ライフサイエンスコーパス: kinin

1 4) or lower degradation of growth-inhibitory kinins.

2 hibition of TK activity and the formation of kinins.

3 r increased degradation of growth-inhibiting kinins.

4 pendent on activation of local production of kinins.

5 t likely secondary to the formation of local kinins.

6 AT2 receptor and is also mediated in part by kinins.

7 cid metabolism, such as prostaglandin E2 and kinins.

8 contribute to the cardioprotective nature of kinins.

9 unological reactions leading to a release of kinins.

10 mmunological reactions leading to release of kinins.

11 ry microvessels, kininogen (the precursor of kinin; 10 micrograms/mL) and three ACE inhibitors (capto

12 beled peptide with the scrambled-sequence of kinin 8 (TMR-Scrambled) did not.

13 The unlabeled kinin 8 peptide competed TMR-RK8, decreasing confocal mi

14 ly-labeled kinin peptide with the endogenous kinin 8 sequence (TMR-RK8), identical in the ticks Rhipi

15 ons or during the development of HF; and (2) kinins acting via the B(2) receptor play an important ro

16 be a mechanism for ACE inhibitors to augment kinin activity at cellular level.

17 The increased kinin activity resulting from CEI treatment may particip

18 nase II, which serves to increase endogenous kinin activity.

19 ion of the B1R, and 2) CPM-generated des-Arg-kinin agonist is efficiently delivered to the B1R.

20 onal activity, subjects were challenged with kinin agonists.

21 Proteolytic processing of kinins alters their affinities toward specific cellular

22 nated "Aedae-KR." We used protease-resistant kinin analogs 1728, 1729, and 1460 to evaluate their eff

23 our knowledge, this is the first report that kinin analogs modulate sucrose perception in any insect.

24 Recent evidence suggests that the kallikrein-kinin and coagulation system might participate in this p

25 nd activation of the inflammatory kallikrein-kinin and complement systems.

26 lished the blood pressure-lowering effect of kinin and kallikrein.

27 sis risk reduction via the plasma kallikrein/kinin and renin angiotensin systems.

28 ctor I (IGF-I) treatment on renal kallikrein-kinin and renin-angiotensin system components.

29 gulation pathway and triggers the kallikrein-kinin and the complement systems.

30 e as a regulator of the biologic activity of kinins and anaphylatoxins, CPN is an important regulator

31 Finally, we assessed the impact of kinins and C5a liberated in parasite-laden tissues on Th

32 endothelium by inflammatory stimuli, such as kinins and cytokines, meets the specifications of the in

33 in the therapeutic effect of the AT1-ant via kinins and other autacoids.

34 erine proteases that catalyze the release of kinins and other vasoactive peptides.

35 ion for understanding the central actions of kinins and their putative role in mediating a number of

36 s encoding the prepropeptides for corazonin, kinin, and allatostatin-A.

37 peptides such as complement anaphylatoxins, kinins, and fibrinopeptides.

38 be mediated partly through kinins; however, kinins appear to play a lesser role in the antihypertrop

39 Here, we use kinins as a model system to address the kinetics and reg

40 We hypothesized that kinins autoregulate B2R and B1R expression in favor of B

41 The kinin B(1) receptor (B(1)R) plays a role in inflammatory

42 d highlight the therapeutic potential of the kinin B(1) receptor in these disease states.

43 The kinin B(1) receptor plays an important role in mediating

44 We demonstrated that rat kinin B(1) receptors displayed a ligand-independent cons

45 vis, Ann Arbor, Michigan); or 4) AT(1)-ant + kinin B(2) receptor antagonist (B(2)-ant) (icatibant) (o

46 interaction of carboxypeptidase M (CPM) and kinin B1 receptor (B1R) enhances B1R signaling in two wa

47 We previously reported upregulated neuronal kinin B1 receptor (B1R) expression in hypertension.

48 Kinin B1 receptor (B1R) expression is induced by injury

49 We reported that the kinin B1 receptor (B1R) heterodimerizes with membrane ca

50 ore microvesicles that were positive for the kinin B1 receptor (P<0.001).

51 s-Arg9-BK (1 microgram kg-1 i.a., a specific kinin B1 receptor agonist), kinin B2 receptor antagonist

52 These results suggest that engagement of the kinin B1 receptor contributes to fibrogenesis through in

53 from blood mononuclear cells (MNCs), whereas kinin B1 receptor expression was barely detectable.

