Inhibition of receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation by pyrroloquinoline quinine (PQQ)

Odkhuu, Erdenezaya; Koide, Naoki; Haque, Abedul; Tsolmongyn, Bilegtsaikhan; Naiki, Yoshikazu; Hirano, Shoji; Komatsu, Takayuki; Yoshida, Tomoaki; Yokochi, Takashi

doi:10.1016/j.imlet.2011.12.001

Cited by 13 publications

(12 citation statements)

References 39 publications

(67 reference statements)

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“…Additionally, mRNA levels of major osteoclast marker TRAP was also inhibited by PQQ. These findings were in agreement with a very recently study showing that PQQ directly affects osteoclast precursors and inhibits the osteoclast generation [18], demonstrating that PQQ inhibited RANKL-induced NF-κB activation and osteoclast formation, it could be expected that the down-regulation of NF-κB could also be a promising target for the reduction of RANKL-induced c-Fos and NFATc1 expression during osteolysis.…”

Section: Discussionsupporting

confidence: 92%

“…While the potential physiological role of PQQ in animals is unclear, it might be involved in bone metabolism via nitric oxide biosynthesis [17]. Previous studies have shown that PQQ acts negative effects on c-Fos expression which suggested it impaired activation of NFATc1 [18]. However, the effects of PQQ on RANKL and M-CSF induced osteoclast differentiation remain unclear, and there is no report about the effects of PQQ on particle-induced osteolysis in vivo .…”

Section: Introductionmentioning

confidence: 99%

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Pyrroloquinoline Quinine Inhibits RANKL-Mediated Expression of NFATc1 in Part via Suppression of c-Fos in Mouse Bone Marrow Cells and Inhibits Wear Particle-Induced Osteolysis in Mice

Kong

Yang

et al. 2013

PLoS ONE

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The effects of pyrroloquinoline quinine (PQQ) on RANKL-induced osteoclast differentiation and on wear particle-induced osteolysis were examined in this study. PQQ inhibited RANKL-mediated osteoclast differentiation in bone marrow macrophages (BMMs) in a dose-dependent manner without any evidence of cytotoxicity. The mRNA expression of c-Fos, NFATc1, and TRAP in RANKL-treated BMMs was inhibited by PQQ treatment. Moreover, RANKL-induced c-Fos and NFATc1 protein expression was suppressed by PQQ. PQQ additionally inhibited the bone resorptive activity of differentiated osteoclasts. Further a UHMWPE-induced murine calvaria erosion model study was performed to assess the effects of PQQ on wear particle-induced osteolysis in vivo. Mice treated with PQQ demonstrated marked attenuation of bone erosion based on Micro-CT and histologic analysis of calvaria. These results collectively suggested that PQQ demonstrated inhibitory effects on osteoclast differentiation in vitro and may suppress wear particle-induced osteolysis in vivo, indicating that PQQ may therefore serve as a useful drug in the prevention of bone loss.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Pyrroloquinoline Quinine Inhibits RANKL-Mediated Expression of NFATc1 in Part via Suppression of c-Fos in Mouse Bone Marrow Cells and Inhibits Wear Particle-Induced Osteolysis in Mice

Kong

Yang

et al. 2013

PLoS ONE

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“…Inflammatory cells, particularly the Kupffer cells, are recruited to the liver in response to liver injury or after exposure to danger signals. PQQ reduced macrophage infiltration in thioacetamide‐induced injury (18) and inhibited osteoclast formation (58), suggesting that PQQ targets macrophage activity. Oxidative stress, associated with maternal obesity (59, 60), may connect the liver to intrauterine programming sequelae in the macrophage, particularly via epigenetic mechanisms (61–64).…”

Section: Discussionmentioning

confidence: 99%

“…formation (58), suggesting that PQQ targets macrophage activity. Oxidative stress, associated with maternal obesity (59,60), may connect the liver to intrauterine programming sequelae in the macrophage, particularly via epigenetic mechanisms (61)(62)(63)(64).…”

