Yasuda K

References (7)

Title : Epicatechin gallate and epigallocatechin gallate are potent inhibitors of human arylacetamide deacetylase - Yasuda_2021_Drug.Metab.Pharmacokinet_39_100397
Author(s) : Yasuda K , Watanabe K , Fukami T , Nakashima S , Ikushiro SI , Nakajima M , Sakaki T
Ref : Drug Metab Pharmacokinet , 39 :100397 , 2021
Abstract : Recently, in addition to carboxylesterases (CESs), we found that arylacetamide deacetylase (AADAC) plays an important role in the metabolism of some clinical drugs. In this study, we screened for food-related natural compounds that could specifically inhibit human AADAC, CES1, or CES2. AADAC, CES1, and CES2 activities in human liver microsomes were measured using phenacetin, fenofibrate, and procaine as specific substrates, respectively. In total, 43 natural compounds were screened for their inhibitory effects on each of these enzymes. Curcumin and quercetin showed strong inhibitory effects against all three enzymes, whereas epicatechin, epicatechin gallate (ECg), and epigallocatechin gallate (EGCg) specifically inhibited AADAC. In particular, ECg and EGCg showed strong inhibitory effects on AADAC (IC(50) values: 3.0 +/- 0.5 and 2.2 +/- 0.2 microM, respectively). ECg and EGCg also strongly inhibited AADAC-mediated rifampicin hydrolase activity in human liver microsomes with IC(50) values of 2.2 +/- 1.4 and 1.7 +/- 0.4 microM, respectively, whereas it weakly inhibited p-nitrophenyl acetate hydrolase activity, which is catalyzed by AADAC, CES1, and CES2. Our results indicate that ECg and EGCg are potent inhibitors of AADAC.
ESTHER : Yasuda_2021_Drug.Metab.Pharmacokinet_39_100397
PubMedSearch : Yasuda_2021_Drug.Metab.Pharmacokinet_39_100397
PubMedID: 34171773

Title : Lung fibroblasts produce IL-33 in response to stimulation with retinoblastoma-binding protein 9 via production of prostaglandin E2 - Adachi_2020_Int.Immunol_32_637
Author(s) : Adachi T , Yasuda K , Muto T , Serada S , Yoshimoto T , Ishii KJ , Kuroda E , Araki K , Ohmuraya M , Naka T , Nakanishi K
Ref : Int Immunol , 32 :637 , 2020
Abstract : Intestinal nematode infection induces pulmonary eosinophilia via IL-33, although the mechanism of pulmonary IL-33 induction remains unclear. Because nematode migration damages lungs, we speculated that lung-derived damage-associated molecular patterns (DAMPs) possess an IL-33-inducing activity (IL33ia). Indeed, intra-nasal administration of a lung extract induced IL-33 production in lungs. Additionally, lung extracts increased Il33 mRNA expression in primary lung fibroblasts. Proteomic analysis identified retinoblastoma-binding protein 9 (RBBP9) as a major DAMP with IL33ia. RBBP9 was originally discovered as a protein that provides cells with resistance to the growth inhibitory effect of transforming growth factor (TGF)-beta1. Here, we found that stimulation by RBBP9 induced primary fibroblasts to produce prostaglandin E2 (PGE2) that, in turn, induced fibroblasts to produce IL-33. RBBP9-activated fibroblasts expressed mRNAs of cyclooxygenase-2 (COX-2) and PGE2 synthase-1 that convert arachidonic acid to PGE2. Furthermore, they expressed PGE2 receptors E-prostanoid (EP) 2 and EP4. Thus, treatment with a COX-2 inhibitor or EP2 and/or EP4 receptor antagonists inhibited RBBP9-induced IL-33 production. Nematode infection induced pulmonary Il33 mRNA expression, which was inhibited by the COX-2 inhibitor or EP2 and EP4 antagonists, suggesting that nematode infection induced pulmonary Il33 mRNA via PGE2. RBBP9 was expressed constitutively in the lung in the steady state, which did not increase after nematode infection. Finally, we found that Rbbp9-deficient mice had a significantly diminished capacity to increase pulmonary Il33 mRNA expression following nematode infection. Thus, the PGE2-EP2/EP4 pathway activated by RBBP9 released from damaged lungs is important for pulmonary IL-33 production in nematode-infected animals.
ESTHER : Adachi_2020_Int.Immunol_32_637
PubMedSearch : Adachi_2020_Int.Immunol_32_637
PubMedID: 32484881
Gene_locus related to this paper: human-RBBP9

