Curcumin suppresses tumor necrosis factor-α-induced matrix metalloproteinase-2 expression and activity in rat vascular smooth muscle cells via the NF-κB pathway

Zhong, Yi; Yu, Wenyan; Feng, Jian; Fan, Zhongcai; Li, Jiafu

doi:10.3892/etm.2014.1647

Cited by 19 publications

(17 citation statements)

References 28 publications

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“…In support of these findings, a recent study reported that activation of the TLR4/NF-κB pathway in microvascular ECs triggered marked upregulation of inflammatory molecules, which play a major role in the cross talk between ECs and monocytes/macrophages, leading to upregulated MMP expression, mainly via IL-6 secretion (Lu et al ., 2012). Moreover, TNF-α induces expression of MMP-2 and MMP-9 in vascular SMCs, through the NF-κB pathway (Zhong et al ., 2014). …”

Section: Discussionmentioning

confidence: 99%

“…These are all important events that contribute to enhancing MMP production and activation, resulting in excessive matrix degradation and the rupture of vulnerable atherosclerotic plaques (Leonarduzzi et al ., 2005; Poli et al ., 2009; Gargiulo et al ., 2011). Of note, among the various MMPs, MMP-9 has been consistently implicated in the pathophysiology of plaque rupture, and various inflammatory molecules, in particular interleukin-6 (IL-6), IL-8, IL-1β, and tumor necrosis factor-α (TNF-α), play crucial roles in the cross talk between vascular cells leading to upregulated MMP expression (Moreau et al ., 1999; Lu et al ., 2012; Zhong et al ., 2014). …”

Section: Introductionmentioning

confidence: 99%

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Relation between TLR4/NF‐κB signaling pathway activation by 27‐hydroxycholesterol and 4‐hydroxynonenal, and atherosclerotic plaque instability

et al. 2015

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It is now thought that atherosclerosis, although due to increased plasma lipids, is mainly the consequence of a complicated inflammatory process, with immune responses at the different stages of plaque development. Increasing evidence points to a significant role of Toll-like receptor 4 (TLR4), a key player in innate immunity, in the pathogenesis of atherosclerosis. This study aimed to determine the effects on TLR4 activation of two reactive oxidized lipids carried by oxidized low-density lipoproteins, the oxysterol 27-hydroxycholesterol (27-OH) and the aldehyde 4-hydroxynonenal (HNE), both of which accumulate in atherosclerotic plaques and play a key role in the pathogenesis of atherosclerosis. Secondarily, it examined their potential involvement in mediating inflammation and extracellular matrix degradation, the hallmarks of high-risk atherosclerotic unstable plaques. In human promonocytic U937 cells, both 27-OH and HNE were found to enhance cell release of IL-8, IL-1β, and TNF-α and to upregulate matrix metalloproteinase-9 (MMP-9) via TLR4/NF-κB-dependent pathway; these actions may sustain the inflammatory response and matrix degradation that lead to atherosclerotic plaque instability and to their rupture. Using specific antibodies, it was also demonstrated that these inflammatory cytokines increase MMP-9 upregulation, thus enhancing the release of this matrix-degrading enzyme by macrophage cells and contributing to plaque instability. These innovative results suggest that, by accumulating in atherosclerotic plaques, the two oxidized lipids may contribute to plaque instability and rupture. They appear to do so by sustaining the release of inflammatory molecules and MMP-9 by inflammatory and immune cells, for example, macrophages, through activation of TLR4 and its NF-κB downstream signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Relation between TLR4/NF‐κB signaling pathway activation by 27‐hydroxycholesterol and 4‐hydroxynonenal, and atherosclerotic plaque instability

et al. 2015

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“…Preparation of nuclear proteins. Nuclear proteins were extracted from cells as previously described (9). Protein content was determined using a Bicinchoninic Acid Protein assay reagent (Beyotime Institute of Biotechnology).…”

Section: Methodsmentioning

confidence: 99%

“…Previous studies have demonstrated that curcumin inhibits the expression and activity of MMP-2 under various experimental conditions and in different cell types. (9,10). However, the potential molecular mechanisms underlying this remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Curcumin prevents lipopolysaccharide-induced matrix metalloproteinase-2 activity via the Ras/MEK1/2 signaling pathway in rat vascular smooth muscle cells

