Pyrroloquinoline Quinone Modulates Mitochondrial Quantity and Function in Mice

Stites, Tracy; Storms, David H.; Bauerly, Kathryn; Mah, James; Harris, Calliandra; Fascetti, Andrea J.; Rogers, Quinton R.; Tchaparian, Eskouhie; Satre, Michael; Rucker, Robert B.

doi:10.1093/jn/136.2.390

Cited by 94 publications

(82 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…More recently, vitamin K 2 , a derivative of menadione, was discovered to function as an important electron carrier in Drosophila mitochondria to help maintain normal ATP production (8). A disordered quinone pool would severely affect the respiratory systems of Drosophila, leading to subsequent changes in cellular metabolism (9)(10)(11). Meanwhile, quinone molecules are also considered a source of exogenous stress: a variety of toxins and antimicrobial compounds contain quinone, such as cercosporin and anthracycline (12)(13)(14).…”

Section: Molecular Mechanism Of Quinone Signaling Mediated Through S-mentioning

confidence: 99%

Molecular mechanism of quinone signaling mediated through S-quinonization of a YodB family repressor QsrR

Zhang

Jones

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Section: Molecular Mechanism Of Quinone Signaling Mediated Through S-mentioning

confidence: 99%

Molecular mechanism of quinone signaling mediated through S-quinonization of a YodB family repressor QsrR

Zhang

Jones

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

“…It has been reported that PQQ can stimulate the activation of cAMP response elementbinding protein (CREB) in combination with some transcription factors such as Nrf1, Nrf2 and mitochondrial transcription factors, enhancing mitochondriogenesis Stites et al, 2006;Zhu et al, 2006;Chowanadisai et al, 2010), whereas the Nrf2/ARE signaling pathway has been recognized as a key contributor to the cellular response to neuronal injury in vitro and in vivo (Shih et al, 2005). In this study, we measured the expression level of Nrf2 and some related transcript factors to demonstrate whether Nrf2/ARE signaling was influenced by PQQ treatment.…”

Section: Discussionmentioning

confidence: 99%

Pyrroloquinoline quinone rescues hippocampal neurons from glutamate-induced cell death through activation of Nrf2 and up-regulation of antioxidant genes

Zhang¹,

Ding²,

Gao³

et al. 2012

Genet. Mol. Res.

View full text Add to dashboard Cite

ABSTRACT. Pyrroloquinoline quinone (PQQ) has been shown to protect primary cultured hippocampal neurons from glutamateinduced cell apoptosis by scavenging reactive oxygen species (ROS) and activating phosphatidylinositol-3-kinase (PI3K)/Akt signaling. We investigated the downstream pathways of PI3K/Akt involved in PQQ protection of glutamate-injured hippocampal neurons. Western blot analysis indicated that PQQ treatment following glutamate stimulation triggers phosphorylation of glycogen synthase kinase 3β, accompanied by maintenance of Akt activation. Immunostaining and quantitative RT-PCR revealed that PQQ treatment promotes nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), and up-regulates mRNA expression of Nrf2 and the antioxidant enzyme genes, heme oxygenase-1 and glutamate cysteine ligase catalytic in glutamate-injured hippocampal neurons; this is a process dependent on the PI3K/Akt pathway, as evidenced by blocking experiments with PI3K inhibitors. In addition, increased ROS production and decreased glutathione ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 11 (3): 2652-2664 (2012) PQQ rescues neurons from death through Nrf2 activation 2653 levels in glutamate-injured hippocampal neurons were found to be reduced by PQQ treatment. Collectively, our findings suggest that PQQ exerts neuroprotective activity, possibly through PI3K/Akt-dependent activation of Nrf2 and up-regulation of antioxidant genes. However, the ability of PQQ to scavenge ROS was not totally regulated by PI3K/Akt signaling; possibly it is governed by other mechanisms.

show abstract

“…This substance, initially identified as a coenzyme necessary for certain oxidation-reduction reactions and cell signaling pathways, has recently become of interest as a potentially critical coenzyme in mammals. [14][15][16][17][18][25][26][27][28][29] The importance of PQQ in mammalian health has been reported based on its omission from chemically defined diets, resulting in a wide range of systemic responses, including growth impairment, compromised immune responsiveness, and abnormal reproductive performance in mouse and rat experimental models. 11-13-13,17,18 In the immune system, PQQ deficiency is associated with a reduction in interleukin (IL)-2 level and decreased Tand B-cell sensitivity to mitogens 12 .…”

Section: Discussionmentioning

confidence: 99%

“…10,11 Previous nutrition studies have indicated a metabolic and nutrition role of PQQ in mammals. [11][12][13][14][15][16][17][18] When mice were…”

mentioning

confidence: 99%

Influence of Adding Pyrroloquinoline Quinone to Parenteral Nutrition on Gut‐Associated Lymphoid Tissue

Omata

Fukatsu

Murakoshi

et al. 2011

J Parenter Enteral Nutr

View full text Add to dashboard Cite

Background: Experimental intravenous (IV) parenteral nutrition (PN) diminishes gut‐associated lymphoid tissue (GALT) cell number and function. PN solution cannot maintain GALT at the same level as a normal diet, even when delivered intragastrically (IG). Previous studies demonstrated pyrroloquinoline quinone (PQQ)–deficient mice to be less immunologically responsive. Because standard (STD) PN solution lacks PQQ, PQQ supplementation may prevent PN‐induced GALT changes. This study was designed to determine the influence of adding PQQ to PN on GALT. Methods: In experiment 1, mice (n = 32) were randomized to chow, IV‐STD‐PN, and IV‐PQQ‐PN groups. The chow group was fed chow with the same caloric content as PN. The IV‐STD‐PN group received STD‐PN solution, whereas the IV‐PQQ‐PN group was given PQQ (3 mcg/d)–enriched PN by the IV route. After 5 days of feeding, lymphocytes were isolated from the Peyer's patch (PPs), intraepithelial space (IE), and lamina propria (LP) of the small intestine. GALT lymphocyte number and phenotype (αβTCR+, γδTCR+, CD4+, CD8+, B220+ cells) and intestinal immunoglobulin A (IgA) level were determined. In experiment 2, mice (n = 28) were randomized to IG‐STD‐PN or IG‐PQQ‐PN group. After IG nutrition supports, GALT mass and function were determined as in experiment 1. Results: The IV‐PQQ‐PN group showed increased PP lymphocyte number and PP CD8+ cell number compared with the IV‐STD PN group. The IG‐PQQ‐PN group had significantly greater PP lymphocyte number and PP CD4+ cell numbers than the IG‐STD‐PN group. Neither IV nor IG PQQ treatment raised IgA level. Conclusions: PQQ added to PN partly restores GALT mass, although its effects on GALT function remain unclear.

show abstract

Pyrroloquinoline Quinone Modulates Mitochondrial Quantity and Function in Mice

Cited by 94 publications

References 46 publications

Molecular mechanism of quinone signaling mediated through S-quinonization of a YodB family repressor QsrR

Molecular mechanism of quinone signaling mediated through S-quinonization of a YodB family repressor QsrR

Pyrroloquinoline quinone rescues hippocampal neurons from glutamate-induced cell death through activation of Nrf2 and up-regulation of antioxidant genes

Influence of Adding Pyrroloquinoline Quinone to Parenteral Nutrition on Gut‐Associated Lymphoid Tissue

Contact Info

Product

Resources

About