Hyaluronic acid regulates a key redox control factor Nrf2 via phosphorylation of Akt in bovine articular chondrocytes

Onodera, Yuta; Teramura, Takeshi; Takehara, Toshiyuki; Fukuda, Kanji

doi:10.1016/j.fob.2015.05.007

Cited by 48 publications

(43 citation statements)

References 50 publications

(59 reference statements)

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“…Numerous studies have confirmed the effect of HA on the activity of these enzymes but in other cells and tissues and not in erythrocytes [75,76]. It was confirmed that HA can reduce cellular superoxide generation and its accumulation through Nrf2 regulation which can induce transcription of antioxidant enzymes such as SOD, GPx, CAT, and others [61]. Supplementary to its primary role in cytoprotection, Nrf2 is also linked to differentiation, proliferation, growth, and apoptosis, and it is thought that Nrf2 has evolved from an original role in hematopoiesis and the regulation of cell differentiation from early lineages [77].…”

Section: Evaluation Of Results Of Administration Of Hyaluronans In Exmentioning

confidence: 98%

“…One important pharmacological function of HA is the reduction of cellular superoxide generation and accumulation through nuclear factor erythroid 2-related factor 2 (Nrf2) regulation, which is a master transcription factor in cellular redox reactions. Antioxidants and phase II detoxifying enzymes such as catalase (CAT), superoxide dismutase (SOD), heme oxygenase-1, glutathione S-transferase, glutathione peroxidase (GPx), and thioredoxin are coordinated at transcription level by Nrf2, so the hyaluronic acid could affect the activity and quantity of these antioxidant enzymes (Figure 7) [61].…”

Section: Hyaluronan In Arthritis: Regulation Of Inflammation Through mentioning

confidence: 99%

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The Role of Endogenous Antioxidants in the Treatment of Experimental Arthritis

Bauerová¹,

Kucharská²,

Poništ³

et al. 2019

Antioxidants

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The pathogenesis of rheumatoid arthritis is poorly understood; however, elevated oxidative stress has been described to be involved. In this chapter, we present experiments with endogenous molecules bearing antioxidative properties. In our studies, we used male Lewis rats, and the arthritis was induced with Mycobacterium butyricum. In the first experiment, we tested coenzyme Q 10 (CoQ 10) in the oral daily dose of 100 mg/kg b.w. Markers of inflammation and total antioxidant status were corrected in the group supplemented. CoQ 10 treatment significantly improved concentrations of the investigated endogenous antioxidants. Further as an important fact, we consider a good bioavailability of used CoQ 10 formulation which was confirmed by increased CoQ concentrations in plasma, tissue, and mitochondria from skeletal muscles. In the second study, we describe the results with hyaluronic acid (HA) administered in oral daily doses of 0.5 mg and 5 mg/kg b.w. and of different molecular weights (0.43, 0.99, and 1.73 MDa). A notable antioxidative effect of HA was assessed: its administration increased the activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase) in erythrocytes and total antioxidant capacity of plasma and reduced the marker of oxidative damage to lipids-plasmatic lipid hydroperoxides. HA with the highest molecular weight showed the most significant effect.

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Section: Evaluation Of Results Of Administration Of Hyaluronans In Exmentioning

confidence: 98%

Section: Hyaluronan In Arthritis: Regulation Of Inflammation Through mentioning

confidence: 99%

The Role of Endogenous Antioxidants in the Treatment of Experimental Arthritis

Bauerová¹,

Kucharská²,

Poništ³

et al. 2019

Antioxidants

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“…It is known that increased adhesion by FN-integrin β1 interaction plays an essential role in regulating cell proliferation, survival, and migration by triggering several signaling pathways (Leiss et al 2008, Schmidt & Friedl 2010, Schiller et al 2013, Nakagawa et al 2014, especially PI-3K-Akt pathway, which is the most important pathway to promote cell survival (Benbrook & Masamha 2011). Interaction of CD44 with its ligands, including FN, can also enhance proliferation, survival, and invasion by activating PI-3K-Akt pathways (Li et al 2015, McFarlane et al 2015, Onodera et al 2015. In this study, we demonstrated that DEX could enhance the activation of Akt, which is a late phase and sustained regulation, suggesting that Akt activation is not a direct effect of DEX, but the result of DEXenhanced cell adhesion.…”