54 Expression of the kinin B1 receptor is up-regulated in chronic inflammator

55 s study, we investigated the presence of the kinin B1 receptor on endothelial microvesicles and its c

56 Activation of the kinin B1 receptor with des-Arg(10)-kallidin stimulated a

57 and has been associated with increased B1R (kinin B1 receptor) activation.

58 Kinin-B1 receptor agonists and antagonists did not affec

59 version of bradykinin or kallidin to des-Arg kinin B1R agonists.

60 We hypothesized that kinin B1R contributes to hypertension via upregulation o

61 We now demonstrate the involvement of the kinin B2 receptor (B(2)R) in the recruitment of CPCs to

62 al cells (HLMVEC), bradykinin (BK) activates kinin B2 receptor (B2R) signaling that results in Ca(2+)

63 Bradykinin, a potent and selective kinin B2 receptor agonist, induces calcium mobilization

64 NPC-17731, another kinin B2 receptor antagonist, had similar inhibitory eff

65 i.a., a specific kinin B1 receptor agonist), kinin B2 receptor antagonists: HOE140 (30 micrograms kg-

66 esults suggest that PKC-alpha is involved in kinin B2 receptor regulation by phorbol esters in A549 c

67 ese hamster ovary cells expressing the human kinin B2 receptor, which internalized approximately 80%

68 bant and dominant-negative Akt, indicating a kinin B2 receptor-Akt-mediated event.

69 ates serosal afferents by a direct action on kinin B2 receptors that are present on serosal afferent

70 iac visceral afferents through activation of kinin B2 receptors.

71 schaemia activates cardiac afferents through kinin B2 receptors.

72 cribe novel functions for bradykinin and the kinin-B2 receptor (B2BkR) in differentiation of neural s

73 Katholiek rats (BNK), which are deficient in kinins because of a mutation in the kininogen gene, and

74 (B1R) enhances B1R signaling in two ways; 1) kinin binding to CPM causes a conformational activation

75 (Gi and Gq) that are coupled to the type II kinin (BK2) receptor.

76 mRNA levels for regulators of the kallikrein-kinin (C1-inhibitor), coagulation (thrombomodulin, endot

77 Complement and the kallikrein-kinin cascade system are both activated in injured tissu

78 ect modulation of complement (MAb 60.11) and kinin cascades (MAb 74.5.2) and/or activation of immune

79 modulating the activation of complement and kinin cascades, gC1qR has been identified as a putative

80 variables contributed to FXII-HAE, with the kinin catabolism enzymes ACE and CPN exhibiting a signif

81 AE is associated with modifiers, for example kinin catabolism enzymes, ACE and CPN, different from th

82 Kinins cleaved from kininogen are agonists of the B2R an

83 ACE activity (r(2)=0.16, P=0.039), and total kinin concentration correlated with net tissue plasminog

84 Instillation of PPE in the lung increased kinin concentrations in BALF, a result consistent with t

85 sociated with severalfold increases in local kinin concentrations.

86 eptibility and activation of the kalli-krein-kinin (contact) system were investigated in experimental

87 cal analysis of parameters of the kallikrein-kinin (contact) system.

88 keletal muscle through increased ACE-related kinin degradation [and reduced activity at the bradykini

89 ecursor for kinin formation or inhibition of kinin degradation by use of ACE inhibitors increases NO

90 human myocardium and that the inhibition of kinin degradation plays an important role in the regulat

91 ted both by angiotensin-converting enzyme, a kinin-degrading peptidase, and by endogenous IL-10.

92 Here, we hypothesize that a kinin-dependent local lung angioedema via B1R and eventu

93 of the RAS, ACEi may also act by inhibiting kinin destruction, whereas AT1-ant may block the RAS at

94 cells L(3,4) in abdominal ganglia coexpress kinins, DH41, and DH30, which together elicit the fictiv

95 basal infoldings of the stellate cells after kinin diuretic peptide stimulation, confirming that thes

96 fe-threatening swelling caused by kallikrein-kinin dysregulation.

97 Kinins exert multiple pathophysiological functions, incl

98 asodilator agonists known and belongs to the kinin family of proinflammatory peptides.

99 ons express numerous neuropeptides including kinin, FMRFamides, eclosion hormone (EH), crustacean car

100 Our data indicate that stimulation of local kinin formation by use of a precursor for kinin formatio

101 al kinin formation by use of a precursor for kinin formation or inhibition of kinin degradation by us

102 Established by means of the kinin formation process, this assay should be preferred

103 ine this factor XII-independent mechanism of kinin formation.

104 ine protease inhibitors, which inhibit local kinin formation.

