the retina. However, recent evidence suggests that DR is a neurovascular disease, characterized by the degeneration of retinal neural tissue and microvascular abnormalities encompassing ischemia, neovascularization, and blood-retinal barrier breakdown, ultimately leading to blindness. The intricate relationship between the retina and vascular cells constitutes a neurovascular unit, a multi-cellular framework of retinal neurons, glial cells, immune cells, and vascular cells, which facilitates neurovascular coupling, linking neuronal activity to blood flow.
View Article and Find Full Text PDFNeurosci Lett
January 2025
Neurophysiology Research Center, Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences, Urmia, Iran. Electronic address:
Brain aging is the leading risk factor for most neurodegenerative diseases and has been linked with high rates of neuron loss. Thus, identifying molecular mechanisms underlying neuron loss and pharmacological modulation may be of great importance for slowing or preventing age-related diseases. Herein, we investigated the roles of miR-92a, Akt, mTOR, and NF-κB in age-associated apoptosis in the hippocampus (a critical structure involved in brain aging) of male rats alone and in combination with prazosin.
View Article and Find Full Text PDFExp Neurol
January 2025
Department of Neurosurgery, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Introduction: Brain damage caused by subarachnoid hemorrhage (SAH) currently lacks effective treatment, leading to stagnation in the improvement of functional outcomes for decades. Recent studies have demonstrated the therapeutic potential of exosomes released from mesenchymal stem cells (MSC), which effectively attenuate neuronal apoptosis and inflammation in neurological diseases. Due to the challenge of systemic dilution associated with intravenous administration, intranasal delivery has emerged as a novel approach for targeting the brain.
View Article and Find Full Text PDFToxicology
January 2025
School of Forensic Medicine, National Health Commission (NHC) Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, Yunnan 650500, China. Electronic address:
Methamphetamine (METH), a synthetic stimulant, has seen an escalating abuse situation globally over the past decade. Although the molecular mechanism underlying METH-induced neurotoxicity has been explored, the dysfunction of brain-derived neurotrophic factor (BDNF) neuroprotection in the context of METH neurotoxicity remains insufficiently understood. Our previous studies have found that METH induced neurotoxicity and BDNF expression in rat primary neurons, necessitating further research into this paradox.
View Article and Find Full Text PDFCell Rep
January 2025
Department of Human Biology, Faculty of Natural Sciences, University of Haifa, Haifa 34988, Israel. Electronic address:
The elimination of superfluous neurons via apoptosis and subsequent glial phagocytosis is crucial for the development of the central nervous system (CNS). In Drosophila, two glial phagocytic receptors, six-microns-under (SIMU) and Draper, mediate the phagocytosis of apoptotic neurons during embryogenesis. However, in simu;draper double-mutant embryos, some apoptotic neurons are still engulfed by the glia, suggesting the involvement of additional receptors.
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