scholarly journals Tryptophan Pathway Abnormalities in a Murine Model of Hereditary Glaucoma

2021 ◽  
Vol 22 (3) ◽  
pp. 1039
Author(s):  
Michal Fiedorowicz ◽  
Tomasz Choragiewicz ◽  
Waldemar A. Turski ◽  
Tomasz Kocki ◽  
Dominika Nowakowska ◽  
...  
Keyword(s):  
Mouse Model ◽  
Murine Model ◽  
Kynurenic Acid ◽  
Pathogenetic Mechanism ◽  
Retinal Tissue ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Pathway ◽  
K Concentration ◽  
And Control

Background: It has been shown that a possible pathogenetic mechanism of neurodegeneration in the mouse model of glaucoma (DBA/2J) may be an alteration of kynurenic acid (KYNA) in the retina. This study aimed to verify the hypothesis that alterations of tryptophan (TRP) metabolism in DBA/2J mice is not limited to the retina. Methods: Samples of the retinal tissue and serum were collected from DBA/2J mice (6 and 10 months old) and control C57Bl/6 mice of the same age. The concentration of TRP, KYNA, kynurenine (KYN), and 3-hydroxykynurenine (3OH-K) was measured by HPLC. The activity of indoleamine 2,3-dioxygenase (IDO) was also determined as a KYN/TRP ratio. Results: TRP, KYNA, L-KYN, and 3OH-K concentration were significantly lower in the retinas of DBA/2J mice than in C57Bl/6 mice. 3OH-K concentration was higher in older mice in both strains. Serum TRP, L-KYN, and KYNA concentrations were lower in DBA/2J than in age-matched controls. However, serum IDO activity did not differ significantly between compared groups and strains. Conclusions: Alterations of the TRP pathway seem not to be limited to the retina in the murine model of hereditary glaucoma.

Effects of carbamylcholine on chick embryo aggregate retina cell cultures

1988 ◽  
Vol 46 ◽  
pp. 350-351
Author(s):  
Glenn M. Cohen ◽  
Radharaman Ray
Keyword(s):  
Cell Cultures ◽  
Single Cells ◽  
Retinal Cell ◽  
Cell Aggregates ◽  
High Concentration ◽  
In Ovo ◽  
Sterile Culture ◽  
Retinal Tissue ◽  
Synaptic Junctions ◽  
And Control

Retinal,cell aggregates develop in culture in a pattern similar to the in ovo retina, forming neurites first and then synapses. In the present study, we continuously exposed chick retinal cell aggregates to a high concentration (1 mM) of carbamylcholine (carbachol), an acetylcholine (ACh) analog that resists hydrolysis by acetylcholinesterase (AChE). This situation is similar to organophosphorus anticholinesterase poisoning in which the ACh level is elevated at synaptic junctions due to inhibition of AChE, Our objective was to determine whether continuous carbachol exposure either damaged cholino- ceptive neurites, cell bodies, and synaptic elements of the aggregates or influenced (hastened or retarded) their development.The retinal tissue was isolated aseptically from 11 day embryonic White Leghorn chicks and then enzymatically (trypsin) and mechanically (trituration) dissociated into single cells. After washing the cells by repeated suspension and low (about 200 x G) centrifugation twice, aggregate cell cultures (about l0 cells/culture) were initiated in 1.5 ml medium (BME, GIBCO) in 35 mm sterile culture dishes and maintained as experimental (containing 10-3 M carbachol) and control specimens.

Indoleamine 2,3-dioxygenase–dependent tryptophan metabolites contribute to tolerance induction during allergen immunotherapy in a mouse model

2008 ◽  
Vol 121 (4) ◽  
pp. 983-991.e2 ◽  
Author(s):  
Yousef A. Taher ◽  
Benoit J.A. Piavaux ◽  
Reneé Gras ◽  
Betty C.A.M. van Esch ◽  
Gerard A. Hofman ◽  
...  
Keyword(s):  
Mouse Model ◽  
Allergen Immunotherapy ◽  
Tolerance Induction ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Metabolites

Relationship between Serum Tryptophan and Tryptophan Metabolite Levels after Tryptophan Ingestion in Normal Subjects and Age-Related Cataract Patients

1995 ◽  
Vol 89 (6) ◽  
pp. 591-599 ◽  
Author(s):  
Roger J. W. Truscott ◽  
Anthony J. Elderfield
Keyword(s):  
Anthranilic Acid ◽  
Kynurenic Acid ◽  
Normal Subjects ◽  
Serum Levels ◽  
Xanthurenic Acid ◽  
Control Subjects ◽  
Age Related ◽  
Hydroxyanthranilic Acid ◽  
And Control ◽  
Cataract Patients

