1,721,044 research outputs found
Increase in ferric and ferrous iron in the mouse lung after asbestos exposure
No full textThe growing amounts of Fe2+ in the lung of asbestos exposed mice could support a continuated generation of oxidative stress resulting in clinical manifestations, which culminate in inflammarory, fibrotic and hyperplastic lesions
, "REGULATION OF BREAST CANCER MIGRATION TO BONE: ROLE OF RANK/RANKL/OPG". ATTI DEL CONVEGNO "32 ND NATIONAL CONGRESS OF THE ITALIAN SOCIETY OF HISTOCHEMISTRY",
No full textMorphological features P2X3 expression in sensory neurons of rodent trigeminal ganglia under different culture conditions
No full textEffect of the neridronate on RANKL release in differentiated primary human osteoblasts
No full textBisphosphonates are important inhibitors of bone resorption and widely used clinically to treat osteoporosis, metabolic bone diseases and other orthopaedic disorders . Inhibiting osteoclasts via the mevalonate pathway is rec- ognized as the primary mechanism of its inhibitory action. Recent evidence suggests that bisphosphonates may regulate essential signaling molecules involved in osteoclastoge- nesis such as RANKL (receptor activator of NF- kB ligand) which are synthesized by osteoblasts. In this report we have investigated into the neridronate-osteoblast interactions in modulating essential signaling molecule such as RANKL
Increased OPG expression and impaired OPG/TRAIL ratio in the aorta of diabetic rats.
No full textDespite accumulating evidence showing that TNF-related apoptosis inducing ligand (TRAIL) plays a role in vascular biology and that its decoy receptor osteoprotegerin (OPG) is expressed in the vessel wall, modulation of these TNF and TNF-R family members in the early phases of diabetes mellitus has not been investigated. The expression of TRAIL and of OPG was examined both at the mRNA and protein levels in control and streptozotocin (SZT)-induced diabetic rats at early time points after the induction of diabetes mellitus. No differences in the steady-state mRNA levels of TRAIL were noticed by quantitative RT-PCR among the two groups of animals. On the other hand, diabetic rats showed a rapid and significant increase of the steady-state mRNA levels of OPG in the aortic wall of diabetic animals with respect to vehicle-treated (control) animals. These findings were confirmed at the protein level by analysing the amount of TRAIL and OPG proteins in aortic lysates by either Western blot or immunohistochemistry. Thus, an abnormal elevation of the OPG/TRAIL ratio in the vessel wall characterizes the early onset of diabetes mellitus and might represent a molecular mechanism involved in the vascular dysfunction characterizing diabetes mellitus
Recombinant TRAIL induces miorelaxating activity in rat aortas, which is abrogated by the induction of diabetes mellitus
No full textTNF-related apoptosis inducing ligand (TRAIL) is a member of the tumor necrosis factor (TNF) family of cytokines, which exist either as type II membrane or as a soluble protein. Although the best-characterized activity of TRAIL is represented by its anti-cancer activity, it has been recently shown that TRAIL serum levels are decreased in patients affected by atherosclerotic cardiovascular disease raising the possibility that circulating soluble TRAIL might also affect vascular biology. In this respect, it has been previously shown that TRAIL induces the in vitro release of nitric oxide by vascular endothelial cells. In order to explore the in vivo relevance of these in vitro findings, we have assessed the vascular reactivity in response to recombinant TRAIL in a more intact paradigm. For this purpose, rings (4mm long) from rat thoracic aorta were obtained by both control (3-month-old male non-diabetic Wistar rats receiving vehicle infusion) and rats in which diabetes mellitus was induced by injecting 40 mg/kg streptozotocin (SZT). After sacrifice of the animals, aortas were harvested, cleaned of connective tissue and vascular reactivity was analyzed in ex vivo immediately after harvest. During submaximal contraction with phenylephrine, incubation of aortic segments in the presence of increasing (up to 1000 ng/ml) concentrations of recombinant human TRAIL, resulted in significant (p<0.01) vaso-relaxation. The effect was dose-dependent and was completely abolished by pre incubation of the rat aortic rings with L-NAME, clearly indicating that the NOS pathway played a key role in mediating the myo-relaxating activity of TRAIL. In parallel, we have investigated whether the induction of diabetes mellitus might affect the relaxating activity of aortic rings in response to TRAIL. Diabetes mellitus was induced by destruction of pancreatic islet cells by treating rats with SZT (40 mg/kg). Non-fasting blood glucose concentrations of both SZT-diabetic rats (SZT, n = 10) and age-matched control non-diabetic rats treated with vehicle (n = 10) were measured at days 5 and 15, when animals were sacrificed with CO2. The loss of insulin secretion triggered stable hyperglycemia, as evaluated by blood glucose measurement: 260±46 and 295±55 in diabetic rats at days 5 and 15 after diabetic induction, respectively, versus 89±8 in control rats. Relaxation to TRAIL was completely abrogated in aortic rings obtained from SZT-induced diabetic rats. To the best of our knowledge, this is the first demonstration that soluble recombinant TRAIL promotes a dose-dependent myo-relaxation activity when added ex vivo to rat aortic rings, thus suggesting that it might play a physiological role in the control of vascular tone regulation. Importantly, such myorelaxating activity was completely abrogated in diabetic rats, as early as 15 days after diabetes mellitus induction by STZ injection. It should be emphasized that diabetic vascular dysfunction is a major clinical problem that predisposes patients to a variety of cardiovascular diseases. In fact, diabetic patients frequently suffer from macroscopic and microscopic vasculopathy and accelerated atherosclerosis. The loss of myo-relaxating activity is a key feature of endothelial dysfunction, which invariably precedes permanent vascular alterations. Taken together with previous data showing that TRAIL significantly counteracts the pro-adhesive activity of inflammatory cytokines on endothelial cells in vitro and displays anti-atherosclerotic activity when injected in vivo in ApoE−/−null mice, our present findings suggest that a therapeutic strategy aimed to restore the miorelaxating response to TRAIL may be suitable for improving the vascular function in diabetes mellitus
Recombinant TRAIL induces miorelaxating activity in rat aortas, which is abrogated by the induction of diabetes mellitus
No full textMethodological approach to scanning near field optical microscope (SNOM) for biological analysis. New prospects for nanobiotechnologies?
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