ROSA MARIA AFFONSO MOYSES
Projetos de Pesquisa
Unidades Organizacionais
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina - Líder
7 resultados
Resultados de Busca
Agora exibindo 1 - 7 de 7
- Turning over renal osteodystrophy dogma: direct actions of FGF23 on osteoblast beta-catenin pathway(2016) SCHIAVI, Susan C.; MOYSES, Rosa M. A.Although recognized as a major complication of chronic kidney disease (CKD), the pathophysiology of the CKD-related mineral and bone disorder (CKD-MBD) is not completely understood. Recently, the inhibition of Wnt/beta-catenin pathway in osteocytes by sclerostin has been shown to play a role in CKD-MBD. The study by Carrilo-Lopez et al. confirms this inhibition in an experimental model of CKD. Moreover, they describe direct actions of FGF23-Klotho on osteoblasts, increasing the expression of DKK1, another Wnt/beta-catenin pathway inhibitor.
- Sevelamer and CKD-associated cardiovascular disease: going further, but far from there(2013) MOYSES, Rosa M. A.; CANZIANI, Maria E. F.Cardiovascular disease is a major complication of chronic kidney disease (CKD), and current data support its link to mineral metabolism disturbances. However, there is an intense debate over whether CKD-mineral and bone disorder therapy could change the cardiovascular burden in CKD. The study by Maizel and colleagues shows the benefits of a phosphate binder, sevelamer, for the progression of aortic stiffness and endothelial dysfunction as well as left ventricular dysfunction and hypertrophy in mice with CKD.
- Peritoneal dialysis per se is a risk factor for sclerostin-associated adynamic bone disease(2015) OLIVEIRA, Rodrigo A. de; BARRETO, Fellype C.; MENDES, Monique; REIS, Luciene M. dos; CASTRO, Joao Henrique; BRITTO, Zita Maria L.; MARQUES, Igor D. B.; CARVALHO, Aluizio B.; MOYSES, Rosa M.; JORGETTI, VandaChronic kidney disease-mineral bone disorder (CKD-MBD) is a complex syndrome influenced by various factors, such as age, CKD etiology, uremic toxins, and dialysis modality. Although extensively studied in hemodialysis (HD) patients, only a few studies exist for peritoneal dialysis (PD) patients. Since most of these older studies contain no bone biopsy data, we studied the pattern of renal osteodystrophy in 41 prevalent PD patients. The most common presentation was adynamic bone disease (49%). There was a significant inverse association between serum sclerostin (a Wnt/beta-catenin pathway inhibitor that decreases osteoblast action and bone formation) and the bone formation rate. Bone alkaline phosphatase had the best sensitivity and specificity to detect both high-and low-turnover diseases. The comparison between nondiabetic PD and HD patients, matched by age, gender, parathyroid hormone level, and length of dialysis, revealed low 25-hydroxyvitamin D levels, worse bone mineralization, and low bone turnover in the nondiabetic PD group. Thus, adynamic bone disease was the most frequent type of renal osteodystrophy in PD patients. Sclerostin seems to participate in the pathophysiology of adynamic bone disease and bone alkaline phosphatase was the best serum marker of bone turnover in these patients.
- The complexity of chronic kidney disease-mineral and bone disorder across stages of chronic kidney disease(2017) GRACIOLLI, Fabiana G.; NEVES, Katia R.; BARRETO, Fellype; BARRETO, Daniela V.; REIS, Luciene M. dos; CANZIANI, Maria E.; SABBAGH, Yves; CARVALHO, Aluizio B.; JORGETTI, Vanda; ELIAS, Rosilene M.; SCHIAVI, Susan; MOYSES, Rosa M. A.Chronic Kidney Disease (CKD)-Mineral and Bone Disorder (CKD-MBD) is a complex disease that is not completely understood. However, some factors secreted by the osteocytes might play an important role in its pathophysiology. Therefore, we evaluated the bone expression of proteins in a group of patients with CKD 2-3, CKD 4, and CKD 5 on dialysis and healthy individuals. We also tested several bone remodeling markers, and correlated these levels with bone biopsy findings. As expected, as serum calcium decreased, serum phosphate, alkaline phosphatase, fibroblast growth factor-23 (FGF-23), parathyroid hormone, and osteoprotegerin increased, as CKD progressed. Additionally, there was a gradual increase in bone resorption associated with a decrease in bone formation and impairment in bone mineralization. Bone expression of sclerostin and parathyroid hormone receptor-1 seemed to be increased in earlier stages of CKD, whereas FGF-23 and phosphorylated beta-catenin had increased expression in the late stages of CKD, although all these proteins were elevated relative to healthy individuals. Immunohistochemical studies showed that FGF-23 and sclerostin did not co-localize, suggesting that distinct osteocytes produce these proteins. Moreover, there was a good correlation between serum levels and bone expression of FGF-23. Thus, our studies help define the complex mechanism of bone and mineral metabolism in patients with CKD. Linkage of serum markers to bone expression of specific proteins may facilitate our understanding and management of this disease.
- Is osteocyte Klotho bad for bone health?(2017) MOYSES, Rosa M. A.; DUSSO, AdrianaThe recent identification of aKlotho protein ( Klotho) in osteocytes led to the generation of an experimental mouse model with osteocyte-specific Klotho ablation. This enabled Komaba et al. to assess the contribution to bone structure and function of osteocyte Klotho per se as compared with that of the systemic fibroblast growth factor 23-Klotho axis. Surprisingly, unlike the osteopenia and low bone turnover of systemic Klotho deletion, osteocyte-specific Klotho ablation resulted in increased osteoblastic activity and bone formation rate.
- Comparison of serum levels with bone content and gene expression indicate a contradictory effect of kidney transplantation on sclerostin(2019) ARAUJO, Maria Julia Correia Lima Nepomuceno; MARQUES, Igor Denizarde Bacelar; GRACIOLLI, Fabiana Giorgetti; FUKUHARA, Luzia; REIS, Luciene Machado dos; CUSTODIO, Melani; JORGETTI, Vanda; ELIAS, Rosilene Mota; DAVID-NETO, Elias; MOYSES, Rosa M. A.In an attempt to clarify the mechanisms of post-transplant bone disease we investigated the bone content and gene expression of several bone-related proteins. After a successful kidney transplant, the content of sclerostin in bone biopsies was found to be increased as measured by immunohistochemistry, multiplex assay, and gene expression despite a concomitant decrease of sclerostin in the serum. The phosphorylation of beta-catenin was increased, confirming Wnt pathway inhibition, an effect accompanied by an increase of the receptor activator of nuclear factor kappa-B ligand (RANKL) and a decrease of osteoprotegerin protein levels in both serum and bone. Thus, changes in circulating biomarkers after kidney transplantation cannot be easily extrapolated to concomitant changes occurring in the bone. Hence, overall treatment decisions post kidney transplant should not be based on serum biochemistry alone.
- Parathyroidectomy: better late than never(2015) ELIAS, Rosilene M.; GOLDENSTEIN, Patricia T.; MOYSES, Rosa M. A.