Inflammatory effects of resistin on human smooth muscle cells: up-regulation of fractalkine and its receptor, CX3CR1 expression by TLR4 and Gi-protein pathways

Gan, Ana-Maria; Butoi, Elena; Manea, Adrian; Simion, Viorel; Stan, Daniela; Parvulescu, M.M.; Calin, Manuela; Manduteanu, Ileana; Simionescu, Maya

doi:10.1007/s00441-012-1510-9

Cited by 39 publications

(43 citation statements)

References 42 publications

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“…This pathway plays an important role in inflammatory activation, proliferation and migration and restenosis of vascular smooth muscle cells. Restenosis requires the acquisition of an inflammatory phenotype of smooth muscle cells, and TLR4/MyD88/NF-κB is a critical promoting factor for the phenotypic acquisition of the cells [40][41][42]. Therefore, activation of the TLR4/MyD88/NF-κB pathway is closely associated with restenosis, and the LPS-induced HCASMC inflammatory activation model can serve as a reliable cell model for research on the restenosis mechanism.…”

Section: Discussionmentioning

confidence: 99%

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Li¹,

Wang²,

Xu³

2018

Cell Physiol Biochem

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Background/Aims: Approximately 10%-20% of patients with acute cardiovascular disease who have received coronary intervention suffer restenosis and high inflammation. The stent compound paclitaxel+hirudin was prepared for the treatment of post-intervention restenosis. This study aimed to explore the anti-inflammatory and anti-restenosis mechanisms of paclitaxel+hirudin with regard to the TLR4/MyD88/NF-κB pathway. Methods: Human coronary artery smooth muscle cells (HCASMCs) at 4-6 generations after in vitro culture were used as a model. Lipopolysaccharide (LPS) was used as an inducer to maximally activate the TLR4/MyD88/NF-κB inflammation pathway. After MyD88 knockdown and selective blocking of MyD88 degradation with epoxomicin, the effects of paclitaxel+hirudin stenting on key sites of the TLR4/MyD88/NF-κB pathway were detected using ELISA, Q-PCR, and western blot analysis. Results: LPS at 1 μg/mL for 48 h was the optimal modeling condition for inflammatory activation of HCASMCs. Paclitaxel+hirudin inhibited the levels of key proteins and the gene expression, except for that of the MyD88 gene, of the TLR4-MyD88 pathway. The trend of the effect of paclitaxel+hirudin on the pathway proteins was similar to that of MyD88 knockdown. After epoxomicin intervention, the inhibitory effects of paclitaxel+hirudin on the key genes and proteins of the TLR4-MyD88 pathway were significantly weakened, which even reached pre-intervention levels. Paclitaxel+hirudin affected the MyD88 protein in a dosage-dependent manner. Conclusion: The paclitaxel+hirudin compound promotes MyD88 degradation in the TLR4/MyD88/NF-κB pathway to reduce the activity of TLR4 and NF-κB p65 and to weaken the LPS-initiated inflammatory reactions of IL-1β, IL-6, and TNF-α.

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Section: Discussionmentioning

confidence: 99%

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Li¹,

Wang²,

Xu³

2018

Cell Physiol Biochem

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“…Under basal conditions, the concentration and activity of AP-1 are relatively low (30). When cells are stimulated, AP-1 expression increases (30). The results of the current study indicated that geniposide reduces AP-1 protein expression in mouse epilepsy.…”

Section: Discussionmentioning

confidence: 48%

“…AP-1 is a homodimer or heterodimer of c-fos and c-jun. Under basal conditions, the concentration and activity of AP-1 are relatively low (30). When cells are stimulated, AP-1 expression increases (30).…”

Section: Discussionmentioning

confidence: 98%

Geniposide attenuates epilepsy symptoms in a mouse model through the PI3K/Akt/GSK‑3β signaling pathway

Wei¹,

Duan²,

He³

et al. 2017

Exp Ther Med

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Abstract. Previous reports on the pharmacological actions of geniposide have indicated that it has anti-asthmatic, anti-inflammatory and analgesic effects in the liver and gallbladder, and therapeutic effects in neurological, cardiovascular and cerebrovascular diseases. The results of the current study demonstrate that geniposide attenuates epilepsy in a mouse model through the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) signaling pathway. A mouse model of epilepsy was induced by maximal electric shock (50 mA, 50 Hz, 1 sec). Epilepsy mice were intragastrically administered with 0, 5, 10 or 20 mg/kg geniposide. Geniposide significantly reduced the incidence and significantly increased the latency of clonic seizures in epileptic mice compared with non-treated epileptic mice (both P<0.01). Geniposide treatment significantly inhibited cyclooxygenase-2 mRNA expression in epilepsy mice (P<0.01). Furthermore, geniposide significantly suppressed the protein expression of activator protein 1, increased the activation of Akt and increased the protein expression of GSK-3β and PI3K in epilepsy mice (all P<0.01). These results suggest that geniposide attenuates epilepsy in mice through the PI3K/Akt/GSK-3β signaling pathway.

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“…Previous studies have reported that resistin may indicate the severity of the disease in patients with neonatal sepsis, in a similar manner to IL-6 and CRP (7,14,23,24). Furthermore, recent studies have demonstrated that resistin may serve a function in inflammation and autoimmunity (5,25). Bokarewa et al reported that the use of recombinant resistin resulted in a marked upregulation in the genes for tumor necrosis factor (TNF)-α and IL-6 (26).…”

Section: Discussionmentioning

confidence: 99%

“…Resistin competes with lipopolysaccharides through binding to Toll-like receptors and may function as a proinflammatory cytokine in human monocytes. In addition, resistin is a member of the cysteine-rich secretory protein family, members of which are also known as resistin-like or ʻfound in inflammatory zoneʼ molecules (5). Serum resistin levels have been observed to increase during severe bacterial and viral infections (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Clinical potential of resistin as a novel prognostic biomarker for cellulitis

Ertürk

Cüre

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. Cellulitis is an acute, subacute or chronic inflammation of the dermis and subdermal tissues, which is typically caused by bacteria, although other causes are possible. The present study aimed to evaluate the association between resistin levels and the recovery time of patients with cellulitis. In addition, the effect of resistin and insulin resistance on the prognosis of cellulitis was investigated. In total, 52 patients with cellulitis (male, 21; female, 31) and an age-matched group of 42 healthy individuals (male, 18; female, 24) were included in the study. The levels of serum resistin, fasting plasma glucose (FPG), homeostasis model assessment-insulin resistance (HOMA-IR), C-reactive protein (CRP) and other biochemical parameters were compared between the groups. The mean resistin levels in the cellulitis and control groups were 9.4±5.3 and 5.8±3.1 ng/ml, respectively. The levels of resistin, FPG, HOMA-IR and CRP were significantly higher in the cellulitis group compared with the control group (P<0.001). Furthermore, the mean recovery time of the patients with cellulitis was 21.2±5.6 days. Thus, increased levels of resistin (P=0.002) and HOMA-IR (P=0.005) could be used as predictive factors for the recovery time. The enhanced levels of resistin and HOMA-IR were shown to correlate with the high CRP levels in the cellulitis group. Therefore, the results indicated that increased levels of resistin may function as a prognostic marker for cellulitis.

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Inflammatory effects of resistin on human smooth muscle cells: up-regulation of fractalkine and its receptor, CX3CR1 expression by TLR4 and Gi-protein pathways

Cited by 39 publications

References 42 publications

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

Geniposide attenuates epilepsy symptoms in a mouse model through the PI3K/Akt/GSK‑3β signaling pathway

Clinical potential of resistin as a novel prognostic biomarker for cellulitis

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