Beta-adrenoceptor Activation by Norepinephrine Enhances Lipopolysaccharide-induced Matrix Metalloproteinase-9 Expression Through the ERK/JNK-c-Fos Pathway in Human THP-1 Cells

Yin, Xiaoxing; Zhou, Linli; Han, Fei; Han, Jie; Zhang, Yuanyuan; Sun, Zewei; Zhao, Wenting; Wang, Zhen; Zheng, Liangrong

doi:10.5551/jat.35204

Cited by 11 publications

(8 citation statements)

References 28 publications

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“…We found that TIMP-1 values were significantly higher in the septic patients treated with vasopressors/inotropes. Clinical studies on this topic are lacking, but experimental models imply that catecholamines have a very complex interaction with MMPs and their inhibitors [ 37 , 38 ] that could be influenced by various medications, none of which are accounted for in this research.…”

Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9 and Tissue Inhibitor of Matrix Metalloproteinase-1 in Sepsis after Major Abdominal Surgery

et al. 2018

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Background The role of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in sepsis after major abdominal surgery and sepsis-associated organ dysfunction is unexplored. Materials and Methods Fifty-three patients with sepsis after major abdominal surgery were compared to 50 operated and 50 nonoperated controls. MMP-9, TIMP-1, biomarkers of inflammation, kidney and liver injury, coagulation, and metabolic disorders were measured daily during 96 h following diagnosis of sepsis and once in controls. MMP-9/TIMP-1 ratios and disease severity scores were calculated. Use of vasopressors/inotropes, mechanical ventilation, and survival were recorded. Results Septic patients had lower MMP-9 and MMP-9/TIMP-1 ratios but higher TIMP-1 levels compared to controls. AUC-ROC for diagnosis of sepsis was 0.940 and 0.854 for TIMP-1 and 0.924 and 0.788 for MMP-9/TIMP-1 ratio (sepsis versus nonoperated and sepsis versus operated controls, resp.). Lower MMP-9 and MMP-9/TIMP-1 ratio and higher TIMP-1 levels were associated with shorter survival. MMP-9, TIMP-1, and MMP-9/TIMP-1 ratio correlated with biomarkers of inflammation, kidney and liver injury, coagulation, metabolic disorders, and disease severity scores. Use of vasopressors/inotropes was associated with higher TIMP-1 levels. Conclusions MMP-9, TIMP-1, and MMP-9/TIMP ratio were good diagnostic or prognostic biomarkers of sepsis after major abdominal surgery and were linked to sepsis-associated organ dysfunction.

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Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9 and Tissue Inhibitor of Matrix Metalloproteinase-1 in Sepsis after Major Abdominal Surgery

et al. 2018

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“…Notably, irisin significantly reduced the severity of aortic atherosclerosis by blocking the activation of p-p38 MAPK in ApoE −/− mice fed on a high-cholesterol diet ( 27 ). In addition, in vitro experiments indicated that norepinephrine enhanced lipopolysaccharide-induced MMP-9 expression as well as MMP-9 activity in human THP-1 cells by promoting the activation of p-JNK ( 28 ). Furthermore, BBR protected against lipopolysaccharide-induced apoptosis by suppressing JNK-mediated signaling ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Suppressive effects of berberine on atherosclerosis via downregulating visfatin expression and attenuating visfatin-induced endothelial dysfunction

et al. 2018

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Berberine (BBR) possesses significant anti-atherosclerosis properties. Visfatin is one of the most promising biomarkers of incoming atherosclerosis. However, research on the effect of BBR on regulating visfatin expression in atherogenesis remains largely unknown. In this study, we investigated the effects of BBR on visfatin expression and atherogenesis in apolipoprotein E knockout (ApoE−/−) mice. The effect of BBR on attenuating visfatin-induced endothelial dysfunction was also evaluated in cultured human umbilical vein endothelial cells (HUVECs). In vivo experiments showed that BBR treatment (5 mg/kg/day) significantly reduced the serum levels of visfatin, lipid, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), the protein expression of visfatin, p-p38 MAPK and p-c-Jun N-terminal kinase (JNK) in mice aorta and the distribution of visfatin in the atherosclerotic lesions in ApoE−/− mice fed with a Western diet. In addition, in vitro experiments indicated that visfatin (100 µg/l) significantly increased apoptosis, the contents of IL-6 and TNF-α, the protein levels of p-p38 MAPK, p-JNK and Bax in HUVECs, which were reversed by BBR administration (50 µmol/l). Our findings suggest that BBR significantly ameliorates Western diet-induced atherosclerosis in ApoE−/− mice via downregulating visfatin expression, which is related to the inhibition of p38 MAPK and JNK signaling pathways and subsequent suppression of visfatin-induced endothelial dysfunction.

