T-kininogen - the major plasma kininogen in rat adjuvant arthritis

Barlas, A.; Okamoto, Hiroshi; Greenbaum, Lowell M.

doi:10.1016/0006-291x(85)91434-2

Cited by 101 publications

(11 citation statements)

References 11 publications

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“…Measurements of kininogen levels were performed as described previously by our laboratory using the protocols described by Barlas et al [7,21]. Total kininogens.…”

Section: Determination Of Kininogensmentioning

confidence: 99%

Expression of Bradykinin B₂Receptor in the Mouse Ovary

et al. 2003

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Background: Previous work by our group and others has implicated a role for kinins in the ovulatory process. The purpose of the present study was to elucidate whether endogenous progesterone, which is an intraovarian regulator of ovulation, might be responsible for induction of the kinin system in the ovary during ovulation. The gonadotropin-primed immature rat was used as the experimental model, and the role of endogenous progesterone was explored using the antiprogestin, RU486.

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“…Measurements of kininogen levels were performed as described previously by our laboratory using the protocols described by Barlas et al [7,21]. Total kininogens.…”

Section: Determination Of Kininogensmentioning

confidence: 99%

Expression of Bradykinin B₂Receptor in the Mouse Ovary

et al. 2003

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“…In the rat there is a third kininogen known as t-kininogen that releases kinins when incubated with trypsin but not tissue or plasma kallikrein and is one of the main acute reactants of inflammation. All kininogens, including LMWK, HMWK, and t-kininogen, also inhibit thiol proteases such as cathepsin M, H, and calpains (16, 86, 193, 194). HMWK is involved in the early stages of surface-activated coagulation (intrinsic coagulation pathway) (69, 120, 277).…”

Section: Introductionmentioning

confidence: 99%

The Kallikrein‐Kinin System as a Regulator of Cardiovascular and Renal Function

Rhaleb

Yang

Carretero

2011

Comprehensive Physiology

109

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Autocrine, paracrine, endocrine, and neuroendocrine hormonal systems help regulate cardiovascular and renal function. Any change in the balance among these systems may result in hypertension and target organ damage, whether the cause is genetic, environmental or a combination of the two. Endocrine and neuroendocrine vasopressor hormones such as the renin-angiotensin system (RAS), aldosterone, and catecholamines are important for regulation of blood pressure and pathogenesis of hypertension and target organ damage. While the role of vasodepressor autacoids such as kinins is not as well defined, there is increasing evidence that they are not only critical to blood pressure and renal function but may also oppose remodeling of the cardiovascular system. Here we will primarily be concerned with kinins, which are oligopeptides containing the aminoacid sequence of bradykinin. They are generated from precursors known as kininogens by enzymes such as tissue (glandular) and plasma kallikrein. Some of the effects of kinins are mediated via autacoids such as eicosanoids, nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), and/or tissue plasminogen activator (†PA). Kinins help protect against cardiac ischemia and play an important part in preconditioning as well as the cardiovascular and renal protective effects of angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor blockers (ARB). But the role of kinins in the pathogenesis of hypertension remains controversial. A study of Utah families revealed that a dominant kallikrein gene expressed as high urinary kallikrein excretion was associated with a decreased risk of essential hypertension. Moreover, researchers have identified a restriction fragment length polymorphism (RFLP) that distinguishes the kallikrein gene family found in one strain of spontaneously hypertensive rats (SHR) from a homologous gene in normotensive Brown Norway rats, and in recombinant inbred substrains derived from these SHR and Brown Norway rats this RFLP cosegregated with an increase in blood pressure. However, humans, rats and mice with a deficiency in one or more components of the kallikrein-kinin-system (KKS) or chronic KKS blockade do not have hypertension. In the kidney, kinins are essential for proper regulation of papillary blood flow and water and sodium excretion. B2-KO mice appear to be more sensitive to the hypertensinogenic effect of salt. Kinins are involved in the acute antihypertensive effects of ACE inhibitors but not their chronic effects (save for mineralocorticoidsalt-induced hypertension). Kinins appear to play a role in the pathogenesis of inflammatory diseases such as arthritis and skin inflammation; they act on innate immunity as mediators of inflammation by promoting maturation of dendritic cells, which activate the body’s adaptive immune system and thereby stimulate mechanisms that promote inflammation. On the other hand, kinins acting via NO contribute to the vascular protective effect of ACE inhibitors during neointima formation. In myocardial i...

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“…A high plasma concentration of CPIs in rats having adjuvant arthritis is almost solely due to the increase in T-kininogen [8]. These findings strongly suggest that CPI-1 and -2 correspond to two species of Tkininogens that have the ability to inhibit cysteine proteinases and markedly increase in an acute phase of inflammation in rats [4][5][6][7][8]181.…”

Section: Discussionmentioning

confidence: 99%

Purification of two species of exudate cysteine‐proteinase inhibitors that are acute‐phase reactants in the carrageenin‐induced inflammation in rats

Nakagawa¹,

Hirata²

1986

FEBS Letters

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Two species of cysteine-proteinase inhibitors (CPIs) have been purified to homogeneity from exudate in the carrageenin-induced inflammation in rats. The exudate CPIs were separated into two forms (named CPI-1 and -2) in affinity chromatography on 4carboxymethyl-papain-Sepharose, the final stage of purification. CPI-1 and -2 gave different mobilities in polyacrylamide gel electrophoresis (PAGE), probably because of different isoelectric points (~14.47 for CPI-1 and ~14.21 for CPI-2). Both CPI-1 and -2 showed immunological identity in double immunodiffusion and same molecular mass of 68 kDa when analysed by SDS-PAGE. These results indicate that CPI-1 and -2 are very similar but distinct CPIs. CPI-1 and -2 are acute-phase reactants and probably represent two species of T-kininogens having inhibitory activity toward cysteine proteinases.

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T-kininogen - the major plasma kininogen in rat adjuvant arthritis

Cited by 101 publications

References 11 publications

Expression of Bradykinin B₂Receptor in the Mouse Ovary

Expression of Bradykinin B₂Receptor in the Mouse Ovary

The Kallikrein‐Kinin System as a Regulator of Cardiovascular and Renal Function

Purification of two species of exudate cysteine‐proteinase inhibitors that are acute‐phase reactants in the carrageenin‐induced inflammation in rats

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T-kininogen - the major plasma kininogen in rat adjuvant arthritis

Cited by 101 publications

References 11 publications

Expression of Bradykinin B2Receptor in the Mouse Ovary

Expression of Bradykinin B2Receptor in the Mouse Ovary

The Kallikrein‐Kinin System as a Regulator of Cardiovascular and Renal Function

Purification of two species of exudate cysteine‐proteinase inhibitors that are acute‐phase reactants in the carrageenin‐induced inflammation in rats

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Product

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Expression of Bradykinin B₂Receptor in the Mouse Ovary

Expression of Bradykinin B₂Receptor in the Mouse Ovary