Activation of hageman factor by collagen

Wilner, George D.; Nossel, Hymie L.; Leroy, Éric

doi:10.1172/jci105943

Cited by 204 publications

(86 citation statements)

References 22 publications

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“…The precise etiologic incitant of lipoid nephrosis is not known but it is possible that subtle damage to the G B M not only leads to contact-activation of Hageman factor (35) and, ultimately, generation of bradykinin, but also initiates the coagulation sequence. The latter is suggested by the finding of platelet thrombi in intimate association with the glomerular capillary wall (12).…”

Section: Resultsmentioning

confidence: 99%

A Study of the Plasma Kinin-generating System in Children with the Minimal Lesion, Idiopathic Nephrotic Syndrome

Kallen

Lee

1975

Pediatr Res

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705the present ones which suggest the existence of a photochemical reaction between D N A and bilirubin are somewhat disquieting, particularly when one considers that mutagens and chemical carcinogens derive their biologic activity from the ability to react with DNA. Our results suggest that phototherapy of neonates is a complex process which may generate a number of potentially dangerous genetic side effects. S U M M A R YThe widespread use of phototherapy in the treatment of neonatal jaundice is causing concern because little information is available on its effects on subcellular structure and function. The present study deals with the effects on the macromolecular structure of D N A illuminated in the presence of bilirubin. The results indicate a bilirubin-induced photodegradation of this biopolymer. ExtractAlthough the precise etiologic incitant of the minimal lesion idiopathic nephrotic syndrome of childhood is not known, it is likely that a host mechanism mediates the permeability alterations of the glomerular capillary wall resulting in massive proteinuria. As a first step in examining the possibility that local kinin release may account for the proteinuria in this disorder, two parameters of the plasma kinin-generating system, plasma prekallikrein and kallikrein inhibitor, were assayed during 27 nephrotic episodes in 21 corticosteroid-responsive children. Plasma kallikrein was assayed by means of its esterase activity on a synthetic arginine ester substrate, N-a-tosyl-L-arginine methyl ester (TAMe), after activation of Hageman factor by kaolin. This activity, after subtraction of spontaneous arginine esterase activity (i.e., TAMe esterase activity measured in plasma not exposed to kaolin) is derived from prekallikrein. Plasma prekallikrein activity in 11 normal children was 99.6 + 2.9 pnol TAMe hydrolyzed/ml plasma/hr (mean + SEM). Kallikrein inhibitor was quantified in arbitrary units. Kallikrein inhibitor activity in 11 normal children was 0.94 + 0.04 units.During the overt nephrotic syndrome, before initiation of intensive daily corticosteroid treatment, mean values were: prekallikrein, 58.5 A 7.24 flmol/ml/hr; and kallikrein inhibitor, 0.35 + 0.06 units. After corticosteroid-induced remission occurred, mean values were: plasma prekallikrein, 118.6 + 3.2 pmol/ml/hr; and kallikrein inhibitor, 0.78 + 0.03 pmol/ml/hr. Both parameters were again assayed in 14 of the 21 children after complete cessation of corticosteroid treatment. Plasma prekallikrein was normal, 99.6 * 4.8 flmol/ml/hr; but kallikrein inhibitor was still somewhat depressed, 0.84 + 0.03 units. A subset of 9 patients had marked depression of plasma prekallikrein to levels less than 20 pmol/ml/hr and essentially undetectable inhibitor acGvity. Serum a-2 macroglobulin was elevated in nephrotic patients: mean value during relapse, 862 + 29 mg/100 ml; during corticosteroid-maintaining remission, 615 * 29 mg/100 ml. After cessation of corticosteroids, mean serum level was 481 + 20 mg/100 ml. The proportional reduction of plasma prekallikrein an...

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Section: Resultsmentioning

confidence: 99%

A Study of the Plasma Kinin-generating System in Children with the Minimal Lesion, Idiopathic Nephrotic Syndrome

Kallen

Lee

1975

Pediatr Res

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“…The activation of Hageman factor by a variety of biologic materials such as collagen (28,29), sodium urate crystals (30), pyrophosphate crystals (30), Lhomocystine crystals (31), and human articular cartilage (32), and the capacity of activated Hageman factor to convert prekallikrein to kallikrein either directly or through its prealbumin fragments (5) offers a nonimmunologic, readily activatable mechanism for the generation of a chemotactic principle independent of the complement system. It is noteworthy that kallikrein is not only chemotactic for human neutrophils but also leads to the generation of the permeability factor bradykinin; two other chemotactic factors, fragments from the third and fifth components of complement both promote leukocyte migra-tion in vitro (33,34) and also increase vascular permeability by virtue of their anaphylatoxic activity (35,36).…”

Section: Discussionmentioning

confidence: 99%

A Prealbumin Activator of Prekallikrein

Kaplan

Kay

Austen

1972

The Journal of Experimental Medicine

229

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Human plasma kallikrein has been shown to directly and selectively attract human neutrophils from a mixed leukocyte population. The capacity of plasma kallikrein to be chemotactic and to generate the nonapeptide bradykinin was maintained during progressive purification. While neither highly purified prekallikrein nor the prealbumin Hageman factor fragments were chemotactic alone, their interaction so as to convert prekallikrein to kallikrein yielded both chemotactic and kinin-generating activity. Both functions of kallikrein were inhibited by treatment with diisopropyl fluorophosphate, indicating an essential role for the active site of the enzyme in the expression of its chemotactic activity.

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“…The properties of collagen which cause the reaction with platelets are not known and it is the purpose of the present communication to describe the results of some studies of this problem. These studies were carried out simultaneously with an investigation of the action of collagen on plasma coagulation (13).…”

Section: Introductionmentioning

confidence: 99%

Aggregation of platelets by collagen

Wilner¹,

Nossel²,

Leroy³

1968

J. Clin. Invest.

Self Cite

172

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A B S T R A C T In studying some of the properties of collagen responsible for the ability to aggregate platelets it was found that thermal treatment at pH 2.5 of acid-soluble human collagen resulted in a sharp reduction in relative viscosity and platelet aggregating activity at about 350C. The reduction in viscosity is known to be associated with structural transition from triple helical to random coil form and it is postulated that the native structure of collagen is essential for its platelet aggregation effect. Blockage of the free amino groups by deamination, N-acetylation, or treatment with dinitrofluorobenzene resulted in over 90%o reduction in platelet aggregating activity. Addition of cationic proteins to collagen, removal of the negatively charged telopeptides by treatment with pepsin, or acetylation of the free carboxyl groups did not significantly affect the platelet aggregating activity of collagen. On the basis of these findings it is suggested that the free amino groups and specifically the epsilon amino groups of lysine are critical for the platelet aggregating activity of collagen whereas the carboxyl groups are of relatively little importance.

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Activation of hageman factor by collagen

Cited by 204 publications

References 22 publications

A Study of the Plasma Kinin-generating System in Children with the Minimal Lesion, Idiopathic Nephrotic Syndrome

A Study of the Plasma Kinin-generating System in Children with the Minimal Lesion, Idiopathic Nephrotic Syndrome

A Prealbumin Activator of Prekallikrein

Aggregation of platelets by collagen

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