Prorenin processing and restricted endoproteolysis by mouse tissue kallikrein family enzymes (mK1, mK9, mK13, and mK22)

Kikkawa, Yamato; Yamanaka, Naoaki; Tada, J; Kanamori, Norio; Tsumura, Keiko; Hosoi, Kazuo

doi:10.1016/s0167-4838(97)00144-1

Cited by 29 publications

(14 citation statements)

References 39 publications

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“…Here the first 20 amino acid residues were identical to those of Klk-13, again except for two unidentified residues. These Klks are known to be heterodimeric molecules consisting of heavy and light chains, and the primary structures of heavy chains are highly homologous (28,29) as represented by the N-terminal sequences shown in Fig. 1D.…”

Section: Anti-salivary Autoantibodies In Iqi/jicmentioning

confidence: 99%

Autoimmunity against a Tissue Kallikrein in IQI/Jic Mice

Takada

Takiguchi

Konno

et al. 2005

Journal of Biological Chemistry

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We have recently characterized IQI/Jic mice as a model for Sjö gren's syndrome (SS), a chronic autoimmune disease in humans. In SS, local lymphocytic infiltrations into salivary and lacrimal glands frequently develop to the involvement of systemic exocrine and nonexocrine organs, and the mechanism for progression of this disease remains obscure. Herein, we report identification of an autoantigen shared by various target organs in IQI/Jic mice. Polypeptides identified based on immunorecognition by autoantibodies in sera from IQI/ Jic mice affected with autoimmune disease (>12 weeks of age) were tissue kallikrein (Klk)-1 and -13 and were cross-reactive to the autoantibodies. Interestingly, Klk-13, but not Klk-1, caused a proliferative response of splenic T cells from IQI/Jic mice from the age of 4 weeks onward. In addition, remarkably enhanced expression of Klk-13 was observed in the salivary glands of the mice in accordance with the development of inflammatory lesions. These results indicate that Klk-13 acts as an autoantigen and may increase T cells responsive to organs commonly expressing Klk-13, playing a pivotal role in the etiology of progression of disease in IQI/Jic mice. Our findings provide insights into the contributions of autoantigens shared by multiple organs in the progress of SS from an organ-specific to a systemic disorder.

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Section: Anti-salivary Autoantibodies In Iqi/jicmentioning

confidence: 99%

Autoimmunity against a Tissue Kallikrein in IQI/Jic Mice

Takada

Takiguchi

Konno

et al. 2005

Journal of Biological Chemistry

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“…It was reported previously that kallikrein mK13 specifically cleaves the peptide bond on the carboxyl side of the Arg at the Lys-Arg or Arg-Arg pair of mouse Ren2 pro-renin to yield mature renin (34,38). As a serine proteinase, the substrate specificity shown here appears to be unusual and has not been widely reported.…”

Section: Discussionmentioning

confidence: 60%

Tissue Kallikrein mK13 Is a Candidate Processing Enzyme for the Precursor of Interleukin-1β in the Submandibular Gland of Mice

Yao¹,

Karabasil²,

Purwanti³

et al. 2006

Journal of Biological Chemistry

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By using Western blot analysis, high levels of 17.5-and 20-kDa interleukin-1␤ (IL-1␤) proteins were detected in the submandibular gland (SMG) of mice. Despite this fact, the amount of pro-IL-1␤ protein, a precursor of IL-1␤, with a molecular size of 35 kDa in this tissue was below the detectable level, although strong expression of pro-IL-1␤ mRNA was observed. A large amount of 17.5-kDa IL-1␤ also appeared in the saliva of mice injected with lipopolysaccharide, suggesting that this IL-1␤ is a secretory form produced by the SMG. The protein for IL-1␤-converting enzyme, a processing enzyme for pro-IL-1␤, was expressed only at a low level in the SMG as compared with its level in various epithelial tissues or lipopolysaccharide-stimulated macrophages. On the other hand, mK1, mK9, mK13, and mK22, members of the kallikrein family, were detected strongly in the SMGbutnotinothertissues.ByincubationwithmK13,butnotwithmK1, mK9, or mK22, the 35-kDa pro-IL-1␤ was cleaved into two major products with molecular masses of 17.5 and 22 kDa, and production was inhibited by phenylmethylsulfonyl fluoride, a serine protease inhibitor, but not byIL-1␤-converting enzyme inhibitors. A peptide segment corresponding to amino acid residues 107-121 of mouse pro-IL-1␤ (

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“…However, tissue kallikrein has been reported as prorenin converting enzyme at pH 8.2. Also, mouse tissue kallikrein mk1, mk9, mk13 and mk22 were shown to be prorenin activator in addition to human tissue kallikrein hk1 21 . Recent studies indicate that the enzyme prolylcarboxypeptidase which is an angiotensin II inactivating enzyme is also a prekallikrein activator.…”

Section: Involvement Of the Kinin System In The Regulation Of Renin Smentioning

confidence: 96%

The Kinin System: Present and Future Pharmacological Targets

Sharma¹

2011

Am. J. Biomed. Sci.

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Kallikrein kinin system (KKS) is a complex system produced in various organs. This system includes kininogen (precursor for kinin), kallikreins and the pharmacologically active bradykinin (BK) which is considered either proinflammatory or cardioprotective. It's a proinflammatory polypeptide that is involved in many pathological conditions and can cause pain, inflammation, increased vascular permeability, vasodilation, contraction of various smooth muscle as well as cell proliferation. On the other hand, it has been shown that BK has cardioprotective effects as all components of KKS are located in the cardiac muscles. Numerous observations obtained show that decreased activity of this system may lead to cardiovascular diseases such as hypertension, cardiac failure and myocardial infarction. BK acts on two receptors, B 1 and B 2 receptors which are linked physiologically through their natural stimuli and their common participation in a variety of inflammatory responses. Recently, numerous BK antagonists have been developed in order to treat several diseases which are due to excessive BK formation. Although BK has many beneficial effects, some undesirable effects have been recognized that can be reversed with BK antagonists. In addition, products of this system have multiple interactions with other important metabolic pathways such as the renin-angiotensin system.

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Prorenin processing and restricted endoproteolysis by mouse tissue kallikrein family enzymes (mK1, mK9, mK13, and mK22)

Cited by 29 publications

References 39 publications

Autoimmunity against a Tissue Kallikrein in IQI/Jic Mice

Autoimmunity against a Tissue Kallikrein in IQI/Jic Mice

Tissue Kallikrein mK13 Is a Candidate Processing Enzyme for the Precursor of Interleukin-1β in the Submandibular Gland of Mice

The Kinin System: Present and Future Pharmacological Targets

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