Effects of nitric oxide from exogenous nitric oxide donors on osteoblastic metabolism

Otsuka, Eri; Hirano, K.; Matsushita, Shouji; Inoue, Atsuto; Hirose, Shigehisa; Yamaguchi, Akira; Hagiwara, Hiromi

doi:10.1016/s0014-2999(98)00190-3

Cited by 49 publications

(40 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Inoue et al (25) reported that the cyclic nucleotides cAMP and cGMP significantly and reciprocally regulate osteocalcin synthesis and AL-P activity and modulate the formation of mineralized nodules by osteoblast-like cells in culture (7). HUVEC could act as a donor of nitric oxide, which is well known to enhance the level of mRNA osteocalcin in osteoblastic cells (40,62) and the rate of production of intracellular cGMP by activation of soluble guanylate cyclase. The identification of the signal transduction pathways involved in these cocultures is now underway.…”

Section: Discussionmentioning

confidence: 99%

Effect of HUVEC on human osteoprogenitor cell differentiation needs heterotypic gap junction communication

Villars

Guillotin

Amédée

et al. 2002

American Journal of Physiology-Cell Physiology

295

238

View full text Add to dashboard Cite

Villars, F., B. Guillotin, T. Amé dé e, S. Dutoya, L. Bordenave, R. Bareille, and J. Amé dé e. Effect of HUVEC on human osteoprogenitor cell differentiation needs heterotypic gap junction communication. Am J Physiol Cell Physiol 282: C775-C785, 2002; 10.1152/ajpcell.00310.2001.-Bone development and remodeling depend on complex interactions between bone-forming osteoblasts and other cells present within the bone microenvironment, particularly vascular endothelial cells that may be pivotal members of a complex interactive communication network in bone. Our aim was to investigate the interaction between human umbilical vein endothelial cells (HUVEC) and human bone marrow stromal cells (HBMSC). Cell differentiation analysis performed with different cell culture models revealed that alkaline phosphatase activity and type I collagen synthesis were increased only by the direct contact of HUVEC with HBMSC. This "juxtacrine signaling" could involve a number of different heterotypic connexions that require adhesion molecules or gap junctions. A dye coupling assay with Lucifer yellow demonstrated a functional coupling between HUVEC and HBMSC. Immunocytochemistry revealed that connexin43 (Cx43), a specific gap junction protein, is expressed not only in HBMSC but also in the endothelial cell network and that these two cell types can communicate via a gap junctional channel constituted at least by Cx43. Moreover, functional inhibition of the gap junction by 18␣-glycyrrhetinic acid treatment or inhibition of Cx43 synthesis with oligodeoxyribonucleotide antisense decreased the effect of HUVEC cocultures on HBMSC differentiation. This stimulation could be mediated by the intercellular diffusion of signaling molecules that permeate the junctional channel.coupling; intercellular messenger; connexin43; osteoblast; endothelial cells ANGIOGENESIS is a tightly regulated process involved in growth, repair, and bone remodeling (9, 11-13, 23, 28, 50, 54, 56). Several studies have shown that there is a reciprocal regulation and functional relationship between endothelial cells and osteoblast-like cells during osteogenesis, in which systemic hormones and paracrine growth factors or cytokines play an active role (4,24,53,55). In a previous study (51), we showed that osteoblast progenitor cells [human bone marrow stromal cells (HBMSC)] behave differently in terms of proliferation and differentiation when cultured in association with endothelial cells [human umbilical vein endothelial cells (HUVEC)] in various coculture models (coculture with or without direct contact, conditioned medium) than when they are cultured alone. An increase in alkaline phosphatase activity (Al-P) was observed only when HBMSC were cocultured in direct contact with HUVEC. The enhancement of this early osteoblastic marker is not provided when HBMSC and HUVEC are cocultured separately with the use of a semipermeable membrane (51) or when HBMSC are seeded onto a matrix obtained from HUVEC cultures (51).Therefore, the intercommunication between endothelial cells and os...

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of HUVEC on human osteoprogenitor cell differentiation needs heterotypic gap junction communication

Villars

Guillotin

Amédée

et al. 2002

American Journal of Physiology-Cell Physiology

295

238

View full text Add to dashboard Cite

show abstract

“…Previous studies have reported that NO decomposed from SNP or other NO donors, including NOC-7 and NOC-18, induces insults to primary osteoblasts or osteoblast-like ROB-C26 and MC3T3-E1cells. [29][30][31] Thus, a high concentration of SNP (2 mM) caused massive oxidative stress via production of intracellular ROS, and induced osteoblast damage or even cell death. SNP at a low concentration of 0.3 mM increased the levels of cellular NO without affecting cell viability but protected osteoblasts from oxidative stress-induced cell insults.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide protects osteoblasts from oxidative stress‐induced apoptotic insults via a mitochondria‐dependent mechanism