Title : Efficacy and safety of teneligliptin in addition to insulin therapy in type 2 diabetes mellitus patients on hemodialysis evaluated by continuous glucose monitoring - Yajima_2016_Diabetes.Res.Clin.Pract_122_78
Author(s) : Yajima T , Yajima K , Hayashi M , Takahashi H , Yasuda K
Ref : Diabetes Res Clin Pract , 122 :78 , 2016
Abstract : AIMS: Appropriate glycemic control without hypoglycemia is important in patients with type 2 diabetes on hemodialysis. Teneligliptin, a novel dipeptidyl peptidase-4 inhibitor, can be used without dose adjustment for these patients. Using continuous glucose monitoring (CGM), we evaluated the efficacy and safety of adding teneligliptin to insulin therapy. METHODS: Twenty-one type 2 diabetes mellitus patients on hemodialysis treated with insulin were enrolled. After the adjustment of insulin dose, their blood glucose level was monitored by CGM. Insulin dose was reduced after teneligliptin administration. RESULTS: The median total daily insulin dose significantly reduced from 18 (9-24)U to 6 (0-14)U (p<0.0001). Maximum, mean, and standard deviation of blood glucose level on the hemodialysis and non-hemodialysis days did not change after teneligliptin administration. However, minimum blood glucose level was significantly elevated on the hemodialysis day after teneligliptin administration (from 3.9+/-1.0mmol/L to 4.4+/-0.9mmol/L, p=0.040). The incidence of asymptomatic hypoglycemia on the hemodialysis day detected by CGM significantly decreased from 38.1% to 19.0% (p=0.049). CONCLUSIONS: Teneligliptin may contribute toward reducing the total daily insulin dose and preventing hypoglycemic events on the hemodialysis day in type 2 diabetes mellitus patients.
ESTHER : Yajima_2016_Diabetes.Res.Clin.Pract_122_78
PubMedSearch : Yajima_2016_Diabetes.Res.Clin.Pract_122_78
PubMedID: 27810689

