4 documents found, page 1 of 1
The role of reactive oxygen species in bone cell physiology and pathophysiology
Carvalho, Adriana Marques; Kim, Ha-Neui; Almeida, MariaHydrogen peroxide (H2O2), superoxide anion radical (O2-•), and other forms of reactive oxygen species (ROS) are produced by the vast majority of mammalian cells and can contribute both to cellular homeostasis and dysfunction. The NADPH oxidases (NOX) enzymes and the mitochondria electron transport chain (ETC) produce most of the cellular ROS. Multiple antioxidant systems prevent the accumulation of excessive am...
ECSIT is essential for RANKL-induced stimulation of mitochondria in osteoclasts...
Carvalho, Adriana Marques; Sardão, Vilma A.; Kim, Ha-Neui; Almeida, Maria SIntroduction: Estrogens inhibit bone resorption and preserve bone mass, at least in part, via direct effects on osteoclasts. The binding of RANKL, the critical cytokine for osteoclast differentiation, to its receptor in osteoclast precursor cells of the monocyte lineage recruits the adaptor protein TRAF6 and activates multiple signaling pathways. Early effects of RANKL include stimulation of mitochondria. 17b-e...
The NAD salvage pathway in mesenchymal cells is indispensable for skeletal deve...
Warren, Aaron; Porter, Ryan M; Reyes-Castro, Olivia; Ali, Md Mohsin; Carvalho, Adriana Marques; Kim, Ha-Neui; Gatrell, Landon B; Schipani, ErnestinaNAD is an essential co-factor for cellular energy metabolism and multiple other processes. Systemic NAD+ deficiency has been implicated in skeletal deformities during development in both humans and mice. NAD levels are maintained by multiple synthetic pathways but which ones are important in bone forming cells is unknown. Here, we generate mice with deletion of Nicotinamide Phosphoribosyltransferase (Nampt), a ...
Estrogens decrease osteoclast number by attenuating mitochondria oxidative phos...
Kim, Ha-Neui; Ponte, Filipa; Nookaew, Intawat; Ucer Ozgurel, Serra; Carvalho, Adriana Marques; Iyer, Srividhya; Warren, Aaron; Aykin-Burns, NukhetLoss of estrogens at menopause is a major cause of osteoporosis and increased fracture risk. Estrogens protect against bone loss by decreasing osteoclast number through direct actions on cells of the myeloid lineage. Here, we investigated the molecular mechanism of this effect. We report that 17β-estradiol (E2) decreased osteoclast number by promoting the apoptosis of early osteoclast progenitors, but not matur...