Browsing by Author "Castro, R. E."
Now showing 1 - 10 of 10
Results Per Page
Sort Options
- 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.
- Differential regulation of cyclin D1 and apoptosis by bile acids in primary rat hepatocytesPublication . Castro, R. E.; Amaral, J. D.; Sola, S.; Kren, B. T.; Steer, C. J.; Rodrigues, C. M.
- MODULATION OF MIRNAS BY BILE ACIDSPublication . Castro, R. E.; Zeng, Y.; Steer, C. J.; Kren, B. T.; Rodrigues, C. M. P.
- Modulation of pro-apoptotic p53 transcriptional targeting by bile acids in primary rat hepatocytesPublication . Amaral, J. D.; Castro, R. E.; Sola, S.; Rodrigues, C. M. R.
- MODULATION OF THE P53 UBIQUITIN-PROTEASOME DEGRADATION PATHWAY BY URSODEOXYCHOLIC ACIDPublication . Amaral, J. D.; Castro, R. E.; Sola, S.; Rodrigues, C. M. P.
- P53 is a specific molecular target of ursodeoxycholic acidPublication . Amaral, J. D.; Castro, R. E.; Sola, S.; Rodrigues, C. M.
- 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
- Role of miR-21 in regenerating rat liverPublication . Castro, R. E.; Santos, D. M.; Zeng, Y.; Steer, C. J.; Rodrigues, C. M.; Kren, B. T.
- 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.