Cyclic AMP increases bradykinin receptor binding affinity in human endothelial cells

Stewen, Pia; Saijonmaa, Outi; Nyman, Tuulikki; Fyhrquist, Frej

doi:10.1016/j.lfs.2003.09.071

Cited by 5 publications

(4 citation statements)

References 31 publications

(54 reference statements)

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“…Since endothelial removal strongly reduced BK-induced relaxation, it is possible to suggest that the relaxation induced by this peptide in the rat carotid is mediated by endothelial B 2 receptors. In fact, imunocytochemistry (Raidoo et al, 1997) and real-time PCR (RT-PCR) (Stewen et al, 2004) in human vascular tissue have previously demonstrated the expression of endothelial B 2 receptors.…”

Section: Discussionmentioning

confidence: 99%

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

2007

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Section: Discussionmentioning

confidence: 99%

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

2007

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“…We have used B1Ra and B2Ra at 2 μ M concentration (28) in some experiments on Matrigel invasion, cell proliferation, capillary morphogenesis, and signal transduction, as further detailed in the text. The cGMP EIA kit and the cAMP EIA kit were used to measure cyclic nucleotide production in normal MVECs after lysis of cell monolayers with 0.1 M HCl, in accordance with the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

The antiangiogenic tissue kallikrein pattern of endothelial cells in systemic sclerosis

Giusti

Serratì

Margheri

et al. 2005

Arthritis & Rheumatism

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Objective. Postnatal angiogenesis relies on a proper response of endothelial cells to angiogenic stimuli. In systemic sclerosis (SSc), endothelial cells are unresponsive to angiogenic factors. Since circumstantial and experimental evidence points to tissue kallikreins as powerful effectors of the angiogenic response, we undertook this study to investigate the kallikrein pattern of normal and SSc endothelial cells in order to identify differences that can account for defective angiogenesis.Methods. Expression of 14 tissue kallikreins was studied by a microarray approach, by reverse transcription-polymerase chain reaction, and by Western blotting in endothelial cells isolated from the skin of clinically healthy subjects and SSc patients. Cell proliferation was quantified by direct cell counting. Invasion and capillary morphogenesis were evaluated in a Boyden chamber and in culture flasks layered with Matrigel. Cyclic nucleotide production was measured by enzyme immunoassay. MAP kinase and ERK activation were measured by Western blotting.Results. Endothelial cells from SSc patients showed poor expression of kallikreins 9, 11, and 12 compared with endothelial cells from normal subjects. Antibodies against the relevant kallikreins on normal endothelial cells revealed that while kallikreins 9, 11, and 12 induced cell growth, only kallikrein 12 regulated invasion and capillary morphogenesis. Buffering of kallikrein 12 with antibodies resulted in the acquisition of an SSc-like pattern by normal cells in in vitro angiogenesis. Reduction of cAMP and cGMP production and of ERK phosphorylation upon administration of antikallikrein antibodies revealed that the activity of kallikreins 9, 11, and 12 was mediated by kinins.Conclusion. Reduction of tissue kallikreins 9, 11, and 12 may be relevant to reduced angiogenesis in SSc patients.

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“…These data may provide evidence of mixed receptor populations or indeed of the presence of a novel receptor subtype identified by the bradykinin analogue, maximakinin. In fact, it has subsequently been shown that human endothelial cells express a functional mixed population of both B 1 ‐ and B 2 ‐subtypes of bradykinin receptors in a constitutive manner (15). For these reasons, we have referred to maximakinin responses as mediated through receptors defined by tissue localization.…”

Section: Discussionmentioning

confidence: 99%

Biotransformation of maximakinin, a bradykinin‐related nonadecapeptide from toad venom, by mammalian kallikrein and salivary proteases

Chen

O’Rourke

McKenna

et al. 2005

The Journal of Peptide Research

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Maximakinin is an N‐terminally extended bradykinin (DLPKINRKGPRPPGFSPFR) from the venom of a Chinese toad (Bombina maxima) that displays highly selective activity at mammalian arterial smooth muscle receptors. In this study, we report that incubation of maximakinin with either kallikrein or human saliva generates catabolites with enhanced bioactivity that retain the tissue selective effects of the parent molecule. In addition, we have observed that kallikrein rapidly cleaves the C‐terminal arginyl residue of both maximakinin and bradykinin – a cleavage hitherto considered to be performed by a carboxypeptidase that facilitates selective bradykinin receptor targeting. Maximakinin has thus evolved as a ‘smart’ defensive weapon in the toad with inherent resistance to the signal‐terminating protease hardware in the potential predator. Thus, natural selection of amphibian skin peptides for antipredator defence, through interspecies delivery by an exogenous secretory mode, produces subtle structural stabilization modifications that can potentially provide new insights for the design of orally active and selectively targeted peptide therapeutics.

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Cyclic AMP increases bradykinin receptor binding affinity in human endothelial cells

Cited by 5 publications

References 31 publications

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

Functional characterization of the mechanisms underlying bradykinin-induced relaxation in the isolated rat carotid artery

The antiangiogenic tissue kallikrein pattern of endothelial cells in systemic sclerosis

Biotransformation of maximakinin, a bradykinin‐related nonadecapeptide from toad venom, by mammalian kallikrein and salivary proteases

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