1. Cataract is the single major cause of blindness worldwide; however, the reasons for the development of this condition remain unknown. It has been suggested that the essential amino acid tryptophan may be implicated in the aetiology but definitive evidence has been lacking. 2. The serum levels of tryptophan and seven of its metabolites have been measured in both cataract patients and control subjects, after administration of tryptophan, in order to determine the typical response profile and to discover whether differences could be found in tryptophan metabolism in the two groups. 3. Tryptophan, kynurenine, kynurenic acid, xanthurenic acid, 3-hydroxyanthranilic acid, 5-hydroxyanthranilic acid, 5-hydroxytryptophan and anthranilic acid were measured by HPLC with dual electrochemical and programmable wavelength fluorescence detection. Fasting cataract patients (n = 42) and control subjects (n = 37) were given an oral dose of l-tryptophan and sera were sampled at 0, 1, 2, 4 and 6 h. 4. Statistically significant differences in the distribution of data between the two groups were observed. The responses of kynurenine and 5-hydroxyanthranilic acid were higher in cataract patients, but those of kynurenic acid and total tryptophan were lower than in control subjects. No statistically significant differences in free tryptophan, anthranilic acid, 3-hydroxyanthranilic acid, xanthurenic acid or 5-hydroxytryptophan levels were noted. 5. We conclude that there is a major subgroup of age-related cataract patients with a dysfunction in the metabolism of tryptophan. This may be related to the onset of cataract. The mechanism remains to be established but may operate via the action of tryptophan metabolites, such as 5-hydroxyanthranilic acid, which become reactive towards protein upon oxidation.

scholarly journals A novel mouse model of creatine transporter deficiency

F1000Research ◽  
2015 ◽  
Vol 3 ◽  
pp. 228
Author(s):  
Laura Baroncelli ◽  
Maria Grazia Alessandrì ◽  
Jonida Tola ◽  
Elena Putignano ◽  
Martina Migliore ◽  
...  
Keyword(s):  
Mouse Model ◽  
Murine Model ◽  
Deficiency Syndrome ◽  
Speech Impairment ◽  
Behavioral Disturbances ◽  
Creatine Transporter ◽  
Creatine Transporter Deficiency ◽  
Creatine Deficiency ◽  
Creatine Deficiency Syndrome ◽  
Transporter Deficiency

Mutations in the creatine (Cr) transporter (CrT) gene lead to cerebral creatine deficiency syndrome-1 (CCDS1), an X-linked metabolic disorder characterized by cerebral Cr deficiency causing intellectual disability, seizures, movement  and behavioral disturbances, language and speech impairment ( OMIM #300352).CCDS1 is still an untreatable pathology that can be very invalidating for patients and caregivers. Only two murine models of CCDS1, one of which is an ubiquitous knockout mouse, are currently available to study the possible mechanisms underlying the pathologic phenotype of CCDS1 and to develop therapeutic strategies. Given the importance of validating phenotypes and efficacy of promising treatments in more than one mouse model we have generated a new murine model of CCDS1 obtained by ubiquitous deletion of 5-7 exons in the Slc6a8 gene. We showed a remarkable Cr depletion in the murine brain tissues and cognitive defects, thus resembling the key features of human CCDS1. These results confirm that CCDS1 can be well modeled in mice. This CrT−/y murine model will provide a new tool for increasing the relevance of preclinical studies to the human disease.

scholarly journals 023 Global knockout of immunomodulatory indoleamine 2,3-dioxygenase has no effect on psoriasiform lesions in the imiquimod-induced mouse model of psoriasis

2019 ◽  
Vol 139 (5) ◽  
pp. S4
Author(s):  
V. Choudhary ◽  
E. Ajebo ◽  
R. Uaratanawong ◽  
S. Chowdhury ◽  
S. Hossack ◽  
...  
Keyword(s):  
Mouse Model ◽  
Indoleamine 2,3 Dioxygenase

Differential tissue expression of erythroblast macrophage protein in a MRL/lpr mouse model of lupus

Lupus ◽  
2019 ◽  
Vol 28 (7) ◽  
pp. 843-853
Author(s):  
H Fan ◽  
N Li ◽  
P Fan ◽  
X Hu ◽  
K Liang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Model ◽  
Mrna Expression ◽  
Lupus Erythematosus ◽  
Tissue Expression ◽  
Expression Rate ◽  
Macrophage Protein ◽  
And Control ◽  
Liver Tissues ◽  
Brain Tissues

