Browsing by Author "Ramos, Patricio"

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    Fungal Endophytes Enhance the Photoprotective Mechanisms and Photochemical Efficiency in the Antarctic Colobanthus quitensis (Kunth) Bartl. Exposed to UV-B Radiation
    (FRONTIERS MEDIA SA, 2020) Barrera, Andrea; Hereme, Rasme; Ruiz Lara, Simon; Larrondo, Luis F.; Gundel, Pedro E.; Pollmann, Stephan; Molina Montenegro, Marco A.; Ramos, Patricio
    Antarctic plants have developed mechanisms to deal with one or more adverse factors which allow them to successfully survive such extreme environment. Certain effective mechanisms to face adverse stress factors can arise from the establishment of functional symbiosis with endophytic fungi. In this work, we explored the role of fungal endophytes on host plant performance under high level of UV-B radiation, a harmful factor known to damage structure and function of cell components. In order to unveil the underlying mechanisms, we characterized the expression of genes associated to UV-B photoreception, accumulation of key flavonoids, and physiological responses of Colobanthus quitensis plants with (E+) and without (E-) fungal endophytes, under contrasting levels of UV-B radiation. The deduced proteins of CqUVR8, CqHY5, and CqFLS share the characteristic domains and display high degrees of similarity with other corresponding proteins in plants. Endophyte symbiotic plants showed lower lipid peroxidation and higher photosynthesis efficiency under high UV-B radiation. In comparison with E-, E+ plants showed lower CqUVR8, CqHY5, and CqFLS transcript levels. The content of quercetin, a ROS-scavenger flavonoid, in leaves of E- plants exposed to high UV-B was almost 8-fold higher than that in E+ plants 48 h after treatment. Our results suggest that endophyte fungi minimize cell damage and boost physiological performance in the Antarctic plants increasing the tolerance to UV-B radiation. Fungal endophytes appear as fundamental biological partners for plants to cope with the highly damaging UV-B radiation of Antarctica.
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    Peroxisome Proliferator-activated Receptor γ Up-regulates the Bcl-2 Anti-apoptotic Protein in Neurons and Induces Mitochondrial Stabilization and Protection against Oxidative Stress and Apoptosis
    (AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2007) Fuenzalida, Karen; Quintanilla, Rodrigo; Ramos, Patricio; Piderit, Daniela; Fuentealba, Rodrigo A.; Martinez, Gabriela; Inestrosa, Nibaldo C.; Bronfman, Miguel
    Peroxisome proliferator-activated receptor gamma(PPAR gamma) has been proposed as a therapeutic target for neurodegenerative diseases because of its anti-inflammatory action in glial cells. However, PPAR gamma agonists prevent beta-amyloid (A beta)-induced neurodegeneration in hippocampal neurons, and PPAR gamma is activated by the nerve growth factor (NGF) survival pathway, suggesting a neuroprotective anti-inflammatory independent action. Here we show that the PPAR gamma agonist rosiglitazone (RGZ) protects hippocampal and dorsal root ganglion neurons against A beta-induced mitochondrial damage and NGF deprivation-induced apoptosis, respectively, and promotes PC12 cell survival. In neurons and in PC12 cells RGZ protective effects are associated with increased expression of the Bcl-2 anti-apoptotic protein. NGF-differentiated PC12 neuronal cells constitutively overexpressing PPAR gamma are resistant to A beta-induced apoptosis and morphological changes and show functionally intact mitochondria and no increase in reactive oxygen species when challenged with up to 50 mu M H2O2. Conversely, cells expressing a dominant negative mutant of PPAR gamma show increased A beta-induced apoptosis and disruption of neuronal-like morphology and are highly sensitive to oxidative stress-induced impairment of mitochondrial function. Cells overexpressing PPAR gamma present a 4-to 5-fold increase in Bcl-2 protein content, whereas in dominant negative PPAR gamma-expressing cells, Bcl-2 is barely detected. Bcl-2 knockdown by small interfering RNA in cells overexpressing PPAR gamma results in increased sensitivity to A beta and oxidative stress, further suggesting that Bcl-2 up-regulation mediates PPAR gamma protective effects. PPAR gamma prosurvival action is independent of the signal-regulated MAPK or the Akt prosurvival pathways. Altogether, these data suggest that PPAR gamma supports survival in neurons in part through a mechanism involving increased expression of Bcl-2.
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    TrkA receptor activation by nerve growth factor induces shedding of the p75 neurotrophin receptor followed by endosomal gamma-secretase-mediated release of the p75 intracellular domain
    (AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC, 2007) Urra, Soledad; Escudero, Claudia A.; Ramos, Patricio; Lisbona, Fernanda; Allende, Edgardo; Covarrubias, Paulina; Parraguez, Jose I.; Zampieri, Niccolo; Chao, Moses V.; Annaert, Wim; Bronfman, Francisca C.
    Neurotrophins are trophic factors that regulate important neuronal functions. They bind two unrelated receptors, the Trk family of receptor-tyrosine kinases and the p75 neurotrophin receptor (p75). p75 was recently identified as a new substrate for gamma-secretase-mediated intramembrane proteolysis, generating a p75-derived intracellular domain (p75-ICD) with signaling capabilities. Using PC12 cells as a model, we studied how neurotrophins activate p75 processing and where these events occur in the cell. We demonstrate that activation of the TrkA receptor upon binding of nerve growth factor (NGF) regulates the metalloprotease-mediated shedding of p75 leaving a membrane-bound p75 C-terminal fragment (p75-CTF). Using subcellular fractionation to isolate a highly purified endosomal fraction, we demonstrate that p75-CTF ends up in endosomes where gamma-secretase-mediated p75-CTF cleavage occurs, resulting in the release of a p75-ICD. Moreover, we show similar structural requirements for gamma-secretase processing of p75 and amyloid precursor protein-derived CTFs. Thus, NGF-induced endocytosis regulates both signaling and proteolytic processing of p75.