Browsing by Author "San Martin, Alejandra"

Now showing 1 - 4 of 4
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    Complementary effects of Mediterranean diet and moderate red wine intake on haemostatic cardiovascular risk factors
    (NATURE PUBLISHING GROUP, 2001) Mezzano, Diego; Leighton Puga, Federico; Martínez, Carlos; Marshall Rivera, Guillermo; Cuevas Marín, Ada Marisa; Castillo Valenzuela, Oscar; Panes Becerra, Olga Teresa; Rozowski Narkunska, Samuel Jaime; Pérez Pons, Druso Diego; Mizón Costa, Claudio Luis Enrique; San Martin, Alejandra; Pereira Pereira, J. Marcello
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    Effect of Mediterranean and occidental diets, and red wine, on plasma fatty acids in humans. An intervention study
    (2004) Urquiaga Reus, Inés; Guasch Castro, Viviana; Marshall Rivera, Guillermo; San Martin, Alejandra; Castillo Valenzuela, Oscar; Rozowski Narkunska, Samuel Jaime; Leighton Puga, Federico
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    HERPUD1 governs tumor cell mitochondrial function via inositol 1,4,5-trisphosphate receptor-mediated calcium signaling
    (2024) Paredes, Felipe; Navarro-Marquez, Mario; Quiroga, Clara; Jimenez-Gallegos, Danica; Yeligar, Samantha M.; Parra, Valentina; Mueller, Marioly; Chiong, Mario; Quest, Andrew F. G.; San Martin, Alejandra; Lavandero, Sergio
    The intricate relationship between calcium (Ca2+) homeostasis and mitochondrial function is crucial for cellular metabolic adaptation in tumor cells. Ca2+-initiated signaling maintains mitochondrial respiratory capacity and ATP synthesis, influencing critical cellular processes in cancer development. Previous studies by our group have shown that the homocysteine-inducible ER Protein with Ubiquitin-Like Domain 1 (HERPUD1) regulates inositol 1,4,5-trisphosphate receptor (ITPR3) levels and intracellular Ca2+ signals in tumor cells. This study explores the role of HERPUD1 in regulating mitochondrial function and tumor cell migration by controlling ITPR3-dependent Ca2+ signals.We found HERPUD1 levels correlated with mitochondrial function in tumor cells, with HERPUD1 deficiency leading to enhanced mitochondrial activity. HERPUD1 knockdown increased intracellular Ca2+ release and mitochondrial Ca2+ influx, which was prevented using the ITPR3 antagonist xestospongin C or the Ca2+ chelator BAPTA-AM. Furthermore, HERPUD1 expression reduced tumor cell migration by controlling ITPR3-mediated Ca2+ signals. HERPUD1-deficient cells exhibited increased migratory capacity, which was attenuated by treatment with xestospongin C or BAPTA-AM. Additionally, HERPUD1 deficiency led to reactive oxygen species -dependent activation of paxillin and FAK proteins, which are associated with enhanced cell migration.Our findings highlight the pivotal role of HERPUD1 in regulating mitochondrial function and cell migration by controlling intracellular Ca2+ signals mediated by ITPR3. Understanding the interplay between HERPUD1 and mitochondrial Ca2+ regulation provides insights into potential therapeutic targets for cancer treatment and other pathologies involving altered energy metabolism.
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    Regulation of total LC3 levels by angiotensin II in vascular smooth muscle cells
    (2022) Mondaca-Ruff, David; Quiroga, Clara; Norambuena-Soto, Ignacio; Riquelme, Jaime A.; San Martin, Alejandra; Bustamante, Mario; Lavandero, Sergio; Chiong, Mario
    Hypertension is associated with high circulating angiotensin II (Ang II). We have reported that autophagy regulates Ang II-induced vascular smooth muscle cell (VSMC) hypertrophy, but the mechanism mediating this effect is still unknown. Therefore, we studied how Ang II regulates LC3 levels in VSMCs and whether Bag3, a co-chaperone known to regulate LC3 total levels, may be involved in the effects elicited by Ang II. A7r5 cell line or rat aortic smooth muscle cell (RASMC) primary culture were stimulated with Ang II 100 nM for 24 h and LC3 I, LC3 II and Bag3 protein levels were determined by Western blot. MAP1LC3B mRNA levels were assessed by RT-qPCR. Ang II increased MAP1LC3B mRNA levels and protein levels of LC3 I, LC3 II and total LC3 (LC3 I + LC3 II). Cycloheximide, but not actinomycin D, abolished LC3 II and total LC3 increase elicited by Ang II in RASMCs. In A7r5 cells, cycloheximide prevented the Ang II-mediated increase of LC3 I and total LC3, but not LC3 II. Moreover, Ang II increased Bag3 levels, but this increase was not observed upon co-administration with either losartan 1 mu M (AT1R antagonist) or Y-27632 10 mu M (ROCK inhibitor). These results suggest that Ang II may regulate total LC3 content through transcriptional and translational mechanisms. Moreover, Bag3 is increased in response to Ang II by a AT1R/ROCK signalling pathway. These data provide preliminary evidence suggesting that Ang II may stimulate autophagy in VSMCs by increasing total LC3 content and LC3 processing.