Advanced glycation end products cause collagen II reduction by activating Janus kinase/signal transducer and activator of transcription 3 pathway in porcine chondrocytes

Huang, Chuan‐Yueh; Lai, Kuan-Yui; Hung, Li-Wen; Wu, Wei; Feng-Cheng, Liu; Ho, Ling‐Jun

doi:10.1093/rheumatology/ker134

Cited by 64 publications

(48 citation statements)

References 33 publications

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“…The AGEs that accumulate in chondrocytes from older individuals appear to activate janus kinase 2 and 3 signal transducer and STAT 3 phosphorylation, and lead to increased MMP13 and ADAMTS-4 and -5 expression and activity (Huang et al. 2011). …”

Section: Articular Cartilagementioning

confidence: 99%

Ageing in the musculoskeletal system

Roberts¹,

Colombier²,

Sowman³

et al. 2016

Acta Orthopaedica

100

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The extent of ageing in the musculoskeletal system during the life course affects the quality and length of life. Loss of bone, degraded articular cartilage, and degenerate, narrowed intervertebral discs are primary features of an ageing skeleton, and together they contribute to pain and loss of mobility. This review covers the cellular constituents that make up some key components of the musculoskeletal system and summarizes discussion from the 2015 Aarhus Regenerative Orthopaedic Symposium (AROS) (Regeneration in the Ageing Population) about how each particular cell type alters within the ageing skeletal microenvironment.

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Section: Articular Cartilagementioning

confidence: 99%

Ageing in the musculoskeletal system

Roberts¹,

Colombier²,

Sowman³

et al. 2016

Acta Orthopaedica

100

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“…Reports showed that disarrangement of F-actin cytoskeleton induced by activation of RhoA/ROCK signaling is the main mechanism in AGEs-RAGE injured endothelial cell hyperpermeability [8]. Moreover, AGE-RAGE initiates the cascades of signaling transduction such as AGE-RAGE-NADPH oxidase (Nox) to aggravate oxidative stress [9], or AGE-RAGE-Jak/Stat to interfere the biosynthesis of collagen in kidney fibroblast [10]. These downstream pathways are involved widely in inflammation, autophagy, and apoptosis exerting an extend influence on cellular metabolism.…”

Section: Introductionmentioning

confidence: 99%

Salvianolic Acid A Protects Against Diabetic Nephropathy through Ameliorating Glomerular Endothelial Dysfunction via Inhibiting AGE-RAGE Signaling

Hou

Qiang

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Glomerular endothelium dysfunction leads to the progression of renal architectonic and functional abnormalities in early-stage diabetic nephropathy (DN). Advanced glycation end products (AGEs) and receptor for AGEs (RAGE) are proved to play important roles in diabetic nephropathy. This study investigated the role of Salvianolic acid A (SalA) on early-stage DN and its possible underlying mechanism. Methods: In vitro AGEs formation and breaking rate were measured to illustrate the effect of SalA on AGEs. Type 2 diabetic nephropathy rats were induced by high-fat diet and low-dose streptozocin (STZ). After eight-week treatment with SalA 1 mg/kg/day, 24h-urine protein, creatinine clearance was tested and renal structural injury was assessed by PAS and PASM staining. Primary glomerular endothelial cell permeability was evaluated after exposed to AGEs. AGEs-induced RhoA/ROCK and subsequently activated disarrange of cytoskeleton were assessed by western blot and immunofluorescence. Results: Biochemical assay and histological examination demonstrated that SalA markedly reduced endothelium loss and glomerular hyperfiltration, suppressed glomerular hypertrophy and mesangial matrix expansion, eventually reduced urinary albumin and ameliorated renal function. Further investigation suggested that SalA exerted its renoprotective effects through inhibiting AGE-RAGE signaling. It not only inhibited formation of AGEs and increased its breaking in vitro, but also reduced AGEs accumulation in vivo and downregulated RAGE expression. SalA restored glomerular endothelial permeability through suppressing AGEs-induced rearrangement of actin cytoskeleton via AGE-RAGE-RhoA/ ROCK pathway. Moreover, SalA attenuated oxidative stress induced by AGEs, subsequently alleviated inflammation and restored the disturbed autophagy in glomerular endothelial cell and diabetic rats via AGE-RAGE-Nox4 axis. Conclusion: Our study indicated that SalA restored glomerular endothelial function and alleviated renal structural deterioration through inhibiting AGE-RAGE, thus effectively ameliorated early-stage diabetic nephropathy. SalA might be a promising therapeutic agent for the treatment of diabetic nephropathy.

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“…In addition to affecting the mechanical properties of tissue, AGEs also affect cell function via the engagement of receptor for AGEs (RAGE), which is the best characterized AGE receptor. AGEs/RAGE stimulate the activation of nuclear factor-κB (NF-κB)-dependent pathways and increase oxidative stress, subsequently inducing production of proinflammatory mediators including tumor necrosis factor-α (TNF-α) and matrix metalloproteinases (MMPs) [8,9]. However, it is recognized that current treatments to interrupt AGE-related signal pathways are inefficient, which limits the efficient treatment for OA.…”

Section: Introductionmentioning

confidence: 99%

Inhibition Effect of Curcumin on TNF-a and MMP-13 Expression Induced by Advanced Glycation End Products in Chondrocytes

Yang

Mao

et al. 2013

Pharmacology

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Aims: Accumulation of advanced glycation end products (AGEs) plays a pivotal role in the mechanism by which aging contributes to osteoarthritis (OA). In the present study, we examined the effect of curcumin, a pharmacologically safe phytochemical agent, on AGE-induced tumor necrosis factor-α (TNF-α) and matrix metalloproteinase-13 (MMP-13) in rabbit chondrocytes. Methods: Chondrocytes were derived from rabbit articular cartilage by enzymatic digestion. TNF-α and MMP-13 mRNA was monitored by RT-PCR. TNF-α protein was determined using cytokine-specific ELISA. The reactive oxygen species was determined by the fluorescent probe 29,79-dichlorofluorescein diacetate. The phosphorylation and nuclear translocation of the nuclear factor-ĸB (NF-ĸB) system were studied by Western blot and immunofluorescence respectively. Results: Curcumin significantly decreased AGE-stimulated TNF-α and MMP-13 mRNA and suppressed the NF-ĸB activation via inhibition of ĸBα (I-ĸBα) phosphorylation, I-ĸBα degradation and p65 nuclear translocation. Conclusions: These novel pharmacological actions of curcumin on AGE-stimulated chondrocytes provide new suggestions that curcumin has nutritional potential as a naturally occurring anti-inflammatory agent for treating OA.

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Advanced glycation end products cause collagen II reduction by activating Janus kinase/signal transducer and activator of transcription 3 pathway in porcine chondrocytes

Cited by 64 publications

References 33 publications

Ageing in the musculoskeletal system

Ageing in the musculoskeletal system

Salvianolic Acid A Protects Against Diabetic Nephropathy through Ameliorating Glomerular Endothelial Dysfunction via Inhibiting AGE-RAGE Signaling

Inhibition Effect of Curcumin on TNF-a and MMP-13 Expression Induced by Advanced Glycation End Products in Chondrocytes

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