105 Recent data suggest that activation of the kinin-forming cascade can occur on the surface of endoth

106 h the mechanism by which Hsp90 activates the kinin-forming cascade is not understood, this protein re

107 ght kininogen is the precursor for two-chain kinin-free kininogen and bradykinin.

108 It has been shown that the two-chain kinin-free kininogen has the properties of anti-adhesion

109 ost-translationally via activation of the B1 kinin G protein-coupled receptor (B1R).

110 The importance of the kinin generating pathway and bradykinin in causing edema

111 he cross-talk between the complement and the kinin generating systems has become particularly relevan

112 actic defect; neither of these corrected the kinin-generating defect.

113 in to correct the coagulation, fibrinolytic, kinin-generating, and chemotactic defects of Fletcher fa

114 human heart, and that there is active local kinin generation in these blood vessels.

115 the complement system, the contact system of kinin generation, and the intrinsic coagulation pathway.

116 kallikrein (TK), the enzyme responsible for kinin generation.

117 ng the relationship between fibrinolysis and kinin generation.

118 sequence of nitric oxide > carbon monoxide = kinins > adenosine.

119 d this effect may be mediated partly through kinins; however, kinins appear to play a lesser role in

120 version of angiotensin (Ang) I to Ang II and kinin hydrolysis.

121 Therefore, the diuretic action of kinin in Drosophila can be explained by an increase in C

122 The myotropic function of kinins in eliciting tick midgut peristalsis was establis

123 d the hypothesis that enhanced reactivity to kinins in inflamed airways was caused by induction of B1

124 We conclude that increased reactivity to kinins in inflamed human airways is mediated, at least i

125 arction (MI) in rats, we studied the role of kinins in the cardioprotective effect of ACEi.

126 angiotensin II type 2 (AT(2)) receptors and kinins in the cardioprotective effect of angiotensin II

127 lecular modeling of the binding modes of the kinins in the homology model of the B1 receptor.

128 f important homeostatic responsibilities for kinins, including those in autocrine and paracrine signa

129 angioedema (HAE) is associated with episodic kinin-induced swelling of the skin and mucosal membranes

130 The kallikrein-kinin (K-K) (contact) system is activated during acute a

131 en the evidence for a broad link between the kinin-kallikrein and complement systems, and suggest a r

132 Notably, variants in kinin-kallikrein genes KNG1, F12, KLKB1, and ACE were as

133 S reference standard, directly activated the kinin-kallikrein pathway in human plasma, which can lead

134 Our results highlight the importance of the kinin-kallikrein system in the regulation of serum pepti

135 in the pathogenesis of severe COVID-19: the kinin-kallikrein system, resulting in acute lung inflamm

136 Insect kinins (leucokinins) are multifunctional peptides acting

137 ensin II levels, ACE inhibitors can increase kinin levels and subsequently increase nitric oxide form

138 ation of glucose metabolism by kallikrein or kinins may only be observed in intact perfused tissues o

139 Conversely, after vascular injury, kinins mediate the beneficial effect of angiotensin-conv

140 Evidence also suggests that kinins mediate the increase in insulin sensitivity after

141 stellate cell and is required for Drosophila kinin-mediated induction of diuresis and chloride shunt

142 Therefore, kinin metabolism and kinin-stimulated production of cyto

143 In the present work, we demonstrate that kinins mobilize dendritic cells to produce IL-12 through

144 hormones (DHs) 41 and 30, eclosion hormone, kinins, myoinhibitory peptides (MIPs), neuropeptide F, a

145 ACE inhibitors potentiate kinin-nitric oxide (NO)-dependent coronary vascular dila

146 ible to demonstrate effects of kallikrein or kinins on glucose metabolism in isolated skeletal muscle

147 previously demonstrated the activity of tick kinins on the cognate G protein-coupled receptor.

148 Rat kallikrein-binding protein, but not kinin or kallikrein, induced vascular relaxation of aort

149 Similarly, kinin or transduction of kallikrein in cultured cardiomy

150 nin B(1) receptor, independent of endogenous kinins or ACE.

151 ng after myocardial infarction (MI), and (2) kinins partially mediate the cardiac beneficial effect o

152 ivation of the bradykinin-forming kallikrein-kinin pathway.

153 g the inflammatory effects of the kallikrein-kinin pathway.

154 hat by inhibiting the contact and kallikrein-kinin pathways and impairing neutrophil activation, CpaA

155 for its roles in the contact and kallikrein-kinin pathways.

