Browsing by Author "Rodrigues, C. M. P."
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- Bile acids differentally regulate cell cycle and apoptosis-related proteins in primary rat hepatocytesPublication . Castro, R. E.; Amaral, J. D.; Borralho, P.; Sola, S.; Kren, B. T.; Steer, C. J.; Rodrigues, C. M. P.
- MODULATION OF MIRNAS BY BILE ACIDSPublication . Castro, R. E.; Zeng, Y.; Steer, C. J.; Kren, B. T.; Rodrigues, C. M. P.
- MODULATION OF THE P53 UBIQUITIN-PROTEASOME DEGRADATION PATHWAY BY URSODEOXYCHOLIC ACIDPublication . Amaral, J. D.; Castro, R. E.; Sola, S.; Rodrigues, C. M. P.
- Monoterpene indole alkaloids from the leaves of Tabernaemontana elegans induce apoptosis activity in human hepatoma cellsPublication . Mansoor, T. A.; Ramalho, R. M.; Rodrigues, C. M. P.; Mulhovo, S.; Ferreira, M. J. U.
- NF-kappa B and apoptosis in colorectal tumourigenesisPublication . Aranha, M. M.; Borralho, P. M.; Ravasco, P.; da Silva, I. B. Moreira; Correia, L.; Fernandes, A.; Camilo, M. E.; Rodrigues, C. M. P.Background Nuclear factor-kappa B (NF-kappa B) may play an important role in colorectal tumourigenesis, controlling cell cycle and apoptosis gene expression. In addition, imbalances between cell proliferation and cell death are thought to underlie neoplas
- Progesterone and caspase-3 activation in equine cyclic corpora luteaPublication . Ferreira-Dias, G.; Mateus, L.; Costa, A. S.; Sola, S.; Ramalho, R. M.; Castro, R. E.; Rodrigues, C. M. P.Soon after ovulation, the newly formed corpus luteum (CL) starts secreting progesterone (P-4), necessary for implantation. The CL, an ovarian transient endocrine organ, undergoes growth and regression throughout its life span. The objective of this study
- Synthetic Condensed 1,4-naphthoquinone Derivative Shifts Neural Stem Cell Differentiation by Regulating Redox StatePublication . Santos, Daniela M.; Santos, Maria M. M.; Moreira, Rui; Solá, Susana; Rodrigues, C. M. P.Naphthoquinones are bioactive compounds widespread in nature that impact on several cellular pathways, including cell proliferation and survival, by acting as prooxidants and electrophiles. We have previously described the role of the synthetic isoxazole condensed 1,4-naphthoquinone derivative 1a in preventing apoptosis induced by distinct stimuli in several cell models. In addition, apoptosis regulators and executioners may control neural stem cell (NSC) fate, without involving cell death per se. Here, we hypothesize that 1a might also play a role in NSC fate decision. We found that exposure to 1a shifts NSC differentiation potential from neurogenic to gliogenic lineage and involves the generation of reactive oxygen species, without increasing cell death. Modulation of caspases and calpains, using cysteine protease inhibitors, failed to mimic 1a effects. In addition, incubation with the naphthoquinone derivative resulted in upregulation and nuclear translocation of antioxidant responsive proteins, Nrf2 and Sirt1, which in turn may mediate 1a-directed shift in NSC differentiation. In fact, antioxidants halted the shift in NSC differentiation potential from neurogenic to gliogenic lineage, while strongly reducing reactive oxygen species generation and Nrf2 and Sirt1 nuclear translocation in NSC exposed to 1a. Collectively, these data support a new role for a specific naphthoquinone derivative in NSC fate decision and underline the importance of redox environment control.
- Tauroursodeoxycholic acid prevents E22Q Alzheimer's A beta toxicity in human cerebral endothelial cellsPublication . Viana, R. J. S.; Nunes, A. F.; Castro, R. E.; Ramalho, R. M.; Meyerson, J.; Fossati, S.; Ghiso, J.; Rostagno, A.; Rodrigues, C. M. P.The vasculotropic E22Q mutant of the amyloid-beta (A beta) peptide is associated with hereditary cerebral hemorrhage with amyloidosis Dutch type. The cellular mechanism(s) of toxicity and nature of the A beta E22Q toxic assemblies are not completely understood. Comparative assessment of structural parameters and cell death mechanisms elicited in primary human cerebral endothelial cells by A beta E22Q and wild-type A beta revealed that only A beta E22Q triggered the Bax mitochondrial pathway of apoptosis. A beta E22Q neither matched the fast oligomerization kinetics of A beta 42 nor reached its predominant beta-sheet structure, achieving a modest degree of oligomerization with a secondary structure that remained a mixture of beta and random conformations. The endogenous molecule tauroursodeoxycholic acid (TUDCA) was a strong modulator of A beta E22Q-triggered apoptosis but did not significantly change the secondary structures and fibrillogenic propensities of A beta peptides. These data dissociate the pro-apoptotic properties of A beta peptides from their distinct mechanisms of aggregation/fibrillization in vitro, providing new perspectives for modulation of amyloid toxicity.. - Fundacao para a Ciencia e a Tecnologia (FCT), Lisbon, Portugal [PTDC/BIABCM/67922/2006, BD/30467/2006, BPD/34603/2007, BPD/30257/2006, BPD/40623/2007]; NIH [NS051715, AG10491]; American Heart Association.. - This work was supported by grant PTDC/BIABCM/67922/2006 from Fundacao para a Ciencia e a Tecnologia (FCT), Lisbon, Portugal; NIH grants NS051715 andAG10491; and the American Heart Association. R.J.S.V. is the recipient of a PhD fellowship from FCT, Portugal (BD/30467/2006); A.F.N., R.E.C. and R. M. R. are recipients of postdoctoral fellowships from FCT, Portugal (BPD/34603/2007, BPD/30257/2006 and BPD/40623/2007, respectively).
- Ursodeoxycholic acid modulates the ubiquitin-proteasome degradation pathway of P53Publication . Amaral, J. D.; Castro, R. E.; Sola, S.; Rodrigues, C. M. P.