Tumor Necrosis Factor and Interleukin-6 Are Not Elevated in Venous Blood from Ischemic Canine Myocardium

Field, Garrett; Conn, Carole A.; McClanahan, Thomas B.; Nao, B S; Kluger, Matthew J.; Gallagher, Kim P.

doi:10.3181/00379727-206-43775

Cited by 4 publications

(2 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IL-6 is a pleiotropic cytokine with a wide range of biological activities in immune regulation, hematopoiesis, inflammation and oncogenesis and IL-6 could play an important role in the generation of inflammation within the cornea (50). A recent study has indicated that IL-6 may rank as important factors in the pathogenesis of keratoconus (25).…”

Section: Discussionmentioning

confidence: 99%

Induction of MMP-1 and −3 by cyclical mechanical stretch is mediated by IL-6 in cultured fibroblasts of keratoconus

Du¹,

Chen²,

Li³

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. In order to understand the effect of mechanical stretch on corneal extracellular matrix remodeling, human keratoconus fibroblasts (HKCFBs) were subjected to cyclic stretch in vitro and the expression of matrix metalloproteinases (MMPs), tissue inhibitor of metalloproteinases (TIMPs), and inflammatory cytokines were evaluated. HKCFBs were seeded into a flexible membrane base and subjected to a cyclic stretch regimen of 10% equibiaxial stretch at a stretching frequency of 1 Hz for 6 h using a Flexcell tension unit. An antibody directed against interleukin-6 (IL-6 Ab) was used to investigate the roles of IL-6 on mechanical stretch mediated regulation of MMP in HKCFBs. Culture supernatants were assayed using an enzyme-linked immunosorbent assay for MMP-1 and -3, TIMP-1 and -2, and IL-6. Total RNA from the cells was extracted, and quantitative polymerase chain reaction was used to determine mRNA for MMP-1 and -3, TIMP-1 and -2, and IL-6. In stretched cells, levels of MMP-1 and -3 demonstrated an increase compared with unstretched cells, but levels of TIMP-1, and -2 revealed a decrease. Mechanical stretch significantly increased the mRNA expression and protein synthesis of IL-6 compared with unstretched cells. IL-6 induced MMP-1 and -3 expression, whereas no significant effects were observed in levels of TIMP-1 and -2 compared with the untreated control groups. Additionally, the IL-6 Ab markedly inhibited the stretch-induced increase in MMP-1 and -3 in culture supernatants in a dose-dependent manner. No significant differences in TIMP-1 and -2 protein levels were detected between stretched cells treated with IL-6 Ab and stretched cells without IL-6 Ab treatment. These results indicate that cyclical mechanical stretch augments IL-6 production and MMP expression, and reduces levels of TIMP in HKCFBs. Thus, it is suggested that IL-6 mediates the stretch-induced MMP expression.

show abstract

Section: Discussionmentioning

confidence: 99%

Induction of MMP-1 and −3 by cyclical mechanical stretch is mediated by IL-6 in cultured fibroblasts of keratoconus

Du¹,

Chen²,

Li³

et al. 2017

Molecular Medicine Reports

View full text Add to dashboard Cite

show abstract

“…Rat enzyme-linked immunosorbent assay kits for IL-6 and IL-8 (IminoBiological Laboratories, Fujioka, Japan) were used to measure their serum levels. We used a lipopolysaccharide (LPS) (Escherichia coli 0111: B4; Sigma) 10 Ìg/kg [15] on baseline point by intravenous injection and detected serum cytokine concentrations. The LPS was dissolved in 0.9% sterile saline at a concentration of 20 Ìg/ml and a well-established stimulant of other cytokine production [15].…”

Section: Peripheral Blood Counts Serum Biochemistry and Cytokine Lementioning

confidence: 99%

Protective Effects of Anti-Neutrophil Antibody against Myocardial Ischemia/Reperfusion Injury in Rats

Kohtani¹,

Abe

Satô³

et al. 2002

Eur Surg Res

View full text Add to dashboard Cite

Neutrophil activation initiates myocardial ischemia/reperfusion (I/R) injuries. The aim of this study is to evaluate the in vitro functions of an anti-neutrophil monoclonal antibody, Urge-8, and its therapeutic efficacy against myocardial ischemia (MI) in rats. We measured in vitro functions of rat neutrophils including chemotactic activity, superoxide production, phagocytic function, and neutrophil degranulation. MI was induced in Wistar rats by clamping the left coronary artery for 1 h. Rats received either isotype-negative control IgG₁ (control group, n = 20), 250 µg/kg of Urge-8 before (pre-treatment group, n = 20) or after (post-treatment group, n = 20) MI. The three groups were compared during the first 24 h after reperfusion with respect to changes in mean arterial pressure, heart rate, body temperature, biochemistry, serum cytokines, myocardial neutrophil infiltration, survival rate, and size of MI. Urge-8 effectively suppressed in vitro functions of rat neutrophils including chemotactic activity, superoxide production, phagocytic function, and neutrophil degranulation. The Urge-8 treated groups showed higher levels of arterial pressure and survival rate, lower values of interleukin-6 and interleukin-8, lower grade of myocardial neutrophil infiltration, and smaller MI size as compared to the control group. In conclusion, Urge-8 is effective against myocardial I/R injury by suppressing certain functions and myocardial infiltration of neutrophils in rats.

show abstract

Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine

Arras¹,

Sträßer²,

Mohri³

et al. 1998

Basic Research in Cardiology

View full text Add to dashboard Cite

The time course of expression of TNF-alpha in myocardial wound healing following ischemic injury was investigated in the porcine heart. Microembolization was used to induce focal ischemia and necrosis in hearts of 39 adult pigs. The animals were sacrificed after 3, 6, 12, 24 h, 3 and 7 days, and after 4 weeks, and the myocardial tissue was studied by immunofluorescence using specific antibodies. TNF-alpha containing cells were identified as monocytes/macrophages by double staining with a muramidase antibody. Monocytes/macrophages were the only source of TNF-alpha. Microembolization caused multiple necrotic foci with loss of myocytes in the left ventricular myocardium. These foci contained numerous monocytes/macrophages and showed an inflammatory reaction typical of wound healing followed by replacement with scar tissue. The number of TNF-alpha positive cells increased after 24 h, peaked between 3-7 days and slowly decreased thereafter. Expression of TNF-alpha in monocytes/macrophages was significantly reduced after pretreatment of pigs with cyclosporine or dexamethasone. It is concluded that 1.) in myocardial tissue monocytes/macrophages are the only cell type expressing TNF-alpha, 2.) TNF-alpha is involved in wound healing after ischemia, and 3.) synthesis of TNF-alpha and inflammatory angiogenesis can be inhibited be treatment with either cyclosporine or dexamethasone.

show abstract

Tumor Necrosis Factor and Interleukin-6 Are Not Elevated in Venous Blood from Ischemic Canine Myocardium

Cited by 4 publications

References 6 publications

Induction of MMP-1 and −3 by cyclical mechanical stretch is mediated by IL-6 in cultured fibroblasts of keratoconus

Induction of MMP-1 and −3 by cyclical mechanical stretch is mediated by IL-6 in cultured fibroblasts of keratoconus

Protective Effects of Anti-Neutrophil Antibody against Myocardial Ischemia/Reperfusion Injury in Rats

Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine

Contact Info

Product

Resources

About