کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1981608 1539419 2015 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hyaluronic acid regulates a key redox control factor Nrf2 via phosphorylation of Akt in bovine articular chondrocytes
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Hyaluronic acid regulates a key redox control factor Nrf2 via phosphorylation of Akt in bovine articular chondrocytes
چکیده انگلیسی


• Hyaluronic acid (HA) has a pharmacological role for reduction of cellular superoxide.
• In HA-treated chondrocytes, expression of Nrf2 and its downstream genes was upregulated.
• Inhibition of Akt or suppression of HA receptors prevented HA-mediated Nrf2 accumulation.
• Nrf2 siRNA inhibited the HA effect on antioxidant enzymes.
• HA might contribute to ROS reduction through Nrf2 regulation by activating Akt.

One important pharmacological function of hyaluronic acid (HA) in chondrocytes is reduction of cellular superoxide generation and accumulation. Here we demonstrated a relationship between HA supplementation and accumulation of Nuclear factor-erythroid-2-related factor 2 (Nrf2), which is a master transcription factor in cellular redox reactions, in cultured chondrocytes derived from bovine joint cartilage. In HA-treated chondrocytes, expression of Nrf2 and its downstream genes was upregulated. In HA-treated chondrocytes, Akt was phosphorylated, and inhibition of Akt activity or suppression of HA receptors CD44 and/or RHAMM with siRNAs prevented HA-mediated Nrf2 accumulation. Furthermore, Nrf2 siRNA inhibited the HA effect on antioxidant enzymes. These results show that HA might contribute to ROS reduction through Nrf2 regulation by activating Akt. Our study suggests a new mechanism for extracellular matrix (ECM)-mediated redox systems in chondrocytes.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: FEBS Open Bio - Volume 5, 2015, Pages 476–484
نویسندگان
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