Title : Effects of ovarian hormone treatment on the gene expression of muscarinic acetylcholine receptors in the ovariectomized rat myometrium - Yasuda_2014_J.Steroid.Biochem.Mol.Biol_143C_81
Author(s) : Yasuda K , Sumi G , Kanamori C , Nakajima T , Tsuzuki T , Cho H , Nishigaki A , Okada H , Kanzaki H
Ref : J Steroid Biochem Mol Biol , 143C :81 , 2014
Abstract : We investigate the effects of ovarian hormone on the gene expression of muscarinic acetylcholine receptors (M1-M5) in the myometrium using real-time PCR and evaluate the relationships between their expression and that of ovarian hormone receptors (ERalpha, ERbeta, and PgR). Wistar rats were sham operated (SO) or ovariectomized (OVX) and treated with vehicle, estradiol (E2), progesterone (P4), or both E2 and P4 for 2 days beginning on postoperative day 33. M1 and M4 mRNA expressions were not detected in the myometrium. M2 mRNA expression did not change significantly in the OVX and OVX+P4 groups compared to the SO group, but increased significantly in the OVX+E2 group and was normalized in the OVX+E2P4 group. M3 mRNA expression increased significantly in the OVX and OVX+P4 groups compared to the SO group, but was normalized in the OVX+E2 and OVX+E2P4 groups. M5 mRNA expression did not change significantly in all experimental groups. ERalpha mRNA expression increased significantly in the OVX, OVX+E2, and OVX+P4 groups compared to the SO group, but was normalized in the OVX+E2P4 group. The changes in ERbeta mRNA expression were similar to those of M3 mRNA expression in all experimental groups. In contrast, the changes in PgR mRNA expression did not correspond with that of M2, M3, or M5 mRNA expression in any of the experimental groups. Additionally, we evaluated the relationship between the expression of muscarinic acetylcholine receptors and ovarian hormone receptors in estrus cycle. M2 mRNA expression increased significantly in diestus and metaestrus compared in proestrus and estrus. M3 mRNA expression increased significantly in only diestrus compared in the other stages. In contrast, M5 mRNA expression did not change in estrus cycle. The changes in ERalpha mRNA expression appeared to be similar to those of M2 in estrus cycle, but no significant difference was found. The changes in ERbeta mRNA expression were similar to those of M3 mRNA expression. The change in PgR mRNA expression increased significantly in diestrus compared in metaestrus, but did not correspond with that of M2, M3, or M5 mRNA expression in estrus cycle. When acetylcholine sensitivity in the myometrium was compared between diestrus and estrus, the sensitivity is significantly lower in estrus than in diestrus. These results suggest that ovarian hormones influence the expression of M2 and M3 in the myometrium by regulating the expression of hormone receptors. E2 may upregulate M2 via ERalpha, but P4 may downregulate M2 by inhibiting ERalpha via PgR. E2 may downregulate M3 by inhibiting ERbeta, but P4 may not regulate the expression of M3 and ERbeta. M5 may be a constitutive muscarinic receptor in the myometrium because neither E2 nor P4 influence the expression of M5. The combination of E2 and P4 may contribute the reproduction by quieting down the acetylcholine-induced myometrial contraction.
ESTHER : Yasuda_2014_J.Steroid.Biochem.Mol.Biol_143C_81
PubMedSearch : Yasuda_2014_J.Steroid.Biochem.Mol.Biol_143C_81
PubMedID: 24583025

Title : Glucose regulation of dipeptidyl peptidase IV gene expression is mediated by hepatocyte nuclear factor-1alpha in epithelial intestinal cells - Gu_2008_Clin.Exp.Pharmacol.Physiol_35_1433
Author(s) : Gu N , Tsuda M , Matsunaga T , Adachi T , Yasuda K , Ishihara A , Tsuda K
Ref : Clinical & Experimental Pharmacology & Physiology , 35 :1433 , 2008
Abstract : 1. Dipeptidyl peptidase IV (DPP-IV) is a new drug target in the treatment of Type 2 diabetes. Dipeptidyl peptidase IV enzyme activity is significantly altered in Type 2 diabetic patients with hyperglycaemia, but the underlying molecular mechanisms remain unclear. 2. The first aim of the present study was to clarify whether glucose regulates DPP-IV enzyme activity. To address this, DPP-IV gene expression and enzyme activity were measured in Caco2 cells cultured in the presence of low (2.5 mmol/L) or high (16.7 mmol/L) concentrations of glucose. We observed that high glucose inhibited DPP-IV gene expression and enzyme activity. 3. The second aim of the present study was to investigate whether hepatocyte nuclear factor (HNF)-1alpha contributes to glucose regulation of DPP-IV gene expression. To explore this question, associations between the gene expression of DPP-IV and HNF-1alpha were examined in Caco-2 cells cultured in the presence of low (2.5 mmol/L) or high (16.7 mmol/L) glucose. We found that the pattern of glucose-regulated DPP-IV gene expression is similar to that of HNF-1alpha. Moreover, to elucidate whether glucose regulation of DPP-IV gene expression is affected when HNF-1alpha is inhibited, we produced two stable cell lines in which a dominant-negative mutant HNF-1alphaR271G or basic vectors were stably expressed. We found that glucose regulation of DPP-IV gene expression was compromised in HNF-1alphaR271G cells, but was well maintained in basic vector cells. 4. These results suggest that glucose regulation of DPP-IV gene expression is mediated by HNF-1alpha.
ESTHER : Gu_2008_Clin.Exp.Pharmacol.Physiol_35_1433
PubMedSearch : Gu_2008_Clin.Exp.Pharmacol.Physiol_35_1433
PubMedID: 18671716

