Intracellular Ca2+ contributes to K+-induced increase in renal kallikrein secretion

Fujita, Tomoe; Ogino, Michiko; Daigo, Futaba; Yamaguchi, Tomoko; Murakami, Masataka

doi:10.1016/j.intimp.2006.05.003

Cited by 3 publications

(4 citation statements)

References 32 publications

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“…It has been suggested that potassium-induced renal kallikrein secretion requires an extracellular Ca 2+ entry through Ca 2+ channels including L-type Ca 2+ channels, and Ca 2+ release from intracellular Ca 2+ stores through inositol trisphosphate (IP 3 ) and ryanodine receptors (Fujita et al, 2006). A high-potassium diet produces hypertrophy and hyperplasia of the kallikrein-producing cells (Vio and Figueroa, 1987), an effect that is linked to increases in both urinary kallikrein activity and renal kallikrein expression, and a significant reduction in blood pressure in the overload proteinuria model (Ardiles et al, 2006).…”

Section: Cellular Localizationmentioning

confidence: 99%

10 Kallikrein-Kinin Cascade: Bioregulation by Human Tissue Kallikrein 1 (hK1, KLK1)

Figueroa¹,

Faußner²,

Bhoola³

2012

Kallikrein-Related Peptidases

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Section: Cellular Localizationmentioning

confidence: 99%

10 Kallikrein-Kinin Cascade: Bioregulation by Human Tissue Kallikrein 1 (hK1, KLK1)

Figueroa¹,

Faußner²,

Bhoola³

2012

Kallikrein-Related Peptidases

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“…The percentage of KLK1-like activity inhibited by DX-2300 is plotted for each sample in Figure 3. KLK1 is present in urine because it is secreted from epithelial cells in the distal tubule of the kidney [13]. DX-2300 completely inhibited the observed KLK1-like activity in human and sheep urine.…”

Section: Dx-2300 Inhibits Klk1 Activity In Biological Samplesmentioning

confidence: 99%

“…To validate the use of DX-2300 for specific KLK1 inhibition, we measured the inhibition of KLK1-like activity in biological samples known to either contain, or be deficient in, active KLK1. KLK1 has been previously demonstrated to be responsible for the kallikrein-like activity observed in urine, saliva and asthmatic BAL fluid [13,14,22]. The percentage of KLK1-like activity inhibited by DX-2300 is plotted for each sample in Figure 3.…”

Section: Dx-2300 Inhibits Klk1 Activity In Biological Samplesmentioning

confidence: 99%

“…Plasma kallikrein is a serine protease with kininogenase activity, but it is not a member of the tissue kallikrein family. Plasma kallikrein is primarily expressed by the liver and circulates as a zymogen, known as prekallikrein [10], whereas KLK1 is secreted in response to various stimuli from cells such as neutrophils and macrophages as well as from tissues such as intestine, kidney, pancreas, salivary glands and tracheobronchial submucosal glands [11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Specific inhibition of tissue kallikrein 1 with a human monoclonal antibody reveals a potential role in airway diseases

Sexton¹,

Chen²,

Martik³

et al. 2009

Biochemical Journal

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KLK1 (tissue kallikrein 1) is a member of the tissue kallikrein family of serine proteases and is the primary kinin-generating enzyme in human airways. DX-2300 is a fully human antibody that inhibits KLK1 via a competitive inhibition mechanism (Ki=0.13 nM). No binding of DX-2300 to KLK1 was observed in a surface-plasmon-resonance biosensor assay when KLK1 was complexed to known active-site inhibitors, suggesting that DX-2300 recognizes the KLK1 active site. DX-2300 did not inhibit any of the 21 serine proteases that were each tested at a concentration of 1 microM. We validated the use of DX-2300 for specific KLK1 inhibition by measuring the inhibition of KLK1-like activity in human urine, saliva and bronchoalveolar lavage fluid, which are known to contain active KLK1. In human tracheobronchial epithelial cells grown at the air/liquid interface, DX-2300 blocked oxidative-stress-induced epidermal-growth-factor receptor activation and downstream mucus cell proliferation and hypersecretion, which have been previously shown to be mediated by KLK1. In an allergic sheep model of asthma, DX-2300 inhibited both allergen-induced late-phase bronchoconstriction and airway hyper-responsiveness to carbachol. These studies demonstrate that DX-2300 is a potent and specific inhibitor of KLK1 that is efficacious in in vitro and in vivo models of airway disease.

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A common polymorphism in the tissue kallikrein gene is associated with increased urinary excretions of calcium and sodium in Japanese volunteers

et al. 2013

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Tissue kallikrein is an enzyme involved in the release of kinin in peripheral tissues. It is believed to regulate hemodynamics and electrolyte transport in the kidney. The present study analyzed polymorphisms of tissue kallikrein in Japanese volunteers and examined the associations between allele H in the promoter region, which has been shown to have decreased promoter activity, and urinary kallikrein activity and physiological parameters in subjects on an ad libitum diet. Ninety and 73 volunteers were analyzed for the promoter and coding regions of the tissue kallikrein gene, respectively. The allelic frequency of allele H was found to be 24%. One synonymous and three non-synonymous polymorphisms were found in the coding regions. Urinary kallikrein activity was not significantly decreased in subjects with allele H compared to those without allele H, although they were low in two homozygotes of allele H. Urinary excretions of calcium and sodium were larger in the subjects with allele H than in those without. It is concluded that allele H is a common polymorphism in Japanese and may contribute to decreased reabsorptions of calcium and sodium in the kidney. Further interventional studies are needed to clarify the phenotype of allele H with respect to renal electrolyte handling.

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Intracellular Ca2+ contributes to K+-induced increase in renal kallikrein secretion

Cited by 3 publications

References 32 publications

10 Kallikrein-Kinin Cascade: Bioregulation by Human Tissue Kallikrein 1 (hK1, KLK1)

10 Kallikrein-Kinin Cascade: Bioregulation by Human Tissue Kallikrein 1 (hK1, KLK1)

Specific inhibition of tissue kallikrein 1 with a human monoclonal antibody reveals a potential role in airway diseases

A common polymorphism in the tissue kallikrein gene is associated with increased urinary excretions of calcium and sodium in Japanese volunteers

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