Tissue kallikrein-binding protein is a serpin. I. Purification, characterization, and distribution in normotensive and spontaneously hypertensive rats.

Chao, Julie; Chai, Karl X.; Chen, L M; Xiong, William; Chao, Steven; Woodley-Miller, C; Wang, L X; Lu, H S; Chao, Lee

doi:10.1016/s0021-9258(17)46236-3

Cited by 129 publications

(10 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…9 Kallistatin is a serine proteinase inhibitor and was initially identified as a tissue kallikrein-binding protein. 10 Kallistatin is mainly produced by the liver and also broadly expressed in other tissues, such as the eye, kidney, heart, and blood vessels. 11,12 Kallistatin inhibits the activity of tissue kallikrein and regulates blood pressure.…”

Section: Introductionmentioning

confidence: 99%

Diabetes‐induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation

Yang

Cheng

et al. 2020

FASEB j.

View full text Add to dashboard Cite

Kallistatin is an inhibitor of tissue kallikrein and also inhibits the Wnt pathway. Its role in diabetic nephropathy (DN) is uncertain. Here we reported that serum kallistatin levels were significantly increased in diabetic patients with DN compared to those in diabetic patients without DN and healthy controls, and positively correlated with urinary albumin excretion. In addition, renal kallistatin levels were significantly upregulated in mouse models of type 1 (Akita, OVE26) and type 2 diabetes (db/db). To unveil the effects of kallistatin on DN and its underlying mechanism, we crossed transgenic mice overexpressing kallistatin with OVE26 mice (KS‐tg/OVE). Kallistatin overexpression exacerbated albuminuria, renal fibrosis, inflammation, and oxidative stress in diabetes. Kallikrein activity was inhibited while the renin‐angiotensin system (RAS) upregulated in the kidney of KS‐tg/OVE mice compared to WT/OVE mice, suggesting a disturbed balance between the RAS and kallikrein‐kinin systems. As shown by immunostaining of endothelial makers, renal vascular densities were decreased accompanied by increased HIF‐1α and erythropoietin levels in the kidneys of KS‐tg/OVE mice. Taken together, high levels of kallistatin exacerbate DN at least partly by inducing RAS overactivation and hypoxia. The present study demonstrated a positive correlation between kallistatin levels and DN, suggesting a potential biomarker for prognosis of DN.

show abstract

Section: Introductionmentioning

confidence: 99%

Diabetes‐induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation

Yang

Cheng

et al. 2020

FASEB j.

View full text Add to dashboard Cite

show abstract

“…In der Tat hemmt Antithombin III die Serinprotease Thrombin (Gettins 2003). Der Serine protease inhibitor A3K ist auch als Kallikrein-bindendes Protein (KBP) bekannt und ist in der Lage, die Serinprotease Kallikrein zu inhibieren (Chao et al 1986;Chao et al 1990;Chai et al 1991). Daher kann davon ausgegangen werden, dass diese beiden Serinprotease-Inhibitoren versuchen dem Fortschreiten des Alport-Syndroms entgegenzuwirken, indem sie einzelne Serinproteasen der Gerinnungskaskade hemmen.…”

Section: Der Podozyt Im Fokus Der Erkrankungunclassified

“…Der Serine protease inhibitor A3K ist als Kallikrein-bindendes Protein (KBP) bekannt und ist in der Lage, die Serinprotease Kallikrein zu hemmen. RCL bindet an Kallikrein, was eine Konformationsänderung zur Folge hat (Chao et al 1986;Chao et al 1990;Chai et al 1991). In der Literatur wird angenommen, dass KBP zunächst einen reversiblen und danach einen irreversiblen Komplex mit Kallikrein formt.…”

Section: Serine Protease Inhibitor A3kunclassified

“…Unter gewissen physiologischen Bedingungen verwandelt sich der Komplex von dem tetraedrischen Überganzszustand in ein Aryl-Enzym-Zwischenprodukt. Hierbei wird ein kleines C-terminales Peptid freigesetzt (Chao et al 1990). Dies würde die dritte Bande von Serine protease inhibitor A3K im Western Blot in Abbildung 3.24a auf Seite 66 im Krankheitsstadium von 6 Wochen erklären.…”

Section: Serine Protease Inhibitor A3kunclassified

“…Dies würde die dritte Bande von Serine protease inhibitor A3K im Western Blot in Abbildung 3.24a auf Seite 66 im Krankheitsstadium von 6 Wochen erklären. Nach Freisetzung des C-Peptids schließt sich der Wandel in einen SDS-und Hitze-resistenten Komplex an (Chao et al 1990). An dieser Stelle bleibt unbeantwortet, ob eine unterschiedlich ausgeprägte Bandenexpression innerhalb der beiden Krankheitsstadien (4,5 und 6 Wochen) eine Krankheitsrelevanz hat.…”

Section: Serine Protease Inhibitor A3kunclassified

See 2 more Smart Citations

Erkennung diagnostischer Frühmarker der Nierenfibrose beim Tiermodell des Alport-Syndroms mittels proteomischer Methoden

Schmidt-Eylers¹

View full text Add to dashboard Cite

Proteins of rat serum: III. Gender-related differences in protein concentration under baseline conditions and upon experimental inflammation as evaluated by two-dimensional electrophoresis

et al. 1999

View full text Add to dashboard Cite

Tissue kallikrein-binding protein is a serpin. I. Purification, characterization, and distribution in normotensive and spontaneously hypertensive rats.

Cited by 129 publications

References 29 publications

Diabetes‐induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation

Diabetes‐induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation

Erkennung diagnostischer Frühmarker der Nierenfibrose beim Tiermodell des Alport-Syndroms mittels proteomischer Methoden

Proteins of rat serum: III. Gender-related differences in protein concentration under baseline conditions and upon experimental inflammation as evaluated by two-dimensional electrophoresis

Contact Info

Product

Resources

About