Title : Peg1\/Mest in obese adipose tissue is expressed from the paternal allele in an isoform-specific manner - Kamei_2007_FEBS.Lett_581_91
Author(s) : Kamei Y , Suganami T , Kohda T , Ishino F , Yasuda K , Miura S , Ezaki O , Ogawa Y
Ref : FEBS Letters , 581 :91 , 2007
Abstract : Paternally expressed 1 (Peg1)/mesoderm specific transcript (Mest) is an imprinted gene, which is only transcribed from the paternal (father's) allele. In some human cancer tissues, an alternatively spliced variant of PEG1/MEST mRNA using a different promoter of a distinct first exon is expressed from both paternal and maternal alleles. We previously reported that Peg1/Mest expression was markedly up-regulated in obese adipose tissue in mice. Moreover, transgenic overexpression of Peg1/Mest in the adipose tissue resulted in the enlargement of adipocytes in size. Given the potential pathophysiologic relevance in obesity, we examined the nature of increased expression of Peg1/Mest in obese adipose tissue. In obese adipose tissue, expression of Peg1/Mest was increased, but not that of other imprinted genes tested. The transcription rate of Peg1/Mest was increased in obese adipose tissue. We found at least four isoforms of mouse Peg1/Mest generated by use of the alternative first exons. We also demonstrated that the abundantly expressed Peg1/Mest in obese adipose tissue retained monoallelic expression. This is the first report of monoallelic induction of Peg1/Mest in adult tissues.
ESTHER : Kamei_2007_FEBS.Lett_581_91
PubMedSearch : Kamei_2007_FEBS.Lett_581_91
PubMedID: 17182038

Title : Presence of platelet-activating factor-acetylhydrolase in milk - Furukawa_1993_J.Lipid.Res_34_1603
Author(s) : Furukawa M , Narahara H , Yasuda K , Johnston JM
Ref : J Lipid Res , 34 :1603 , 1993
Abstract : Human milk contains numerous factors such as immunoglobulins, lactoferrin, lysozyme, macrophages, etc., which serve an immunoprotective role. Platelet-activating factor (PAF) is one of the most proinflammatory agents thus far described. PAF is metabolized to the biologically inactive lysoPAF by the enzyme PAF-acetylhydrolase (PAF-AH). In the present study we have demonstrated that PAF-AH activity is present in human milk. The activity was associated with aqueous phase and was not stimulated by the addition of bile salts or Ca2+. The activity of PAF-AH in human milk was not affected by the addition of propranolol or NaCl. PAF, and 1-acyl-2-acetyl-glycerophosphocholine were the only substrates cleaved by the enzyme. Based on these properties it is concluded that the milk PAF-AH is not the lipoprotein or bile salt-stimulated lipase known to be present in milk. Inhibitor studies revealed that the enzyme in human milk was the plasma type PAF-AH. The activity of PAF-AH was stable at pH 4.0 at 37 degrees C and the activity varied in milk samples obtained from various species. The enzyme was secreted by milk macrophages. The presence of PAF-AH in human milk may explain, in part, the beneficial effects of breast feeding in the prevention of necrotizing enterocolitis by inactivating the potent proinflammatory autacoid, PAF.
ESTHER : Furukawa_1993_J.Lipid.Res_34_1603
PubMedSearch : Furukawa_1993_J.Lipid.Res_34_1603
PubMedID: 8228643
Gene_locus related to this paper: human-PLA2G7