Quantification of rat T-kininogen using immunological methods

Adam, Albert; Damas, Jacques; Calay, G; Renard, Claire; Remacle-Volon, Gabrielle; Bourdon, Victor

doi:10.1016/0006-2952(89)90303-1

Cited by 31 publications

(25 citation statements)

References 20 publications

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“…These findings suggest that the contact system may play an important role in human reproduction. Interestingly, the female reproductive tract is the second richest site for kininogen and its metabolic products in the body [35][36][37][38]. Adam et al [38] measure 12.2, 10.9, 0.4 and 1.2 g/mg T-kininogen in rat plasma, uterus, liver, and kidney, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, the female reproductive tract is the second richest site for kininogen and its metabolic products in the body [35][36][37][38]. Adam et al [38] measure 12.2, 10.9, 0.4 and 1.2 g/mg T-kininogen in rat plasma, uterus, liver, and kidney, respectively. The kininogen concentration in reproductive tissues and plasma was reported to fluctuate during ovulation, pregnancy, and parturition [38].…”

Section: Discussionmentioning

confidence: 99%

“…Adam et al [38] measure 12.2, 10.9, 0.4 and 1.2 g/mg T-kininogen in rat plasma, uterus, liver, and kidney, respectively. The kininogen concentration in reproductive tissues and plasma was reported to fluctuate during ovulation, pregnancy, and parturition [38]. Why the reproductive system is so rich in kininogen and how this fluctuation in kininogen concentration occurs at the local level remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

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Certain Autoantibodies to Phosphatidylethanolamine (aPE) Recognize Factor XI and Prekallikrein Independently or in Addition to the Kininogens

Sugi

McIntyre

2001

Journal of Autoimmunity

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Certain Autoantibodies to Phosphatidylethanolamine (aPE) Recognize Factor XI and Prekallikrein Independently or in Addition to the Kininogens

Sugi

McIntyre

2001

Journal of Autoimmunity

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“…PE is a major component of both the outer and inner leaflets of cell plasma membranes and makes a complex with several plasma proteins, such as high-molecular weight kininogen, low-molecular weight kininogen, and proteins in complex with high-molecular weight kininogen, factor XI, or prekallikrein (40,41). Kininogen and its metabolites are abundantly expressed in the female reproductive system (42)(43)(44)(45). Furthermore, in antiphospholipid syndrome, which is clinically characterized by systemic thrombosis and recurrent pregnancy loss, anti-PE antibody recognizes the PE-binding proteins (40,41).…”

Section: Figure 10mentioning

confidence: 99%

Maternal disturbance in activated sphingolipid metabolism causes pregnancy loss in mice

Mizugishi

Li²,

Olivera³

et al. 2007

J. Clin. Invest.

137

116

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Uterine decidualization, a process that occurs in response to embryo implantation, is critical for embryonic survival and thus is a key event for successful pregnancy. Here we show that the sphingolipid metabolic pathway is highly activated in the deciduum during pregnancy and disturbance of the pathway by disruption of sphingosine kinase (Sphk) genes causes defective decidualization with severely compromised uterine blood vessels, leading to early pregnancy loss. Sphk-deficient female mice (Sphk1 -/-Sphk2 +/-) exhibited both an enormous accumulation of dihydrosphingosine and sphingosine and a reduction in phosphatidylethanolamine levels in pregnant uteri. These mice also revealed increased cell death in decidual cells, decreased cell proliferation in undifferentiated stromal cells, and massive breakage of decidual blood vessels, leading to uterine hemorrhage and early embryonic lethality. Thus, sphingolipid metabolism regulates proper uterine decidualization and blood vessel stability. Our findings also suggest that disturbance in sphingolipid metabolism may be considered as a cause of pregnancy loss in humans. IntroductionEmbryonic implantation is a complex series of processes that establishes the connection between maternal and embryonic tissues and requires an intricate program of uterine preparation (1, 2). Very soon after implantation, which occurs in the mouse on day 4.5 postcoitum (pc) (day 0.5 - vaginal plug), endometrial stromal cells surrounding implanting blastocysts undergo dramatic transformation (decidualization), during which they proliferate and differentiate into decidual cells. Decidualization begins in the stromal region immediately surrounding the embryo (antimesometrial site). Next to the implanting blastocyst, thin, dense, avascular cell layers, called the primary decidual zone, are formed. Adjacent to the primary decidual zone, the broad secondary decidual zone is fully developed by day 6.5 pc, and is characterized by terminally differentiated decidual polyploidy with acquisition of large mono- or binucleated cells (3). The decidua provides a vascular network for nutrition and gas exchange for the developing embryo before a functional placenta is established (4). It also acts as a barrier to uncontrolled trophoblast proliferation.The sphingolipid metabolic pathway produces bioactive signaling metabolites as well as complex lipids that are utilized in membrane organization and structure. A very prominent signaling lipid is sphingosine-1-phosphate (S1P), which enhances cell survival and growth (5-8). Recent studies have demonstrated its physiologic importance in the development of the vascular and nervous system (9-12), the heart (13), and the immune system (14-16) by signaling through a family of G protein-coupled receptors designated S1P 1-5 . In contrast, 2 precursors of S1P,