Chang

Liao

Lin

et al. 2006

Journal Orthopaedic Research

View full text Add to dashboard Cite

Nitric oxide (NO) contributes to the regulation of osteoblast activities. In this study, we evaluated the protective effects of NO pretreatment on oxidative stress-induced osteoblast apoptosis and its possible mechanism using neonatal rat calvarial osteoblasts as the experimental model. Exposure of osteoblasts to sodium nitroprusside (SNP) at a low concentration of 0.3 mM significantly increased cellular NO levels without affecting cell viability. However, when the concentration reached a high concentration of 2 mM, SNP increased the levels of intracellular reactive oxygen species and induced osteoblast injuries. Thus, administration of 0.3 and 2 mM SNP in osteoblasts were respectively used as sources of NO and oxidative stress. Pretreatment with NO for 24 h significantly ameliorated the oxidative stress-caused morphological alterations and decreases in alkaline phosphatase activity, and reduced cell death. Oxidative stress induced osteoblast death via an apoptotic mechanism, but NO pretreatment protected osteoblasts against the toxic effects. The mitochondrial membrane potential was significantly reduced following exposure to the oxidative stress. However, pretreatment with NO significantly lowered the suppressive effects. Oxidative stress increased cellular Bax protein production and cytochrome c release from mitochondria. Pretreatment with NO significantly decreased oxidative stress-caused augmentation of Bax and cytochrome c protein levels. In parallel with cytochrome c release, oxidative stress induced caspase-3 activation and DNA fragmentation. Pretreatment with NO significantly reduced the oxidative stress-enhanced caspase-3 activation and DNA damage. Results of this study show that NO pretreatment can protect osteoblasts from oxidative stress-induced apoptotic insults. The protective action involves a mitochondria-dependent mechanism. ß

show abstract

“…Given that spontaneous and evoked APs in B5 neurons depended on Ca channels, we next questioned whether the NO-mediated Ca influx reported in the previous study could have resulted from NO acting as a modulator of neuronal firing activity. To characterize the effect of NO on the spontaneous firing activity of B5 neurons, we bath applied the NO donor NOC-7 (100 M) [half-life: 5-10 min at physiological pH (Otsuka et al, 1998;Onodera et al, 2000)] and recorded neurons in whole-cell current-clamp configuration. In a first set of experiments, spontaneously firing neurons were held in A, Left, Example of a mature B5 neuron with well developed neurites and a large growth cone.…”

Section: Initial Characterization Of Basic Membrane Properties and Elmentioning

confidence: 99%

Nitric Oxide Acts as a Volume Transmitter to Modulate Electrical Properties of Spontaneously Firing Neurons via Apamin-Sensitive Potassium Channels

Artinian

Tornieri²,

Zhong³

et al. 2010

J. Neurosci.

View full text Add to dashboard Cite

Nitric oxide (NO) is a radical and a gas, properties that allow NO to diffuse through membranes and potentially enable it to function as a "volume messenger." This study had two goals: first, to investigate the mechanisms by which NO functions as a modulator of neuronal excitability, and second, to compare NO effects produced by NO release from chemical NO donors with those elicited by physiological NO release from single neurons. We demonstrate that NO depolarizes the membrane potential of B5 neurons of the mollusk Helisoma trivolvis, initially increasing their firing rate and later causing neuronal silencing. Both effects of NO were mediated by inhibition of Ca-activated iberiotoxin-and apamin-sensitive K channels, but only inhibition of apamin-sensitive K channels fully mimicked all effects of NO on firing activity, suggesting that the majority of electrical effects of NO are mediated via inhibition of apamin-sensitive K channels. We further show that single neurons release sufficient amounts of NO to affect the electrical activity of B5 neurons located nearby. These effects are similar to NO release from the chemical NO donor NOC-7 [3-(2-hydroxy-1-methyl-2-nitrosohydazino)-N-methyl-1-propyanamine], validating the use of NO donors in studies of neuronal excitability. Together with previous findings demonstrating a role for NO in neurite outgrowth and growth cone motility, the results suggest that NO has the potential to shape the development of the nervous system by modulating both electrical activity and neurite outgrowth in neurons located in the vicinity of NO-producing cells, supporting the notion of NO functioning as a volume messenger.

show abstract

Effects of nitric oxide from exogenous nitric oxide donors on osteoblastic metabolism

Cited by 49 publications

References 25 publications

Effect of HUVEC on human osteoprogenitor cell differentiation needs heterotypic gap junction communication

Effect of HUVEC on human osteoprogenitor cell differentiation needs heterotypic gap junction communication

Nitric oxide protects osteoblasts from oxidative stress‐induced apoptotic insults via a mitochondria‐dependent mechanism

Nitric Oxide Acts as a Volume Transmitter to Modulate Electrical Properties of Spontaneously Firing Neurons via Apamin-Sensitive Potassium Channels

Contact Info

Product

Resources

About