Section: Discussionmentioning

confidence: 99%

“…The interaction of FN-integrin β1 or FN-CD44 mediates the cell adhesion, and induces signaling, such as activating PI-3K-Akt pathway (Schmidt & Friedl 2010, Nakagawa et al 2014, Li et al 2015, Onodera et al 2015, McFarlane et al 2015, which is an important pathway to promote cell survival (Benbrook & Masamha 2011). We then examined whether PI-3K-Akt pathway was involved in the prosurvival effect of DEX in ovarian cancer cells.…”

Section: Activation Of Akt Pathway Is Involved In Pro-survival Effectmentioning

confidence: 99%

The pro-adhesive and pro-survival effects of glucocorticoid in human ovarian cancer cells

Yin

Fang

Song

et al. 2016

Journal of Molecular Endocrinology

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Cell adhesion to extracellular matrix (ECM) is controlled by multiple signaling molecules and intracellular pathways, and is pivotal for survival and growth of cells from most solid tumors. Our previous works demonstrated that dexamethasone (DEX) significantly enhances cell adhesion and cell resistance to chemotherapeutics by increasing the levels of integrin β1, α4, and α5 in human ovarian cancer cells. However, it is unclear whether the components of ECM or other membrane molecules are also involved in the proadhesive effect of DEX in ovarian cancer cells. In this study, we demonstrated that the treatment of cells with DEX did not change the expression of collagens (I, III, and IV), laminin, CD44, and its principal ligand hyaluronan (HA), but significantly increased the levels of intracellular and secreted fibronectin (FN). Inhibiting the expression of FN with FN1 siRNA or blocking CD44, another FN receptor, with CD44 blocking antibody significantly attenuated the pro-adhesion of DEX, indicating that upregulation of FN mediates the pro-adhesive effect of DEX by its interaction with CD44 besides integrin β1. Moreover, DEX significantly enhanced cell resistance to the chemotherapeutic agent paclitaxel (PTX) by activating PI-3K-Akt pathway. Finally, we found that DEX also significantly upregulated the expression of MUC1, a transmembrane glycoprotein. Inhibiting the expression of MUC1 with MUC1 siRNA significantly attenuated the DEX-induced effects of pro-adhesion, Akt-activation, and pro-survival. In conclusion, these results provide new data that upregulation of FN and MUC1 by DEX contributes to DEX-induced pro-adhesion and protects ovarian cancer cells from chemotherapy.

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“…The major structural component of brain extracellular matrix (ECM) is hyaluronan (HA), which not only serves as the main anchoring point for brain cells but is also an important facilitator of intracellular signaling. CD44 and RHAMM are primary receptors for HA that signal to AKT upon binding (Lin, Chang, & Ying, 2007;Onodera, Teramura, Takehara, & Fukuda, 2015;Trapasso & Allegra, 2012, p. 44…”

Section: Ha-akt Signalingmentioning

confidence: 99%

Investigating Autophagy Dysfunction Induced by a Parkinson's Disease-Causing Mutation in VPS35

Rahman¹

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Hyaluronic acid regulates a key redox control factor Nrf2 via phosphorylation of Akt in bovine articular chondrocytes

Cited by 48 publications

References 50 publications

The Role of Endogenous Antioxidants in the Treatment of Experimental Arthritis

The Role of Endogenous Antioxidants in the Treatment of Experimental Arthritis

The pro-adhesive and pro-survival effects of glucocorticoid in human ovarian cancer cells

Investigating Autophagy Dysfunction Induced by a Parkinson's Disease-Causing Mutation in VPS35

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