scholarly journals p75NTRin the spleen: Age-dependent changes, effect of NGF and 4-methylcatechol treatment, and structural changes in p75NTR-deficient mice

2003 ◽  
Vol 270A (2) ◽  
pp. 117-128 ◽  
Author(s):  
M. Pérez-Pérez ◽  
O. García-Suárez ◽  
I. Esteban ◽  
A. Germanà ◽  
I. Fariñas ◽  
...  
Keyword(s):  
Structural Changes ◽  
Age Dependent ◽  
Deficient Mice

scholarly journals Rescue from excitotoxicity and axonal degeneration accompanied by age-dependent behavioral and neuroanatomical alterations in caspase-6-deficient mice

2012 ◽  
Vol 21 (9) ◽  
pp. 1954-1967 ◽  
Author(s):  
Valeria Uribe ◽  
Bibiana K.Y. Wong ◽  
Rona K. Graham ◽  
Corey L. Cusack ◽  
Niels H. Skotte ◽  
...  
Keyword(s):  
Axonal Degeneration ◽  
Age Dependent ◽  
Caspase 6 ◽  
Deficient Mice

Abstract 3863: Deletion Of Integrin Alpha7 Leads To Altered Cardiac Conduction And Sudden Death Associated With Connexin43 Downregulation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Raja Nadif ◽  
Michael Emerson ◽  
Ulrike Mayer ◽  
Ludwig Neyses ◽  
Elizabeth Cartwright
Keyword(s):  
Atrial Fibrillation ◽  
Extracellular Matrix ◽  
Ventricular Hypertrophy ◽  
Structural Changes ◽  
Cellular Adhesion ◽  
Left Ventricular ◽  
Cardiac Conduction ◽  
Cardiac Phenotype ◽  
One Year ◽  
Deficient Mice

Effective propagation of the electrical impulse throughout the myocardium is highly dependent on cell-to-cell and cell-to-extracellular matrix interactions. Increasing evidence indicates that dysregulation of cellular adhesion is a critical determinant in the genesis of arrhythmia. Null mutations in the integrin α7 gene, an essential mediator of cellular adhesion in cardiac and skeletal muscles, have been linked to myopathy in humans, however, the in vivo role of the integrin α7 subunit in the heart is undefined. The mouse model of integrin α7 deletion dies prematurely at one year of age. We therefore analysed the cardiac phenotype in integrin α7 deficient mice (α7 −/− ) to determine whether their premature death was associated with altered cardiac conduction. One year old integrin α7 −/− mice exhibited altered cardiac conduction characterised by spontaneous atrial fibrillation and prolonged QTc duration (α7 −/− : 25.7±0.74ms, α7 +/+ : 19.5±0.61ms; n=6; p<0.001, QTc=QT/(RR/100) 1/2 ). The abnormal cardiac conduction was associated with downregulation of connexin43. However, no significant changes were observed in the expression of ion chanels that have been linked to long QT syndrome or atrial fibrillation (kv1.1, kv1.5, kcne1, kcnq1, erg1, Cav1.2 and Cav1.3). In addition, α7 −/− mice displayed increased susceptibility to drug-induced arrhythmias: treatment with ouabain (2mg/kg BW) in combination with isoprenaline (2.5mg/kg BW) induced atrial fibrillation and ventricular tachycardia and eventually death in 6 month-old integrin α7 −/− mice, but not in α7 +/+ mice. Interestingly, α7 −/− also displayed concentric ventricular hypertrophy with increased septal wall thickness and reduced left ventricular end-diastolic diameter starting from 6 months of age. These structural changes were accompanied by an increase in myocyte size and increased ERK1/2 phosphorylation. In conclusion, deletion of the integrin α7 gene in mice leads to ventricular hypertrophy and to abnormal cardiac conduction. The integrin α7 deficient mice have a marked propensity to lethal arrhythmias through alterations in gap junctions but not ion channels. The integrin α7 knockout model provides new insight into the link between the extracellular matrix and cardiac conduction.