156 Kinin peptide binding to CPM causes a conformational cha

157 A fluorescently-labeled kinin peptide with the endogenous kinin 8 sequence (TMR-

158 Our data thus indicate that kinin peptides can serve as danger signals that trigger

159 oited the fact that high-affinity binding of kinin peptides to the human B1 receptor subtype requires

160 timulation of the AT1 receptor, ARB lack the kinin-potentiating effects of ACEI.

161 15-ml chilled ethanol to prevent artifactual kinin production and degradation.

162 man heart and to determine the role of local kinin production in the elaboration of nitric oxide by h

163 In conclusion, kallikrein/kinin protects against cardiomyocyte apoptosis in vivo a

164 acutely up-regulated by activation of the B1-kinin receptor (B1R) in human endothelial cells or trans

165 thylthio-ATP, ATP, ADP, and UTP, but not the kinin receptor agonist bradykinin, suggesting that deple

166 r administration of one of two dissimilar B2 kinin receptor antagonists (BK2As), or vehicle.

167 Kinin receptor antagonists to bradykinin-evoked release

168 ty of better kallikrein inhibitors, specific kinin receptor antagonists, and techniques of genetic ma

169 by reintroduction of recombinant NEP and the kinin receptor antagonists.

170 ntractions by activating a G protein-coupled kinin receptor designated "Aedae-KR." We used protease-r

171 r study was to investigate coronary vascular kinin receptor function in patients with atherosclerosis

172 Using B(2) kinin receptor gene knockout mice (B(2)(-/-)), we tested

173 d to the live midgut the TMR-RK8 labeled the kinin receptor in muscles while the labeled peptide with

174 n we uncovered the physiological role of the kinin receptor in the tick midgut.

175 We now show that the B2 kinin receptor is expressed in rat dorsal horn neurons a

176 n the basal state, P2Y receptors but not the kinin receptor may be compartmented to cholesterol-depen

177 arinic receptor with relative sparing of the kinin receptor pathways.

178 a pivotal role in shifting the repertoire of kinin receptor subtypes in favor of B1R during inflammat

179 d functional characteristics of the human B1 kinin receptor, a stable clone of Chinese hamster ovary

180 d by HOE 140, which blocks the bradykinin B2-kinin receptor, and serine protease inhibitors, which in

181 d beta-turn, required for activity at the B2 kinin receptor, the topological orientation of the side

182 ni required for agonistic activity at the B1 kinin receptor.

183 oplasmic carboxyl termini of human B1 and B2 kinin receptors (B1KR and B2KR, respectively) in the int

184 rapid ligand-induced sequestration of human kinin receptors and internalization of their agonists.

185 flamed airways was caused by induction of B1-kinin receptors by comparing the effects of the selectiv

186 We concluded that (1) lack of B(2) kinin receptors does not affect cardiac phenotype or fun

187 significantly different roles for B1 and B2 kinin receptors in vascular smooth muscle cells.

188 Stimulation of B1 and B2 kinin receptors on cultured rabbit superior mesenteric a

189 and inhibition of kallikrein or blockade of kinin receptors reduces GFR and RPF.

190 on pattern or contribution of the individual kinin receptors to pathological prostate cell growth is

191 Experiments excluded a putative kinin release by proteases.

192 PKa-catalyzed kinin release from HK and LK was not affected by the Lys

193 However, kinin release from HK-Lys379 and LK-Lys379 catalyzed by

194 Increased kinin release was evident when fibrinolysis was induced

195 Mass spectrometry revealed that the kinin released from wild-type and variant kininogens by

196 Therefore, kinin metabolism and kinin-stimulated production of cytokines may play a pivo

197 arization of transepithelial potential after kinin stimulation.

198 This implicated local kinin synthesis as an intermediate step in the productio

199 allikrein, again suggesting a role for local kinin synthesis.

200 ulation cascade components of the kallikrein-kinin system (KKS) and downregulation of kininogen prior

201 The kallikrein-kinin system (KKS) comprises a cascade of proteolytic en

202 The plasma kallikrein-kinin system (KKS) consists of serine proteases, prekall

203 The kallikrein-kinin system (KKS) has been postulated to play a role in

204 Modulation of the kallikrein-kinin system (KKS) has been shown to have beneficial eff

205 is study examines the role of the kallikrein-kinin system (KKS) in RIHD by investigating the cardiac

206 at rapidly inhibits PKa activity, kallikrein kinin system activation and HK cleavage in plasma.