Objective The objective of this study was to observe the expression features of erythroblast macrophage protein (EMP) between the tissues of MRL/lpr mice, a mouse model of systemic lupus erythematosus (SLE), and control mice. Methods We examined the serum ANA in both mice groups through indirect immunofluorescence (IIF). Expression features of EMP in bone marrow, liver, renal, spleen, brain, and lung tissues of the MRL/lpr mice and control mice groups were followed using quantitative real-time polymerase chain reaction (Q-PCR). Meanwhile, the expression of EMP was located through immunohistochemical (IHC) studies and the expressive cell identified through double immunofluorescent labeling. Results IIF showed that lupus mice have strong positive fluorescence, but no significant fluorescence was observed in control mice. Q-PCR detection revealed that EMP was expressed in the marrow, liver, renal, spleen, lung, and brain tissues of lupus mice. The highest levels were observed in the bone marrow, but there was no statistical difference between these tissues. EMP mRNA expression in the liver ( t = 2.747, p = 0.01) and bone marrow ( t = 3.853, p = 0.008) of lupus mice was significantly higher than in the control mice. However, no differences in EMP mRNA expression were observed in the renal, spleen, lung, and brain tissues between the lupus and control mice ( p > 0.05). In addition, the IHC results showed that EMP protein is ubiquitously expressed in all of the tissues of the lupus and control mice. The positive expression rate in the bone marrow and liver tissues of the lupus mice was higher than in the control mice, but without an obvious difference in the other tissues. The double IF staining method shows that EMP protein was expressed in macrophages in the tissues of the lupus mice and the control mice. Conclusions Our data showed that EMP is ubiquitously expressed in macrophages at all of the tissues of the lupus and control mice. However, the expression of EMP in bone marrow and liver tissues of lupus mice was higher than in the control mice, which indicates that EMP may be important in the development of SLE.

The therapeutic effect of dendritic cells expressing indoleamine 2,3-dioxygenase (IDO) on an IgA nephropathy mouse model

2020 ◽  
Vol 52 (2) ◽  
pp. 399-407 ◽  
Author(s):  
Kanghan Liu ◽  
Yiya Yang ◽  
Yinyin Chen ◽  
Shiyao Li ◽  
Yuting Gong ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mouse Model ◽  
Iga Nephropathy ◽  
Therapeutic Effect ◽  
Indoleamine 2,3 Dioxygenase

scholarly journals Delayed Administration of Recombinant Plasma Gelsolin Improves Survival in a Murine Model of Penicillin-Susceptible and Penicillin-Resistant Pneumococcal Pneumonia

2019 ◽  
Vol 220 (9) ◽  
pp. 1498-1502 ◽  
Author(s):  
Zhiping Yang ◽  
Alice Bedugnis ◽  
Susan Levinson ◽  
Mark Dinubile ◽  
Thomas Stossel ◽  
...  
Keyword(s):  
Weight Loss ◽  
Antimicrobial Resistance ◽  
Mouse Model ◽  
Murine Model ◽  
Pneumococcal Pneumonia ◽  
Preclinical Models ◽  
Antibiotic Resistant ◽  
Plasma Gelsolin ◽  
Beneficial Effects ◽  
Serious Infections

Abstract Therapy to enhance host immune defenses may improve outcomes in serious infections, especially for antibiotic-resistant pathogens. Recombinant human plasma gelsolin (rhu-pGSN), a normally circulating protein, has beneficial effects in diverse preclinical models of inflammation and injury. We evaluated delayed therapy (24–48 hours after challenge) with rhu-pGSN in a mouse model of pneumococcal pneumonia. rhu-pGSN without antibiotics increased survival and reduced morbidity and weight loss after infection with either penicillin-susceptible or penicillin-resistant pneumococci (serotypes 3 and 14, respectively). rhu-pGSN improves outcomes in a highly lethal pneumococcal pneumonia model when given after a clinically relevant delay, even in the setting of antimicrobial resistance.

Treatment of Skin Injury due to Vinorelbine Extravasation Using bFGF and rhGM-CSF: An Experimental Study in a Murine Model

2010 ◽  
Vol 13 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Chunhua Yu ◽  
Jin Wang ◽  
Yan Fu ◽  
Yongqiu Mao ◽  
Yongshun Chen ◽  
...  
Keyword(s):  
Murine Model ◽  
Maximum Size ◽  
Experimental Models ◽  
Control Group ◽  
Skin Injury ◽  
Macrophage Colony Stimulating Factor ◽  
The Difference ◽  
Macrophage Colony ◽  
And Control

Background and objective: A murine model of skin injury from vinorelbine extravasation was established to evaluate the treatment efficacy of basic fibroblast growth factor (bFGF) and recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF). Materials and method: Experimental models were divided into bFGF, rhGM-CSF, and control (saline) groups, with 40 mice in each group. Edema and ulceration were measured on Days 1, 3, 5, 7, 10, 14, and 18 after the onset of extravasation; injuries were examined pathomorphologically in three mice/group/time point. Results: Edema reached maximum size on Day 3 in the bFGF and rhGM-CSF groups and Day 5 in the control group. The difference between the two experimental groups was not significant; differences between the control group and the experimental groups were statistically significant at all time points. Edema and ulceration began to improve on Day 10 in the bFGF and rhGM-CSF groups and Day 18 in the control group. Healing duration was 14—18 days in the experimental groups, with a (not significantly) shorter duration in the bFGF group. Healing was completed by Day 27.5 in the control group. Pathomorphological evaluation showed regular reepithelization and newly formed granulation tissue in the bFGF and rhGM-CSF groups on Day 13. In the control group, wounds were partially healed, edema and shallow ulcers existed, and epithelization was fragile and disorganized on Day 18. Conclusions: bFGF and rhGM-CSF are useful for the treatment of skin injury due to vinorelbine extravasation, but bFGF may be slightly more effective in decreasing time and improving quality of healing.

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