Kallikrein–kinin system in hepatic experimental models

Kouyoumdjian, Maria; Nagaoka, Márcia Regina; Borges, Durval Rosa

doi:10.1016/j.peptides.2005.03.024

Cited by 17 publications

(15 citation statements)

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“…As factor XIIa cleaves PK to kallikrein and HMWK to bradykinin, contact system activation is expected to decrease both PK and HMWK and increase both kallikrein and bradykinin (14). However, because PK and HMWK are acute-phase reactants (15,16), their levels can be elevated in hyperthyroidism through active hepatic synthesis. Indeed, the circulating levels of PK and HMWK as well as factor XIIa and bradykinin were elevated in our hyperthyroidism patients.…”

Section: Discussionmentioning

confidence: 99%

Contact system activation and high thrombin generation in hyperthyroidism

Kim

Yoo

et al. 2017

European Journal of Endocrinology

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Section: Discussionmentioning

confidence: 99%

Contact system activation and high thrombin generation in hyperthyroidism

Kim

Yoo

et al. 2017

European Journal of Endocrinology

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“…Animal models have been widely used to comprehend mechanisms underlying acute and chronic liver injury (20,30,31) . In our study, we analyzed early stages of BDL on rats' liver cells and ECM in order to understand effects of extrahepatic cholestasis and its pathological changes.…”

Section: Discussionmentioning

confidence: 99%

Increase of Glycosaminoglycans and Metalloproteinases 2 and 9 in Liver Extracellular Matrix on Early Stages of Extrahepatic Cholestasis

Guedes

Castañon

Nagaoka

et al. 2014

Arq. Gastroenterol.

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-Context -Cholestasis produces hepatocellular injury, leukocyte infiltration, ductular cells proliferation and fibrosis of liver parenchyma by extracellular matrix replacement. Objective -Analyze bile duct ligation effect upon glycosaminoglycans content and matrix metalloproteinase (MMPs) activities. Methods -Animals (6-8 weeks; n = 40) were euthanized 2, 7 or 14 days after bile duct ligation or Sham-surgery. Disease evolution was analyzed by body and liver weight, seric direct bilirubin, globulins, gamma glutamyl transpeptidase (GGT), alkaline phosphatase (Alk-P), alanine and aspartate aminotransferases (ALT and AST), tissue myeloperoxidase and MMP-9, pro MMP-2 and MMP-2 activities, histopathology and glycosaminoglycans content. Results -Cholestasis caused cellular damage with elevation of globulins, GGT, Alk-P, ALT, AST. There was neutrophil infiltration observed by the increasing of myeloperoxidase activity on 7(P = 0.0064) and 14 (P = 0.0002) groups which leads to the magnification of tissue injuries. Bile duct ligation increased pro-MMP-2 (P = 0.0667), MMP-2 (P = 0.0003) and MMP-9 (P<0.0001) activities on 14 days indicating matrix remodeling and establishment of inflammatory process. Bile duct ligation animals showed an increasing on dermatan sulfate and/or heparan sulfate content reflecting extracellular matrix production and growing mitosis due to parenchyma depletion. ConclusionCholestasis led to many changes on rats' liver parenchyma, as so as on its extracellular matrix, with major alterations on MMPs activities and glycosaminoglycans content. HEADINGS -Extrahepatic cholestasis. Glycosaminoglycans. Matrix metalloproteinases.

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“…During acute‐phase reactions (inflammation), FXII levels become lowered, while PPK and HK levels increase . The lowered expression of FXII is explained by the inhibiting effect of interleukin‐6 on the production of FXII by hepatocytes .…”

Section: The Contact System In Health and Diseasementioning

confidence: 99%

Tracking down contact activation – from coagulation in vitro to inflammation in vivo

Maat

Tersteeg

Herczenik

et al. 2014

Int J Lab Hematology

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Summary The contact system is a volatile and versatile enzyme system in blood plasma that responds to the presence of nonphysiological surface materials by spontaneous generation of enzymatic activity. In subsequent steps, it can trigger blood coagulation and is responsible for the generation of the proinflammatory peptide bradykinin. The physiological role of the contact system is presently unknown, but it is commonly used to trigger coagulation in a diagnostic setting. In this three‐part review, we will first describe the molecular mechanisms that drive contact activation on nonphysiological materials. Next, we will summarize and compare a number of bioassays, which are commonly used to investigate the contact system in health and disease. Finally, we will discuss recent findings from both fundamental and clinical studies on the contributions of contact system to cardiovascular, infectious, and inflammatory disease.

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Kallikrein–kinin system in hepatic experimental models

Cited by 17 publications

References 50 publications

Contact system activation and high thrombin generation in hyperthyroidism

Contact system activation and high thrombin generation in hyperthyroidism

Increase of Glycosaminoglycans and Metalloproteinases 2 and 9 in Liver Extracellular Matrix on Early Stages of Extrahepatic Cholestasis

Tracking down contact activation – from coagulation in vitro to inflammation in vivo

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