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1.
Biol Pharm Bull ; 46(7): 969-978, 2023.
Article in English | MEDLINE | ID: mdl-37394647

ABSTRACT

11ß-Hydroxysteroid dehydrogenase type 1 (11ß-HSD1) is the only enzyme that converts inactive glucocorticoids to active forms and plays an important role in the regulation of glucocorticoid action in target tissues. JTT-654 is a selective 11ß-HSD1 inhibitor and we investigated its pharmacological properties in cortisone-treated rats and non-obese type 2 diabetic Goto-Kakizaki (GK) rats because Asians, including Japanese, are more likely to have non-obese type 2 diabetics. Systemic cortisone treatment increased fasting plasma glucose and insulin levels and impaired insulin action on glucose disposal rate and hepatic glucose production assessed by hyperinsulinemic-euglycemic clamp, but all these effects were attenuated by JTT-654 administration. Cortisone treatment also reduced basal and insulin-stimulated glucose oxidation in adipose tissue, increased plasma glucose levels after administration of the pyruvate, the substrate of gluconeogenesis, and increased liver glycogen content. Administration of JTT-654 also inhibited all of these effects. Cortisone treatment decreased basal and insulin-stimulated 2-deoxy-D-[1-3H]-glucose uptake in 3T3-L1 adipocytes and increased the release of free fatty acids and glycerol, a gluconeogenic substrate, from 3T3-L1 adipocytes, and JTT-654 significantly attenuated these effects. In GK rats, JTT-654 treatment significantly reduced fasting plasma glucose and insulin levels, enhanced insulin-stimulated glucose oxidation in adipose tissue, and suppressed hepatic gluconeogenesis as assessed by pyruvate administration. These results demonstrated that glucocorticoid was involved in the pathology of diabetes in GK rats, as in cortisone-treated rats, and that JTT-654 ameliorated the diabetic conditions. Our results suggest that JTT-654 ameliorates insulin resistance and non-obese type 2 diabetes by inhibiting adipose tissue and liver 11ß-HSD1.


Subject(s)
Cortisone , Diabetes Mellitus, Type 2 , Insulin Resistance , Rats , Animals , Glucocorticoids/therapeutic use , 11-beta-Hydroxysteroid Dehydrogenase Type 1 , Cortisone/therapeutic use , Cortisone/pharmacology , Blood Glucose , Diabetes Mellitus, Type 2/drug therapy , Obesity/pathology , Insulin , Glucose
2.
Clin Exp Pharmacol Physiol ; 48(3): 381-388, 2021 03.
Article in English | MEDLINE | ID: mdl-33068442

ABSTRACT

G protein-coupled receptor 119 (GPR119) expression in pancreatic ß-cells and intestinal L-cells is a potential therapeutic target for the treatment of type 2 diabetes. Previously, we have reported that the GPR119 agonist JTP-109192 improves glucose metabolism with single and repeated administration. Conversely, overexpression of the Gpr119 gene reportedly regulates cholesterol transporter expression in animal models, and a natural GPR119 agonist, oleoylethanolamide (OEA), improves atherosclerosis. Therefore, improving dyslipidaemia is considered a possible feature of GPR119 agonists. In the present study, the lipid-lowering effect of JTP-109192 was examined in BALB/c background spontaneously hyperlipidaemic (SHL) mice with repeated administration, once daily for 12 weeks. On repeated administration, JTP-109192 revealed a cholesterol-lowering effect and improved atherosclerosis following histopathological examination. With further investigation, the cholesterol-lowering effect and subsequent antiatherosclerotic effect of JTP-109192 was attributed to changes in intestinal cholesterol metabolism gene expression. Based on these results, JTP-109192 represents a new potential antihypercholesterolaemic agent for the treatment of dyslipidaemia.


