Glucosamine promotes osteoblast proliferation by modulating autophagy via the mammalian target of rapamycin pathway

Wang, Lu; Zhu, Xiongbai; Lin, Wenjun; Chen, Xin; Huang, Zhengxiang; Huang, Lintuo; Yang, Shengwu

doi:10.1016/j.biopha.2018.01.066

Cited by 34 publications

(24 citation statements)

References 29 publications

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“…After exposure to bubbles for 30 minutes, autophagy markers LC3‐II/I ratio (the ratio of LC3‐II to LC3‐I), Beclin‐1 and P62 were determined at 2, 4, 8, 12 and 24 hours by Western blotting (WB). Since the expressions of these proteins were consistent after different intensities of stimuli, the peak or valley time were selected as the follow‐up detection time . The number of autophagosomes was determined by transmission electron microscopy (TEM).…”

Section: Methodsmentioning

confidence: 99%

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Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

Wang¹,

Zhang²,

Nie³

et al. 2019

J Cellular Molecular Medi

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Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble‐induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3‐methyladenine (3‐MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3‐II/I ratio and Beclin‐1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase‐3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3‐II/I ratio and partially reversed by 3‐MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre‐conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre‐conditioning, and 30‐minutes pre‐conditioning induced opposing changes, all of which were inhibited by 3‐MA. In conclusion, autophagy was involved and played a biphasic role in bubble‐induced endothelial injury.

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Section: Methodsmentioning

confidence: 99%

“…Since the expressions of these proteins were consistent after different intensities of stimuli, the peak or valley time were selected as the follow-up detection time. 23,24 The number of autophagosomes was determined by transmission electron microscopy (TEM). LC3-II/I ratio,…”

Section: Part 1: Effects Of Different Durations Of Bubble Contact Omentioning

confidence: 99%

Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

Wang¹,

Zhang²,

Nie³

et al. 2019

J Cellular Molecular Medi

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“…Glucosamine induces autophagy in simian virus 40-transformed monkey kidney COS-7 cells [99], primary rat nucleus pulposus cells [100], human retinal pigment epithelial cells [101], human cervical adenocarcinoma Hela cells [99], and the nematode Caenorhabditis elegans [102]. However, the direct evidence of the role of glucosamine-induced autophagy in OA is scarce [103][104][105]. Glucosamine hydrochloride induces autophagy in primary chondrocytes derived from normal human articular cartilage [103,104] and hFOB1.19 osteoblasts [105].…”

Section: Activation Of Autophagy By Glucosaminementioning

confidence: 99%

“…However, the direct evidence of the role of glucosamine-induced autophagy in OA is scarce [103][104][105]. Glucosamine hydrochloride induces autophagy in primary chondrocytes derived from normal human articular cartilage [103,104] and hFOB1.19 osteoblasts [105]. Oral and intraperitoneal administration of glucosamine (250 mg/kg body weight/day) on green fluorescent protein fused to light chain 3 (GFP-LC3)-transgenic mice for 7 days has induced autophagy in the liver and knee joint cartilage of mice, the magnitude of autophagy activation is greater than that of starvation [104].…”

Section: Activation Of Autophagy By Glucosaminementioning

confidence: 99%

“…The upstream initiation of glucosamine-mediated autophagy remains elusive. Current findings suggested that glucosamine-mediated chondrocyte autophagy may be associated with the protein kinase B (PKB or Akt)/Forkhead box O3 (FoxO3)/mammalian target of rapamycin (mTOR) pathway [104,105]. A remarkable and concurrent inhibition of Akt, FoxO3, and ribosomal protein S6 protein (a mTOR downstream target) phosphorylation is detected along with glucosamine-induced autophagy [104].…”

Section: Activation Of Autophagy By Glucosaminementioning

confidence: 99%

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Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

et al. 2019

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Osteoarthritis (OA) is a joint disease resulting from cartilage degeneration and causing joint pain and stiffness. Glucosamine exerts chondroprotective effects and effectively reduces OA pain and stiffness. This review aims to summarise the mechanism of glucosamine in protecting joint health and preventing OA by conducting a literature search on original articles. Current evidence has revealed that glucosamine exhibits anti-inflammatory effects by reducing the levels of pro-inflammatory factors (such as tumour necrosis factor-alpha, interleukin-1, and interleukin-6) and enhancing the synthesis of proteoglycans that retard cartilage degradation and improve joint function. Additionally, glucosamine improves cellular redox status, reduces OA-mediated oxidative damages, scavenges free radicals, upregulates antioxidant proteins and enzyme levels, inhibits the production of reactive oxygen species, and induces autophagy to delay OA pathogenesis. In conclusion, glucosamine prevents OA and maintains joint health by reducing inflammation, improving the redox status, and inducing autophagy in joints. Further studies are warranted to determine the synergistic effect of glucosamine with other anti-inflammatory and/or antioxidative agents on joint health in humans.

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Glucosamine suppresses oxidative stress and induces protective autophagy in osteoblasts by blocking the ROS/Akt/mTOR signaling pathway

Huang

et al. 2022

Cell Biology International

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Oxidative stress is the crucial pathogenic factor in osteoporosis. Cell autophagy, a major form of self-digestion, plays critical functions in different forms of stress by devouring harmful cytosolic proteins or organelles for the renewal of organelles and to maintain cellular homeostasis. Glucosamine (GlcN) has been widely utilized in treatments for patients with osteoarthritis-related joint pain. It has potential antioxidant effects and its pharmacological effect in osteoblasts remains unclear.The present study aimed to investigate whether autophagy participates in the protective effects of GlcN in osteoblasts under oxidative stress and the possible mechanism. First of all, MC3T3-E1 cells were treated with hydrogen peroxide (H 2 O 2 ) to induce oxidative stress, as assessed by viability assays, apoptosis, the intracellular reactive oxygen species production. GlcN was capable of inducing autophagy and protected osteoblasts from those cytotoxic effects. Moreover, it significantly attenuated H 2 O 2 -induced oxidative stress as measured by malondialdehyde, glutathione, nitrite, and superoxide dismutase levels. Importantly, the autophagy level increased in osteoblasts treated with GlcN as represented by an increase in both Beclin1 expression and the LC3 II/I ratio. Immunofluorescence analysis of autophagosomes also confirmed the above results. In addition, GlcN decreased the mammalian target of rapamycin (mTOR) and protein kinase B (Akt). However, the Akt activator (SC79) suppressed the autophagy level induced by GlcN in osteoblasts.Consequently, the antioxidant effects of GlcN were mediated, at least in part, by enhancing autophagy through the Akt/mTOR pathway. These results suggested that GlcN might be a promising candidate for osteoporosis treatment.

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Glucosamine promotes osteoblast proliferation by modulating autophagy via the mammalian target of rapamycin pathway

Cited by 34 publications

References 29 publications

Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

Biphasic effects of autophagy on decompression bubble‐induced endothelial injury

Multifaceted Protective Role of Glucosamine against Osteoarthritis: Review of Its Molecular Mechanisms

Glucosamine suppresses oxidative stress and induces protective autophagy in osteoblasts by blocking the ROS/Akt/mTOR signaling pathway

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