207 cts of KVD900 on PKa activity and kallikrein kinin system activation in whole plasma were measured in

208 antibody C11C1 attenuates plasma kallikrein-kinin system activation, local and systemic inflammation

209 iguing possibility that decreased kallikrein-kinin system activity may play an important role in the

210 be mediated via changes in renal kallikrein-kinin system activity.

211 mbly and activation of the plasma kallikrein/kinin system and discusses its influence on vascular bio

212 lammatory pathways, including the kallikrein-kinin system and leukocyte activity.

213 e close interrelation between the kallikrein-kinin system and the RAAS.

214 The renal kallikrein-kinin system and the renin-angiotensin system are implic

215 reported that alterations of the kallikrein-kinin system are associated with formation of aortic ane

216 The opposing effects of the kallikrein-kinin system are mediated by bradykinin acting on B1 and

217 The principal effectors of the kallikrein-kinin system are plasma and tissue kallikreins, protease

218 ce and significance of the plasma kallikrein/kinin system as a risk factor for the development of vas

219 d in the liver that regulates the kallikrein-kinin system at multiple points.

220 One of the kallikrein-kinin system components, kallikrein-binding protein, bin

221 he local release of bradykinin (BK) or other kinin system constituents into the mammary vasculature h

222 modeling and the up-regulation of Kallikrein-kinin system contribute, at least in part, to the antihy

223 c disease that is associated with kallikrein-kinin system dysregulation.

224 is is the first report of a local kallikrein-kinin system in adrenergic nerve endings capable of gene

225 indings underline the role of the kallikrein-kinin system in angiogenesis.

226 To explore the role of the kallikrein-kinin system in relation to ischemia/reperfusion injury

227 The kinin system is activated during vasculitis and may cont

228 ulators of the renin-angiotensin-aldosterone-kinin system is an effective strategy to forestall the p

229 The kallikrein-kinin system is developmentally expressed in newborn kid

230 n perfused limbs suggest that the kallikrein-kinin system may participate in the regulation of substr

231 It has been postulated that the mammary kinin system may play a role in modulating mammary blood

232 The kallikrein-kinin system participates in blood pressure regulation.

233 in II levels, suggesting that the kallikrein-kinin system partly mediates the effects of the polymorp

234 and the components of the plasma kallikrein-kinin system resulted in decreased bradykinin production

235 coagulation and functions in the kallikrein-kinin system to generate bradykinin.

236 KNG) is a central constituent of the contact-kinin system which represents an interface between throm

237 between CpaA, FXII, and the KKS (kallikrein-kinin system) and to determine the downstream consequenc

238 The kallikrein-kinin system, along with the interlocking renin-angioten

239 Hemodialysis activates the kallikrein-kinin system, increasing bradykinin.

240 C1-inhibitor is the main inhibitor of the kinin system.

241 the fibrinolytic system, and the kallikrein-kinin system.

242 y constituent of the proinflammatory contact-kinin system.

243 ole in the assembly of the plasma kallikrein-kinin system.

244 central role in activation of the kallikrein-kinin system.

245 nd proliferation; cell stress responses; the kinin system; and angiogenesis.

246 mbly of the vasoregulatory plasma kallikrein-kinin system; thus we explored whether MPO and high mole

247 llopeptidases in the natriuretic peptide and kinin systems and renin-angiotensin-aldosterone system,

248 The renin-angiotensin and kallikrein-kinin systems are key regulators of vascular tone and in

249 Kallikrein-kininogen-kinin systems are now topics of widespread interest.

250 The renin-angiotensin and kallikrein-kinin systems engage in cross-talk at multiple levels, i

251 oles of the renin-angiotensin and kallikrein-kinin systems in vivo, the distinct properties of arrest

252 urbed balance between the RAS and kallikrein-kinin systems.

253 also inhibits the contact, coagulation, and kinin systems.

254 renin-angiotensin-aldosterone and kallikrein-kinin systems.

255 at link the renin-angiotensin and kallikrein-kinin systems.

256 In addition to generation of C5a and kinins via parasite-derived cruzipain, we demonstrate th

257 Interestingly, the hemodynamic response to kinins was altered in transgenic mice, with des-Arg(9)-b

258 y regarded as the physiological regulator of kinins, was much less efficient than TAFIa.

259 inin B2 antagonist, NPC-567 (indicating that kinins were generated), but not DN-Prolastin or the elas

260 he effect of the ACEi is mediated in part by kinins, whereas that of the AT1-ant is triggered by acti

261 critical residues for the interaction of the kinins with human bradykinin receptor 1 (B1) using site-