Subject(s)
Diabetes Mellitus, Type 2 , Hypercholesterolemia , Animals , Hypoglycemic Agents , Insulin Secretion , Insulin-Secreting Cells , Mice , Receptors, G-Protein-Coupled
3.
Elife ; 82019 09 23.
Article in English | MEDLINE | ID: mdl-31545169

ABSTRACT

In overloaded and regenerating muscle, the generation of new myonuclei depends on muscle satellite cells (MuSCs). Because MuSC behaviors in these two environments have not been considered separately, MuSC behaviors in overloaded muscle remain unexamined. Here, we show that most MuSCs in overloaded muscle, unlike MuSCs in regenerating muscle, proliferate in the absence of MyoD expression. Mechanistically, MuSCs in overloaded muscle sustain the expression of Heyl, a Notch effector gene, to suppress MyoD expression, which allows effective MuSC proliferation on myofibers and beneath the basal lamina. Although Heyl-knockout mice show no impairment in an injury model, in a hypertrophy model, their muscles harbor fewer new MuSC-derived myonuclei due to increased MyoD expression and diminished proliferation, which ultimately causes blunted hypertrophy. Our results show that sustained HeyL expression is critical for MuSC proliferation specifically in overloaded muscle, and thus indicate that the MuSC-proliferation mechanism differs in overloaded and regenerating muscle.


Subject(s)
Basic Helix-Loop-Helix Transcription Factors/biosynthesis , Cell Proliferation , Gene Expression Regulation , Hypertrophy , Muscles/physiology , Regeneration , Satellite Cells, Skeletal Muscle/metabolism , Animals , Basic Helix-Loop-Helix Transcription Factors/deficiency , Mice , Mice, Knockout , Muscles/cytology , MyoD Protein/metabolism
4.
Clin Exp Pharmacol Physiol ; 46(10): 910-919, 2019 10.
Article in English | MEDLINE | ID: mdl-31380572

ABSTRACT

G-protein coupled receptor 119 (GPR119) expression in pancreatic ß-cells and intestinal L cells is a potential therapeutic target for treating type 2 diabetes. A natural GPR119 agonist oleoylethanolamide is well known to enhance a glucose-stimulated insulin secretion (GSIS) and glucagon-like peptide-1 (GLP-1) secretion by elevating intracellular cAMP levels. In the present study, a glucose lowering effect of the GPR119 agonist, JTP-109192 leading to improvement of insulin sensitivity was examined in Zucker Fatty (ZF) rats. We investigated the in vitro effects of JTP-109192 on GSIS in the rat pancreatic ß-cell line (INS1E) cells and on GLP-1 secretion in the murine enteroendocrine cell line (GLUTag) cells. We also investigated the effect of JTP-109192 on GSIS in Sprague-Dawley (SD) rats with single administration and its effect on glucose metabolism in ZF rats with repeated administration once daily for about 6 weeks. After repeated administration, the hyperinsulinaemic euglycaemic glucose clamp test was performed to evaluate insulin sensitivity. JTP-109192 increased intracellular cAMP levels (EC50 value: 3.6 nmol/L) and enhanced GSIS in the INS1E cells and GLP-1 secretion in GLUTag cells. In SD rats, a single administration of JTP-109192 enhanced GSIS at high blood glucose levels. The repeated administrations in ZF rats improved glucose metabolism without lack of drug efficacy (tachyphylaxis) and increased glucose infusion rates due to improvement of insulin sensitivity.


Subject(s)
Receptors, G-Protein-Coupled/agonists , Animals , Dose-Response Relationship, Drug , Glucose/metabolism , HEK293 Cells , Humans , Insulin Secretion/drug effects , Mice , Rats , Rats, Zucker , Time Factors
5.
Bioorg Med Chem Lett ; 29(16): 2100-2106, 2019 08 15.
Article in English | MEDLINE | ID: mdl-31288965

ABSTRACT

We describe here a novel GPR119 agonist 24, which showed a potent and long-acting hypoglycemic effect in rats via oral dosing. For the discovery of 24, we chose compound 5, which possessed an oxadiazole linker, as a lead compound among our spirocyclic cyclohexane GPR119 agonist series, taking into account its lower plasma protein binding nature. 3,5-Difluoro and 4-methylsulfonylmethy groups on the left side phenyl group, and a gem-difluoro group on the right side of 24 are important for its agonist potency and metabolic stability, respectively.