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“…Plasma T-kininogen was measured by sandwich enzyme-linked immunoabsorbent assay, as described previously (1).…”

Section: Production Of Hk-deficient Lewis Rat the Brown-norwaymentioning

confidence: 99%

Kininogen deficiency modulates chronic intestinal inflammation in genetically susceptible rats

Isordia‐Salas

Pixley

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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ert W. Colman. Kininogen deficiency modulates chronic intestinal inflammation in genetically susceptible rats. Am J Physiol Gastrointest Liver Physiol 283: G180-G186, 2002. First published March 6, 2002 10.1152/ajpgi.00514.2001.-Genetically susceptible Lewis rats injected in the intestinal wall with peptidoglycan-polysaccharide (PG-APS) polymers develop chronic granulomatous enterocolitis concomitant with activation of the kallikrein-kinin system. To elucidate the role of high-molecular-weight kininogen (HK) in chronic enterocolitis, we back crossed Brown-Norway rats having a HK deficiency with Lewis rats for five generations. Two new strains were produced, wild-type F5 (F5WT) and HK deficient (F5HKd), each with a ϳ97% Lewis genome. The HK values of F5WT and F5HKd rat plasma were 0.62 Ϯ 0.20 and 0.08 Ϯ 0.03 U/ml, respectively. In PG-APS-injected rats, chronic inflammation was measured by using gross gut score, histological inflammation, liver granuloma, and white blood cell count. The mean gross gut scores were significantly lower in the F5HKd than in the F5WT rats. Plasma T-kininogen was significantly less in F5HKd. These results indicate the importance of the kallikrein-kinin system in this model of chronic enterocolitis and systemic inflammation. inflammatory bowel disease; experimental colitis; kallikreinkinin system; contact system INFLAMMATORY BOWEL DISEASES (IBDs), including Crohn's disease and ulcerative colitis, are disorders characterized by local and systemic chronic inflammation with unpredictable relapses and remissions (10). These disorders are immunologically mediated and have a genetic component (10,20). In animal models, the aggressiveness and chronicity of the inflammatory process is dependent on the genetic background of the host (9).Previous studies from our laboratory have used a rat model of acute and chronic granulomatous enterocolitis that permits detailed examination of the mechanisms of the genetically determined intestinal and sys-

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Quantification of rat T-kininogen using immunological methods

Cited by 31 publications

References 20 publications

Certain Autoantibodies to Phosphatidylethanolamine (aPE) Recognize Factor XI and Prekallikrein Independently or in Addition to the Kininogens

Certain Autoantibodies to Phosphatidylethanolamine (aPE) Recognize Factor XI and Prekallikrein Independently or in Addition to the Kininogens

Maternal disturbance in activated sphingolipid metabolism causes pregnancy loss in mice

Kininogen deficiency modulates chronic intestinal inflammation in genetically susceptible rats

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