Section: Discussionmentioning

confidence: 99%

Early PQQ supplementation has persistent long‐term protective effects on developmental programming of hepatic lipotoxicity and inflammation in obese mice

et al. 2016

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Nonalcoholic fatty liver disease (NAFLD) is widespread in adults and children. Early exposure to maternal obesity or Western-style diet (WD) increases steatosis and oxidative stress in fetal liver and is associated with lifetime disease risk in the offspring. Pyrroloquinoline quinone (PQQ) is a natural antioxidant found in soil, enriched in human breast milk, and essential for development in mammals. We investigated whether a supplemental dose of PQQ, provided prenatally in a mouse model of diet-induced obesity during pregnancy, could protect obese offspring from progression of NAFLD. PQQ treatment given pre- and postnatally in WD-fed offspring had no effect on weight gain but increased metabolic flexibility while reducing body fat and liver lipids, compared with untreated obese offspring. Indices of NAFLD, including hepatic ceramide levels, oxidative stress, and expression of proinflammatory genes (, ,, and ), were decreased in WD PQQ-fed mice, concomitant with increased expression of fatty acid oxidation genes and decreased expression. Notably, these changes persisted even after PQQ withdrawal at weaning. Our results suggest that supplementation with PQQ, particularly during pregnancy and lactation, protects offspring from WD-induced developmental programming of hepatic lipotoxicity and may help slow the advancing epidemic of NAFLD in the next generation.-Jonscher, K. R., Stewart, M. S., Alfonso-Garcia, A., DeFelice, B. C., Wang, X. X., Luo, Y., Levi, M., Heerwagen, M. J. R., Janssen, R. C., de la Houssaye, B. A., Wiitala, E., Florey, G., Jonscher, R. L., Potma, E. O., Fiehn, O. Friedman, J. E. Early PQQ supplementation has persistent long-term protective effects on developmental programming of hepatic lipotoxicity and inflammation in obese mice.

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“…PQQ regulates MAPk kinase activation and tyrosyl phosphorylation of ERK2 by production of CD4+T lymphocytes [116] having immune response by interleukin-2, and growth factors reduced when T-cell proliferation occurs [117]. When PQQ supplemented orally in nano-amounts alleviates the mitogens of B and T cells [118].…”

Section: Pqq Role In Immunitymentioning

confidence: 99%

The Life History of Pyrroloquinoline Quinone (PQQ): A Versatile Molecule with Novel Impacts on Living Systems

Naveed¹

2016

IJMBOA

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Pyrroloquinoline quinone (PQQ) acting as redox cofactor of Glucose dehydrogenase is orthocyclic antioxidant acting under multifarious environmental stress and rich conditions in prokaryotes as well as eukaryotes. Microbes are the exclusive source of PQQ biosynthesis and for biocatalysis of glucose into gluconic acid and 2-ketogluconic acid by gram positive and negative bacteria. This study focus to describe PQQ biography highlighted its applications acts as biocatalyst by enhanced production of NADH from pqqC, involved in several important mechanisms like bacterial energy transduction by m-ATPase, production of biocontrol substances, growth stimulating activities and DNA repair. PQQ acting as anti-neurological, anti-degenerative, anti-melanogenic and anti-cancer agent due to its antioxidant nature by scavenging free radicals. PQQ is modulator of immunity by CD4 cells count and IL-2, sleep maintenance by PGC-1 alpha pathway and inflammation due to ROS. The mineral phosphate solubilization results in plant growth promotional, biocontrol, antifungal and ISR activities. PQQ nanoparticles used for production of Biofuels cells and sulfonated polymers. It acts as a modulator of diverse signaling pathways like STAT, MAPK, JAK, JNK, P13K/Akt, mTOR, EGFR and Raps for cell proliferation, differentiation, apoptosis, Box translocation and metabolic pathways by phosphorylation of ADP and suppression of reactive oxygen species. It protects from oxidative stress by acting as Alpha AA modulator of lysine metabolism, TrxR1 in selenium metabolism, low density lipoprotein in lipid metabolism, ATP production in Energy, Glucose and carbohydrate metabolism. It has been structurally characterized with bioinformatics tools and future perspectives being molecular modeling and docking for analytical drug design.

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Inhibition of receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation by pyrroloquinoline quinine (PQQ)

Cited by 13 publications

References 39 publications

Pyrroloquinoline Quinine Inhibits RANKL-Mediated Expression of NFATc1 in Part via Suppression of c-Fos in Mouse Bone Marrow Cells and Inhibits Wear Particle-Induced Osteolysis in Mice

Pyrroloquinoline Quinine Inhibits RANKL-Mediated Expression of NFATc1 in Part via Suppression of c-Fos in Mouse Bone Marrow Cells and Inhibits Wear Particle-Induced Osteolysis in Mice

Early PQQ supplementation has persistent long‐term protective effects on developmental programming of hepatic lipotoxicity and inflammation in obese mice

The Life History of Pyrroloquinoline Quinone (PQQ): A Versatile Molecule with Novel Impacts on Living Systems

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