Subject(s)
Cyclohexanes/pharmacology , Hypoglycemic Agents/pharmacology , Oxadiazoles/pharmacology , Receptors, G-Protein-Coupled/agonists , Spiro Compounds/pharmacology , Animals , Cyclohexanes/chemical synthesis , Cyclohexanes/pharmacokinetics , Drug Stability , Humans , Hypoglycemic Agents/chemical synthesis , Hypoglycemic Agents/pharmacokinetics , Microsomes, Liver/metabolism , Molecular Structure , Oxadiazoles/chemical synthesis , Oxadiazoles/pharmacokinetics , Rats, Sprague-Dawley , Spiro Compounds/chemical synthesis , Spiro Compounds/pharmacokinetics , Structure-Activity Relationship
6.
Bioorg Med Chem Lett ; 29(3): 373-379, 2019 02 01.
Article in English | MEDLINE | ID: mdl-30587450

ABSTRACT

We describe here the generation of a lead compound and its optimization studies that led to the identification of a novel GPR119 agonist. Based on a spirocyclic cyclohexane structure reported in our previous work, we identified compound 8 as a lead compound, being guided by ligand-lipophilicity efficiency (LLE), which linked potency and lipophilicity. Subsequent optimization studies of 8 for improvement of solubility afforded representative 21. Compound 21 had no inhibitory activity against six CYP isoforms and showed favorable pharmacokinetic properties and hypoglycemic activity in rats.


Subject(s)
Cyclohexanes/pharmacology , Cytochrome P-450 Enzyme Inhibitors/pharmacology , Hypoglycemic Agents/pharmacology , Receptors, G-Protein-Coupled/agonists , Spiro Compounds/pharmacology , Animals , Cyclohexanes/chemical synthesis , Cyclohexanes/chemistry , Cytochrome P-450 Enzyme Inhibitors/chemical synthesis , Cytochrome P-450 Enzyme Inhibitors/chemistry , Cytochrome P-450 Enzyme System/metabolism , Dose-Response Relationship, Drug , Humans , Hypoglycemic Agents/chemical synthesis , Hypoglycemic Agents/chemistry , Ligands , Microsomes, Liver/chemistry , Microsomes, Liver/metabolism , Molecular Structure , Rats , Rats, Sprague-Dawley , Receptors, G-Protein-Coupled/metabolism , Spiro Compounds/chemical synthesis , Spiro Compounds/chemistry , Structure-Activity Relationship
7.
Bioorg Med Chem Lett ; 28(7): 1228-1233, 2018 04 15.
Article in English | MEDLINE | ID: mdl-29519733

ABSTRACT

Exploration of alternative structures of the substituted piperidine or piperazine ring which are characteristic in most of the reported GPR119 agonists provided novel spirocyclic cyclohexane derivatives. The representative 17 with a high three-dimensionality exhibited potent agonistic activity (EC50 = 4 nM) with no CYP inhibitory activity (IC50 >10 µM). Compound 17 also displayed hypoglycemic activity with insulin secretion dependent on glucose concentration in an intraperitoneal glucose tolerance test in rats.


Subject(s)
Cyclohexanes/pharmacology , Drug Design , Hypoglycemic Agents/pharmacology , Receptors, G-Protein-Coupled/agonists , Spiro Compounds/pharmacology , Animals , Cyclohexanes/chemical synthesis , Cyclohexanes/chemistry , Dose-Response Relationship, Drug , Glucose/administration & dosage , Glucose/analysis , Glucose Tolerance Test , Humans , Hypoglycemic Agents/chemical synthesis , Hypoglycemic Agents/chemistry , Injections, Intraperitoneal , Insulin/metabolism , Molecular Structure , Rats , Rats, Sprague-Dawley , Receptors, G-Protein-Coupled/metabolism , Spiro Compounds/chemical synthesis , Spiro Compounds/chemistry , Structure-Activity Relationship
8.
PLoS One ; 12(5): e0177516, 2017.
Article in English | MEDLINE | ID: mdl-28498863

ABSTRACT

Myogenic stem cells are a promising avenue for the treatment of muscular disorders. Freshly isolated muscle stem cells have a remarkable engraftment ability in vivo, but their cell number is limited. Current conventional culture conditions do not allow muscle stem cells to expand in vitro with their bona fide engraftment efficiency, requiring the improvement of culture procedures for achieving successful cell-therapy for muscle disorders. Here we expanded mouse muscle stem cells and human myoblasts with Notch ligands, DLL1, DLL4, and JAG1 to activate Notch signaling in vitro and to investigate whether these cells could retain their engraftment efficiency. Notch signaling promotes the expansion of Pax7+MyoD- mouse muscle stem-like cells and inhibits differentiation even after passage in vitro. Treatment with Notch ligands induced the Notch target genes and generated PAX7+MYOD- stem-like cells from human myoblasts previously cultured on conventional culture plates. However, cells treated with Notch ligands exhibit a stem cell-like state in culture, yet their regenerative ability was less than that of freshly isolated cells in vivo and was comparable to that of the control. These unexpected findings suggest that artificial maintenance of Notch signaling alone is insufficient for improving regenerative capacity of mouse and human donor-muscle cells and suggest that combinatorial events are critical to achieve muscle stem cell and myoblast engraftment potential.


