Fibrinolysis is down-regulated in mouse collagen-induced arthritis, but its normalization does not alleviate the course of disease

Kwieciński, Jakub; Josefsson, Elisabet; Jin, Tao

doi:10.1007/s00011-011-0363-0

Cited by 13 publications

(11 citation statements)

References 36 publications

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“…Furthermore, pharmacological inhibition of thrombin via hirudin resulted in a significant reduction in synovial inflammation and disease severity in two different animal models of RA (see Table 3 ) ( 80 , 81 ). In this context, it could be shown that the plasmin activity is decreased, while PAI-1 levels are increased in both blood and inflamed joints of mice with collagen-induced arthritis (CIA) ( 82 ).…”

Section: Resultsmentioning

confidence: 99%

The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders—A Systematic Review

et al. 2018

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BackgroundThe interaction of coagulation factors has been shown to go beyond their traditional roles in hemostasis and to affect the development of inflammatory diseases. Key molecular players, such as fibrinogen, thrombin, or factor XII have been mechanistically and epidemiologically linked to inflammatory disorders like multiple sclerosis (MS), rheumatoid arthritis (RA), and colitis.ObjectivesTo systematically review the evidence for a role of coagulation factors, especially factor XII, fibrinogen, and thrombin in inflammatory disorders like MS, RA, and bowel disorders.MethodsA systematic literature search was done in the PubMed database to identify studies about coagulation factors in inflammatory diseases. Original articles and reviews investigating the role of the kallikrein–kinin and the coagulation system in mouse and humans were included.ResultsWe identified 43 animal studies dealing with inflammatory disorders and factors of the kallikrein–kinin or the coagulation system. Different immunological influences are described and novel molecular mechanisms linking coagulation and inflammation are reported.ConclusionA number of studies have highlighted coagulation factors to tip the balance between hemostasis and thrombosis and between protection from infection and extensive inflammation. To optimize the treatment of chronic inflammatory disorders by these factors, further studies are necessary.

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Section: Resultsmentioning

confidence: 99%

The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders—A Systematic Review

et al. 2018

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“…Myeloperoxidase (MPO) activity was measured in infected skin biopsies. Homogenized biopsies were placed in 1 mL of lysis buffer for 1 h at 4 °C, centrifuged at 1500 g for 15 min at 4 °C and supernatant was centrifuged again at 16 000 g , 4 °C, 5 min. Supernatants (50 μL, diluted 5× with distilled H 2 O) were mixed with 100 μL of 1,2‐phenylenediamine dihydrochloride (7 mg/mL, Dako AB, Stockholm, Sweden) and 10 μL of 30% H 2 O 2 and incubated at room temperature for 1 h. MPO activity resulted in colour development, measured as a change in absorbance at 450 nm.…”

Section: Methodsmentioning

confidence: 99%

Surface proteins ofStaphylococcus aureusplay an important role in experimental skin infection

Kwieciński

Jin

Josefsson

2014

APMIS

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Staphylococcus aureus is the most common cause of skin infections that range from mild diseases up to life-threatening conditions. Mechanisms of S. aureus virulence in those infections remain poorly studied. To investigate the impact of S. aureus surface proteins on skin infection, we used mouse models of skin abscess formation and skin necrosis, induced by a subcutaneous injection of bacteria. In the skin abscess model, a sortase-deficient S. aureus strain lacking all of its cell-wall anchored proteins was less virulent than its wild-type strain. Also, strains specifically lacking protein A, fibronecting binding proteins, clumping factor A or surface protein SasF were impaired in their virulence. When a model of dermonecrosis was studied, the S. aureus surface proteins could not be shown to be involved. In summary, surface proteins play an important role in virulence of S. aureus skin abscess infections, but not in formation of skin necrosis.

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“…Urokinase plasminogen activator (uPA), a serine protease that binds to the uPA receptor (uPAR), regulates various processes including neo-vascularization, inflammation, tumor invasion, and metastasis (Ossowski and Aguirre-Ghiso, 2000;Kwiecinski et al, 2011;Mahmood et al, 2018). Sodium azide synergized with LPS for the expression of both uPA and uPAR ( Figure 4A).…”

Section: Synergizes With Lps For the Expression Of Upa And Upar Thmentioning

confidence: 99%

ER stress differentially affects pro‐inflammatory changes induced by mitochondrial dysfunction in the human monocytic leukemia cell line, THP‐1

Heo

Kim

Lim

et al. 2019

Cell Biology International

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The functional and physical interaction between mitochondria and the endoplasmic reticulum (ER) has been the subject of intense study. To test the effect of this interaction on macrophage inflammatory activation, the human macrophage‐like monocytic leukemia cell line THP‐1 was treated with oligomycin, rotenone, or sodium azide, which induce mitochondrial dysfunction (MD) by blocking the electron transport chain (ETC). MD induced by these agents triggered activation of various sensors and markers of ER stress. This linkage affected macrophage function since LPS‐induced expression of IL‐23 was enhanced by the MD inducers, and this enhancing effect was abolished by inhibition of pancreatic endoplasmic reticulum kinase (PERK) activity. This MD‐mediated ER stress may be universal since it was observed in human embryonic kidney HEK293 cells and colon cancer SW480 cells. On the other hand, MD regulated LPS‐induced activation of the AKT/GSK3β/β‐catenin pathway in a manner not affected by inhibition of PERK or inositol‐requiring enzyme 1α (IRE1α) activities. These results indicate that the occurrence of MD can lead to ER stress and these two events, separately or in combination, can affect various cellular processes.

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Fibrinolysis is down-regulated in mouse collagen-induced arthritis, but its normalization does not alleviate the course of disease

Abstract: Fibrinolytic changes in CIA parallel changes in RA, making CIA a suitable model to study fibrinolysis in RA. Normalization of plasmin activity in CIA after treatment with plasminogen activators had no effect on disease severity.

Cited by 13 publications

References 36 publications

The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders—A Systematic Review

The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders—A Systematic Review

Surface proteins ofStaphylococcus aureusplay an important role in experimental skin infection

ER stress differentially affects pro‐inflammatory changes induced by mitochondrial dysfunction in the human monocytic leukemia cell line, THP‐1

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