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“…Phloroglucinol administration in platelets is helpful to cardiovascular health by modulating Cox-2 activity through repressing ERK/p38 signaling [ 44 ]. In THP-1 cells, norepinephrine (NE) can induce the secretion of matrix metalloproteinase-9 (MMP-9) and augmented the progression of AS through promoting ERK/JNK-c-Fos pathway [ 45 ]. Plentiful evidence has also indicated that MAPKs and PI3K-Akt signal pathway can activate the downstream NF- κ B and enhance the progression of atherosclerosis [ 46 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

Papain Ameliorates the MPAs Formation-Mediated Activation of Monocytes by Inhibiting Cox-2 Expression via Regulating the MAPKs and PI3K/Akt Signal Pathway

Fei

Yuan

Zhao

et al. 2018

BioMed Research International

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Monocytes activation and subsequent inflammatory response mediated by monocyte-platelet aggregates (MPAs) formation play the key roles in the early pathogenesis of atherosclerosis (AS). Exploration of novel drugs to ameliorate MPAs formation-mediated monocytes activation would be helpful for the treatment of AS patients. Papain has definite pharmacological effects including antiplatelet, thrombolysis, and anti-inflammation. However, its effect on MPAs formation and the following monocytes activation remains vague. This study aimed to illustrate the underlying mechanisms of papain on MPAs formation-initiated monocytes activation in vitro. In this study, Papain, Cox-2 inhibitor (NS-398), and NF-κB agonist (TNF-α) were used as the treating agents, respectively. MPAs formation and activated monocytes were measured by flow cytometry (FCM). Cox-2 mRNA, MCP-1, and proteins of Cox-2 and NF-κB signal pathway were detected by qRT-PCR, ELISA, and western blotting, respectively. As we observed, papain exhibited the powerful inhibitory effects on thrombin-mediated MPAs formation and monocytes activation in a concentration-dependent manner as what Cox-2 inhibitor demonstrated. However, the inhibitory tendency was significantly reversed by TNF-α. We also discovered that both Cox-2 mRNA and protein expression as well as the release of MCP-1 of monocyte was inhibited by either papain or NS-398, but TNF-α stimulated Cox-2 expression and release of MCP-1. The results of western blotting assay indicated that thrombin-mediated proteins expression of MAPKs and PI3K/Akt signal pathway was inhibited by papain and NS-398. However, TNF-α notably abated the inhibitory effects of papain on the process of MPAs-initiated monocytes activation. Our findings suggest that papain can inhibit the MPAs formation-mediated activation of monocytes by inhibiting the MAPKs and PI3K/Akt signal pathway.

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Beta-adrenoceptor Activation by Norepinephrine Enhances Lipopolysaccharide-induced Matrix Metalloproteinase-9 Expression Through the ERK/JNK-c-Fos Pathway in Human THP-1 Cells

Cited by 11 publications

References 28 publications

Matrix Metalloproteinase-9 and Tissue Inhibitor of Matrix Metalloproteinase-1 in Sepsis after Major Abdominal Surgery

Matrix Metalloproteinase-9 and Tissue Inhibitor of Matrix Metalloproteinase-1 in Sepsis after Major Abdominal Surgery

Suppressive effects of berberine on atherosclerosis via downregulating visfatin expression and attenuating visfatin-induced endothelial dysfunction

Papain Ameliorates the MPAs Formation-Mediated Activation of Monocytes by Inhibiting Cox-2 Expression via Regulating the MAPKs and PI3K/Akt Signal Pathway

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