Subject(s)
Muscle Cells/cytology , Receptors, Notch/metabolism , Stem Cells/cytology , Stem Cells/metabolism , Animals , Calcium-Binding Proteins , Cell Differentiation/genetics , Cell Differentiation/physiology , Cells, Cultured , Immunohistochemistry , Intercellular Signaling Peptides and Proteins/genetics , Intercellular Signaling Peptides and Proteins/metabolism , Intracellular Signaling Peptides and Proteins/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Jagged-1 Protein/genetics , Jagged-1 Protein/metabolism , Membrane Proteins/genetics , Membrane Proteins/metabolism , Mice , Muscle Development/genetics , Muscle Development/physiology , MyoD Protein/genetics , MyoD Protein/metabolism , Myoblasts/cytology , Myoblasts/metabolism , PAX7 Transcription Factor/genetics , PAX7 Transcription Factor/metabolism , Real-Time Polymerase Chain Reaction , Receptors, Notch/genetics , Regeneration/genetics , Regeneration/physiology , Signal Transduction/genetics , Signal Transduction/physiology
9.
PLoS One ; 10(9): e0138517, 2015.
Article in English | MEDLINE | ID: mdl-26418810

ABSTRACT

Nrf2 is a master regulator of oxidative stresses through the induction of anti-oxidative genes. Nrf2 plays roles in maintaining murine hematopoietic stem cells and fly intestinal stem cells. The canonical Notch signaling pathway is also crucial for maintaining several types of adult stem cells including muscle stem cells (satellite cells). Here, we show that Dll1 induced Nrf2 expression in myogenic cells. In addition, primary targets of Notch signaling, Hesr1 and Hesr3, were involved in the up-regulation of Nrf2 mRNA and expression of its target genes. In vitro, Nrf2 had anti-myogenic and anti-proliferative effects on primary myoblasts. In vivo, although Nrf2-knockout mice showed decreased expression of its target genes in muscle stem cells, adult muscle stem cells of Nrf2-knockout mice did not exhibit the phenotype. Taken together, in muscle stem cells, the Notch-Hesr-Nrf2 axis is a pathway potentially inducing anti-oxidative genes, but muscle stem cells either do not require Nrf2-mediated anti-oxidative gene expression or they have a complementary system compensating for the loss of Nrf2.


Subject(s)
Basic Helix-Loop-Helix Transcription Factors/genetics , Cell Cycle Proteins/genetics , NF-E2-Related Factor 2/genetics , Receptors, Notch/metabolism , Satellite Cells, Skeletal Muscle/cytology , Adult Stem Cells/cytology , Animals , Antioxidants/metabolism , Basic Helix-Loop-Helix Transcription Factors/metabolism , CHO Cells , Calcium-Binding Proteins , Cell Cycle Proteins/metabolism , Cell Differentiation/genetics , Cell Line , Cricetulus , Intercellular Signaling Peptides and Proteins/metabolism , Mice , Mice, Knockout , Muscle Cells/cytology , Muscle Cells/metabolism , Muscle Development/genetics , NF-E2-Related Factor 2/metabolism , Satellite Cells, Skeletal Muscle/metabolism , Signal Transduction
10.
J Diabetes Res ; 2014: 680348, 2014.
Article in English | MEDLINE | ID: mdl-24987707

ABSTRACT

Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of leptin signaling as well as insulin signaling. JTT-551 is a new PTP1B inhibitor, which is reported to improve glucose metabolism by enhancement of insulin signaling. We have evaluated an antiobesity effect of JTT-551 using diet-induced obesity (DIO) mice. A single administration of JTT-551 was provided to DIO mice with or without leptin, and DIO mice were given food containing JTT-551 for six weeks. A single administration of JTT-551 with leptin treatment enhanced the food inhibition and the signal transducer and activator of transcription 3 (STAT3) phosphorylation in hypothalamus. Moreover, chronic administration of JTT-551 showed an antiobesity effect and an improvement of glucose and lipid metabolism in DIO mice. JTT-551 shows an antiobesity effect possibly by enhancement of leptin signaling and could be useful in the treatment of type 2 diabetes and obesity.