Zhong

Feng

et al. 2017

Molecular Medicine Reports

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The aim of the present study was to examine the effect of curcumin treatment on lipopolysaccharide (LPS)-induced matrix metalloproteinase‑2 (MMP‑2) activity, and assess whether the effects are mediated by the Ras/mitogen‑activated protein kinase kinase 1/2 (MEK1/2) signaling pathway in vascular smooth muscle cells (VSMCs). VSMCs were isolated from male Sprague‑Dawley rats. Protein expression levels were analyzed by western blotting. The activity of MMP‑2 was measured with gelatin zymography, and an electrophoretic mobility shift assay was used to detect the DNA binding activity of nuclear factor‑κB (NF‑κB). Curcumin treatment was demonstrated to inhibit LPS‑induced MMP‑2 activity in rat VSMCs. This inhibitory effect was partially blocked by ammonium pyrrolidinedithiocarbamate, an inhibitor of NF‑κB activation, and farnesylthiosalicylic acid, an inhibitor of Ras. In addition, the results of the present study indicated that LPS‑induced phosphorylation of Ras homolog family member A and MEK1/2 was significantly decreased by curcumin. Furthermore, NF‑κB p65 expression in the nucleus and the DNA binding activity of NF‑κB in rat LPS‑exposed VSMCs was decreased by curcumin. Taken together, these findings suggest that curcumin prevents of LPS‑induced MMP‑2 activity through Ras/MEK1/2 and NF‑κB signaling.

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“…Chondrocytes are a distinct cell type that are targets for proinflammatory cytokines during the pathogenesis of OA. These cytokines induce the expression of matrix metalloproteinases (MMPs), which subsequently cleave various components of the ECM (1)(2)(3)(4). However, the mechanisms by which TNF-α increases the expression of MMP-13 in chondrocytes are yet to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Lentivirus-induced knockdown of LRP1 induces osteoarthritic-like effects and increases susceptibility to apoptosis in chondrocytes via the nuclear factor-κB pathway

Yang

Zheng

Peng

et al. 2015

Experimental and Therapeutic Medicine

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Low-density lipoprotein receptor-related protein 1 (LRP1) is known to regulate cell survival and inflammation. The present study investigated the involvement of LRP1 in the regulation of tumor necrosis factor (TNF)-α-induced expression of matrix metalloproteinase (MMP)-13. Furthermore, the study aimed to elucidate the mechanisms underlying the effects of LRP1 on TNF-α-induced inflammation and apoptosis of chondrocytes. Lentivirus-mediated RNA interference techniques were used to knockdown the LRP1 gene. Subsequently, the effects of LRP1 on TNF-α-induced MMP-13 expression were determined using quantitative polymerase chain reaction, western blot analysis and ELISA. Furthermore, the TNF-α-induced intracellular pathway was investigated using a nuclear factor (NF)-κB inhibitor (Bay 11-7082). In addition, the effect of LRP1 regulation on growth and apoptosis in chondrocytes was investigated using western blot analysis and a TUNEL assay. LRP1 knockdown was shown to increase TNF-α-induced MMP-13 expression via the activation of the NF-κB (p65) pathway, which reduced the expression of collagen type II and cell viability. In addition, LRP1 inhibited cell apoptosis by increasing the expression of phospho-Akt and B-cell lymphoma 2 (Bcl-2), while suppressing the expression of caspase-3 and Bcl-2-associated X protein. The results of the present study indicated that LRP1 was able to inhibit TNF-α-induced apoptosis and inflammation in chondrocytes. Therefore, LRP1 may be an effective osteoarthritis inhibitor, potentially providing a novel approach for antiarthritic therapeutics.

show abstract

Curcumin suppresses tumor necrosis factor-α-induced matrix metalloproteinase-2 expression and activity in rat vascular smooth muscle cells via the NF-κB pathway

Cited by 19 publications

References 28 publications

Relation between TLR4/NF‐κB signaling pathway activation by 27‐hydroxycholesterol and 4‐hydroxynonenal, and atherosclerotic plaque instability

Relation between TLR4/NF‐κB signaling pathway activation by 27‐hydroxycholesterol and 4‐hydroxynonenal, and atherosclerotic plaque instability

Curcumin prevents lipopolysaccharide-induced matrix metalloproteinase-2 activity via the Ras/MEK1/2 signaling pathway in rat vascular smooth muscle cells

Lentivirus-induced knockdown of LRP1 induces osteoarthritic-like effects and increases susceptibility to apoptosis in chondrocytes via the nuclear factor-κB pathway

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