Exercise Can Reverse the Phenotype of Biglycan Deficient Mice

2003 ◽  
Author(s):  
Joseph M. Wallace ◽  
Rupak M. Rajachar ◽  
Xiao-Dong Chen ◽  
Songtao Shi ◽  
Matthew R. Allen ◽  
...  
Keyword(s):  
Skeletal Development ◽  
Skeletal Growth ◽  
Treadmill Running ◽  
Wild Type ◽  
Connective Tissues ◽  
Cross Sectional ◽  
Age Dependent ◽  
Skeletal Phenotype ◽  
Deficient Mice ◽  
Wild Type Control

Biglycan (Bgn) is a small leucine-rich proteoglycan (SLRP) that is enriched in bone and other skeletal connective tissues and is responsible, in part, for the regulation of postnatal skeletal growth (Bianco, 1990). Mice lacking Bgn display reduced skeletal development and a lower peak bone mass that leads to age-dependent osteopenia (Xu, 1998). We hypothesized that mechanical loading could reverse the skeletal phenotype of Bgn knockout mice. To test this hypothesis, we determined the effects of treadmill running on the geometric, mechanical and mineral properties of Bgn deficient mice bones. After sacrifice, femora and tibiae were tested in 4 point bending and cross-sectional geometric properties and bone mineral parameters were measured. Exercise was able to partially reverse the skeletal phenotype of the Bgn knockouts by increasing both the geometric and mechanical properties of the tibiae to values equal to or greater than those of wild type control mice.

scholarly journals Age-dependent dystonia in striatal Gγ7 deficient mice is reversed by the dopamine D2 receptor agonist pramipexole

2013 ◽  
Vol 124 (6) ◽  
pp. 844-854 ◽  
Author(s):  
Keita Sasaki ◽  
Tatsuro Yamasaki ◽  
Idowu O. Omotuyi ◽  
Masayoshi Mishina ◽  
Hiroshi Ueda
Keyword(s):  
Receptor Agonist ◽  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Dopamine D2 ◽  
Age Dependent ◽  
D2 Receptor Agonist ◽  
Deficient Mice

scholarly journals Impaired liver regeneration and lipid homeostasis in CCl4 treated WDR13 deficient mice

2019 ◽  
Author(s):  
Arun Prakash Mishra ◽  
Archana B Siva ◽  
Chandrashekaran Gurunathan ◽  
Y Komala ◽  
B Jyothi Lakshmi
Keyword(s):  
De Novo ◽  
Recovery Period ◽  
Lipid Homeostasis ◽  
Hepatic Regeneration ◽  
Impaired Liver ◽  
Age Dependent ◽  
Regeneration Phase ◽  
Mild Obesity ◽  
Deficient Mice ◽  
Ppar Pathway

AbstractBackground and AimWDR13 - a WD repeat protein, is abundant in pancreas, liver, ovary and testis. Absence of this protein in mice has been seen to be associated with pancreatic β-cell proliferation, hyperinsulinemia and age dependent mild obesity. Previously, we have reported that the absence of WDR13 in diabetic Leprdb/db mice helps in amelioration of fatty liver phenotype along with diabetes and systemic inflammation. This intrigued us to study direct liver injury and hepatic regeneration in Wdr13−/0 mice using hepatotoxin CCl4.MethodsMice were injected with CCl4 twice a week for 8 consecutive weeks. Controls were injected with vehicle (olive oil) similarly. After the last injection, mice were given a 10-days of recovery period and then sacrificed for physiological and molecular analyses.ResultsIn the present study we report slower hepatic regeneration in Wdr13−/0 mice as compared to their wild type littermates after CCl4 administration. Interestingly, during the regeneration phase, hepatic hypertriglyceridemia was observed in Wdr13−/0 mice. Further analyses revealed an upregulation of PPAR pathway in the liver of CCl4-administered Wdr13−/0 mice, causing de novo lipogenesis.ConclusionsThe slower hepatic regeneration observed in CCl4 administered Wdr13−/0 mice, may be linked to liver hypertriglyceridemia because of activation of PPAR pathway.

Age-dependent Alteration in Mitochondrial Dynamics and Autophagy in Hippocampal Neuron of Cannabinoid CB1 Receptor-deficient Mice

2020 ◽  
Vol 160 ◽  
pp. 40-49 ◽  
Author(s):  
Kosuke Kataoka ◽  
Andras Bilkei-Gorzo ◽  
Chihiro Nozaki ◽  
Akinobu Togo ◽  
Keiichiro Nakamura ◽  
...  
Keyword(s):  
Hippocampal Neuron ◽  
Mitochondrial Dynamics ◽  
Cb1 Receptor ◽  
Cannabinoid Cb1 Receptor ◽  
Age Dependent ◽  
Deficient Mice

Atm-deficient mice Purkinje cells show age-dependent defects in calcium spike bursts and calcium currents

Neuroscience ◽  
2000 ◽  
Vol 96 (3) ◽  
pp. 575-583 ◽  
Author(s):  
N Chiesa ◽  
C Barlow ◽  
A Wynshaw-Boris ◽  
P Strata ◽  
F Tempia
Keyword(s):  
Purkinje Cells ◽  
Calcium Currents ◽  
Age Dependent ◽  
Deficient Mice ◽  
Spike Bursts
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