Subject(s)
Glycine/analogs & derivatives , Obesity/drug therapy , Protein Tyrosine Phosphatase, Non-Receptor Type 1/antagonists & inhibitors , Thiazoles/pharmacology , Animals , Blood Glucose/analysis , Body Weight , Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Type 2/blood , Diabetes Mellitus, Type 2/drug therapy , Glucose/metabolism , Glycine/pharmacology , Hypothalamus/metabolism , Leptin/metabolism , Lipid Metabolism , Male , Mice , Mice, Inbred C57BL , Mice, Obese , Obesity/therapy , Protein Tyrosine Phosphatases/pharmacology , STAT3 Transcription Factor/metabolism , Signal Transduction
11.
Exp Diabetes Res ; 2009: 715057, 2009.
Article in English | MEDLINE | ID: mdl-19696902

ABSTRACT

Spontaneously Diabetic Torii-fa/fa (SDT fatty) rat is a new model of obese type 2 diabetes. SDT fatty rat exhibits obesity associated with hyperphagia. In this study, SDT fatty rats were subjected to pair-feeding with SDT-+/+ (SDT) rats from 6 to 22 weeks of age. The ratio of visceral fat weight to subcutaneous fat weight (V/S) decreased at 12 weeks of age in the pair-feeding rats. The intraperitoneal fat weight such as epididymal and retroperitoneal fat weight decreased, whereas mesenteric fat weight had no change. Cell size of the epididymal fat in the pair-feeding rats tended to decrease. Glucose oxidation level in epididymal fat in the pair-feeding rats at 12 weeks of age was recovered to a similar level with that in SDT rats. These results indicated that SDT fatty rat is a useful model to evaluate the functional or the morphological features in adipose tissue and develop a novel drug for antiobesity.


Subject(s)
Adipose Tissue/pathology , Caloric Restriction , Diabetes Mellitus, Type 2/diet therapy , Obesity/diet therapy , Acetyltransferases/genetics , Adipocytes/pathology , Adipose Tissue/metabolism , Animals , Base Sequence , Cell Size , DNA Primers/genetics , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/pathology , Disease Models, Animal , Glucose/metabolism , Glucose Transporter Type 4/genetics , Lipoprotein Lipase/genetics , Male , Obesity/genetics , Obesity/metabolism , Obesity/pathology , Oxidation-Reduction , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats , Rats, Mutant Strains , Rats, Zucker , Tumor Necrosis Factor-alpha/genetics
12.
Exp Anim ; 58(4): 363-74, 2009 Jul.
Article in English | MEDLINE | ID: mdl-19654434

ABSTRACT

The Spontaneously Diabetic Torii (SDT) rat is a new model for non-obese type 2 diabetes. In the present study, we investigated changes in insulin secretion from the pancreas of male SDT rats aged 8, 16, and 24 weeks in order to analyze pancreatic function. An analysis of glucose-stimulated insulin secretion (GSIS) in isolated islets showed a marked reduction in insulin secretion in pre-diabetic 16-week-old SDT rats. When the islets were treated with tolbutamide or glucagon-like peptide-1 (7-36) amide (tGLP-1) in the presence of 11.2 mM glucose, however, insulin levels were restored to levels of normal rats. In vivo study, SDT rats exhibited a marked reduction in GSIS from 16 weeks of age. However, tolbutamide or JTP-76209, which is a novel dipeptidyl peptidase IV (DPP IV) inhibitor, increased insulin release after glucose loading and improved glucose tolerance. A marked reduction in GSIS was observed in pre-diabetic SDT rats and the reduction was improved by tolbutamide, tGLP-1, and the DPP IV inhibitor. Therefore, we concluded that the SDT rat is useful, as a model of non-obese insulin secretory disorder, for the analysis of the onset of type 2 diabetes and the development of antidiabetic agents.


