Localization and Expression of Tissue Kallikrein and Kallistatin in Human Blood Vessels

Wolf, W. Clark; Harley, Russell A.; Sluce, Dan; Chao, Lee; Chao, Julie

doi:10.1177/002215549904700210

Cited by 73 publications

(55 citation statements)

References 28 publications

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“…Evidence that SC5-9 incubated with endothelial cells promotes the release and accumulation of BK-like material in the medium is also supported by the observation that the culture medium collected after a 30-min incubation of HUVECs with SC5b-9 induces a prompt BSA leakage very similar to that of BK. These findings indicate that SC5-9 interacts with endothelial cells and promotes the formation of BK possibly from a complex kininogen-prekallikrein present on the surface of the endothelium (39,40). A similar mechanism has been proposed by Katada and Majima (41) to explain the release of BK and the arterial vasodilatation observed in isolated and perfused mesenteric artery following the interaction of angiotensin II with its type 2 receptor.…”

Section: Discussionmentioning

confidence: 90%

Platelet-Activating Factor and Kinin-Dependent Vascular Leakage as a Novel Functional Activity of the Soluble Terminal Complement Complex

Bossi¹,

Fischetti

Pellis³

et al. 2004

The Journal of Immunology

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The infrequent occurrence of septic shock in patients with inherited deficiencies of the terminal complement components experiencing meningococcal disease led us to suspect that the terminal complement complex is involved in vascular leakage. To this end, the permeabilizing effect of the cytolytically inactive soluble terminal complement complex (SC5b-9) was tested in a Transwell system measuring the amount of fluorescein-labeled BSA (FITC-BSA) leaked through a monolayer of endothelial cells. The complex caused increased permeability to FITC-BSA after 15 min as opposed to the prompt response to bradykinin (BK). The effect of SC5b-9 was partially reduced by HOE-140 or CV-3988, two selective antagonists of BK B2 and platelet-activating factor receptors, respectively, and was completely neutralized by the mixture of the two antagonists. Also, DX-88, a specific inhibitor of kallikrein, partially inhibited the activity of SC5b-9. The permeabilizing factor(s) released after 30 min of incubation of endothelial cells with SC5b-9 caused a prompt leakage of albumin like BK. Intravital microscopy confirmed both the extravasation of circulating FITC-BSA across mesenteric microvessels 15 min after topical application of SC5b-9 and the complete neutralization by the mixture of HOE-140 and CV-3988. SC5b-9 induced opening of interendothelial junctions in mesenteric endothelium documented by transmission electron microscopy.

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Section: Discussionmentioning

confidence: 90%

Platelet-Activating Factor and Kinin-Dependent Vascular Leakage as a Novel Functional Activity of the Soluble Terminal Complement Complex

Bossi¹,

Fischetti

Pellis³

et al. 2004

The Journal of Immunology

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“…40 In diabetic retinopathy, unregulated angiogenesis is observed. 41 Therefore, we expected to find high serum kallistatin levels in our studied patients with diabetic retinopathy.…”

Section: Discussionmentioning

confidence: 99%

Kallistatin as a marker of microvascular complications in children and adolescents with type 1 diabetes mellitus: Relation to carotid intima media thickness

et al. 2015

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In diabetes, angiogenesis is disturbed, contributing to proliferative retinopathy, nephropathy and neuropathy. Kallistatin, a serine proteinase inhibitor, has anti-angiogenic effects. We assessed serum kallistatin in children and adolescents with type 1 diabetes as a potential marker for microvascular complications and its relation to carotid intima media thickness (CIMT). Sixty patients with type 1 diabetes were divided into two groups according to the presence of microvascular complications and compared with 30 healthy controls. High-sensitivity C-reactive protein (hs-CRP), HbA1c, urinary albumin creatinine ratio (UACR), kallistatin levels and CIMT were assessed. Kallistatin levels were significantly higher in patients with microvascular complications (9.9 ± 2.38 ng/mL) and those without complications (5.0 ± 1.5 ng/mL) than in healthy controls (1.39 ± 0.55 ng/mL; p<0.001). Kallistatin was increased in patients with microalbuminuria compared with the normoalbuminuric group (p<0.001). Positive correlations were found between kallistatin and disease duration, fasting blood glucose, HbA1c, triglycerides, total cholesterol, hs-CRP, UACR and CIMT (p<0.05). A kallistatin cut-off value at 6.1 ng/mL could differentiate patients with and without microvascular complications, with a sensitivity of 96.87% and specificity of 93.75%. Increased kallistatin levels in type 1 diabetes and its relation with CIMT may reflect vascular dysfunction and suggest a link between micro-and macro-angiopathy.

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“…Tissue kallikrein cleaves low-molecular-weight kininogen, leading to the release of potent vasodilator kinins. Intact BK exerts its bioactive functions via binding to G protein-coupled receptors [28][29][30]. To date, two types of kinin G protein-coupled receptors, B 1 and B 2 , have been characterized.…”

Section: Discussionmentioning

confidence: 99%

Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats

Wan

et al. 2008

Human Gene Therapy

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The tissue kallikrein-kinin system is important in regulating cardiovascular and renal function, and dysregulation of the system has been implicated in heart and kidney pathologies. These findings suggest that if balance can be restored to the kallikrein-kinin axis, then associated disease progression may be attenuated. To test this hypothesis, recombinant adeno-associated virus (rAAV)-mediated human tissue kallikrein (HK) expression was induced in a rodent model of chronic renal failure involving 5/6 nephrectomy. rAAV-HK treatment attenuated the rise in blood pressure, glomerular sclerosis, and tubulointerstitial injury observed in this model. rAAV-HK treatment also attenuated renal function decline as measured by urinary microalbumin, osmolarity and cGMP levels. RT-PCR analysis showed that rAAV-HK treated rats had higher levels of bradykinin-B 2 receptor (B 2 R) and dopamine D 1 -like receptor mRNAs. In contrast, angiotensin II receptor 1, endothelin ET A receptor, and vasopressin V 2 receptor mRNAs were markedly downregulated in kidneys from HK-treated rats. Bradykinin induced similar changes in receptor levels and prevented TGF-β1-induced tubulointerstitial fibrosis. The effects of bradykinin could be reversed by the B 2 R antagonist HOE-140. Together, these findings suggest that restoration of the kallikrein-kinin system reduces kidney injury and protects renal function in 5/6 nephrectomized rats via changes in the expression and activation of G-protein coupled receptors including B 2 R.

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Localization and Expression of Tissue Kallikrein and Kallistatin in Human Blood Vessels

Cited by 73 publications

References 28 publications

Platelet-Activating Factor and Kinin-Dependent Vascular Leakage as a Novel Functional Activity of the Soluble Terminal Complement Complex

Platelet-Activating Factor and Kinin-Dependent Vascular Leakage as a Novel Functional Activity of the Soluble Terminal Complement Complex

Kallistatin as a marker of microvascular complications in children and adolescents with type 1 diabetes mellitus: Relation to carotid intima media thickness

Delivery of Recombinant Adeno-Associated Virus-Mediated Human Tissue Kallikrein for Therapy of Chronic Renal Failure in Rats

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