Subject(s)
Diabetes Mellitus, Type 2/metabolism , Disease Models, Animal , Insulin/metabolism , Obesity/metabolism , Pancreas/metabolism , Animals , Arginine , Benzoates/pharmacology , Body Weight/drug effects , Diabetes Mellitus, Type 2/genetics , Diabetes Mellitus, Type 2/pathology , Dipeptidyl-Peptidase IV Inhibitors , Enzyme Inhibitors/pharmacology , Glucagon/metabolism , Glucagon-Like Peptide 1/pharmacology , Glucose Tolerance Test , Hypoglycemic Agents/pharmacology , Insulin Secretion , Islets of Langerhans/drug effects , Islets of Langerhans/metabolism , Male , Obesity/genetics , Organ Culture Techniques , Pancreas/drug effects , Peptide Fragments/pharmacology , Rats , Rats, Sprague-Dawley , Tolbutamide/pharmacology
13.
J Vet Med Sci ; 70(11): 1239-45, 2008 Nov.
Article in English | MEDLINE | ID: mdl-19057144

ABSTRACT

The Spontaneously Diabetic Torii (SDT) rat has recently been established as a new model of non-obese type 2 diabetes. In this study, we examined changes in hepatic glucose metabolism in prediabetic and diabetic SDT rats compared with age-matched control rats. The prediabetic state was confirmed at 16 weeks of age, and the diabetic state was confirmed at 24 and 32 weeks of age. Decreases in glucokinase mRNA levels and activity were observed in the prediabetic state. In this state, glycogen synthase activity and glycogen content were also decreased in the SDT rat. In addition to the above changes, glycogen phosphorylase mRNA and activity were decreased and gluconeogenetic enzyme mRNA levels were significantly increased in the diabetic state. These results indicate there is a great potential that abnormalities in hepatic glucose metabolism play a role in the progression to onset of diabetes. We suggest that the SDT rat is a valuable diabetic model for investigations into mechanisms or causes of progression to diabetes.


Subject(s)
Diabetes Mellitus, Type 1/genetics , Glucose Intolerance/metabolism , Liver/metabolism , Aging , Animals , Cholesterol/blood , DNA Primers , Diabetes Mellitus, Type 1/enzymology , Disease Progression , Glucokinase/genetics , Glucokinase/metabolism , Gluconeogenesis/genetics , Hypoglycemic Agents/therapeutic use , Insulin/therapeutic use , Liver/enzymology , Male , Prediabetic State/metabolism , RNA, Messenger/genetics , Rats , Rats, Inbred Strains , Triglycerides/blood
14.
J Immunol ; 171(10): 5507-13, 2003 Nov 15.
Article in English | MEDLINE | ID: mdl-14607957

ABSTRACT

We examined the severity of experimental colitis induced by dextran sulfate sodium (DSS) using immunologically manipulated mice. C57BL/6 mice showed more severe colitis than BALB/c mice, but mice of both strains recovered fully from the disease after the removal of DSS from their drinking water. The infiltrated cells at the lesions were mainly granulocytes in normal littermates. However, C.B-17 scid, IL-7Ralpha deficient, and TCR-Cbetadelta double-deficient mice showed severe colitis and did not recover from the disease even after the removal of DSS. It was found that the infiltrated cells at the lesions in the lethal strains were monocytes. Although both TCR-Cdelta(-/-) and TCR-Cbeta(-/-) mice showed severe colitis phenotypes, infiltration in the former is monocyte-dominant while that in the latter is granulocyte-dominant. Thus the type of cells that infiltrate at the lesions of DSS-induced experimental colitis may be controlled by functional T cell subsets. Immunohistological and RT-PCR analyses of the inflamed colon revealed that the murine homologue of human GROalpha released by some cells under the control of gammadeltaT cells is a possible candidate determining the severity of DSS-induced experimental colitis.


Subject(s)
Colitis/immunology , Colitis/pathology , Receptors, Antigen, T-Cell, gamma-delta/physiology , T-Lymphocyte Subsets/immunology , T-Lymphocyte Subsets/metabolism , Animals , Cell Division/genetics , Cell Division/immunology , Cell Movement/genetics , Cell Movement/immunology , Colitis/chemically induced , Colitis/genetics , Dextran Sulfate/administration & dosage , Female , Genes, T-Cell Receptor beta/genetics , Genes, T-Cell Receptor delta/genetics , Intestinal Mucosa/immunology , Intestinal Mucosa/metabolism , Intestinal Mucosa/pathology , Male , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Mice, Knockout , Mice, SCID , RNA, Messenger/biosynthesis , Receptors, Antigen, T-Cell, gamma-delta/biosynthesis , Receptors, Antigen, T-Cell, gamma-delta/deficiency , Receptors, Antigen, T-Cell, gamma-delta/genetics , Reverse Transcriptase Polymerase Chain Reaction
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