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The Jackson Laboratory wild type wt mice
$Atrial Energetics and Mitochondrial Dysfunction in Mouse Model of Atrial Fibrillation with Heart Failure. A, B C) As opposed to <t>wild</t> <t>type</t> <t>(WT)</t> <t>mice,</t> a novel mouse model of atrial fibrillation (AF) shows significant electrical and structural remodeling. Electrocardiograms demonstrate sinus rhythm (SR) in wild type (WT) ( A ) and LKB1 knockout (KO) mice ( B ). LKB1 KO mice develop spontaneous AF ( C) and then heart failure (HF). Cardiac magnetic resonance imaging showed significant right and left atrial enlargement in LKB1 KO mice in AF and HF ( lower panel ). D) ECG analysis demonstrated heart rate was similar in WT and KO mice in SR while ventricular rate was slower in KO in AF and HF. E ). Atrial size significantly increased in AF and HF with progressive right and left atrial enlargement compare to WT mice. F ) Left ventricular ejection fraction was reduced in AF. G, H I ) Disrupted atrial energetics and metabolism was associated with development of atrial remodeling, AF and HF. Atrial myocardial content of nucleotides including ATP ( G ) and ADP ( H ) was significantly lower in LKB1 KO mice in SR and AF compare to WT mice. As shown by high performance liquid chromatography measurement ( G ), ATP was significantly depleted in LKB1 KO atrial myocardium starting in SR and further decrease in AF. Metabolic stress, as reflected in AMP/ATP ratio ( I ), was more significant in LKB1 KO hearts with AF than in WT. Thus, AF is associated with impaired myocardial energetics and metabolism. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P$
Wild Type Wt Mice, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 92/100, based on 250 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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wild type wt mice - by Bioz Stars, 2021-01

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1) Product Images from "MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION"

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION

Journal: Journal of cardiac failure

doi: 10.1016/j.cardfail.2019.08.005

$Atrial Energetics and Mitochondrial Dysfunction in Mouse Model of Atrial Fibrillation with Heart Failure. A, B C) As opposed to wild type (WT) mice, a novel mouse model of atrial fibrillation (AF) shows significant electrical and structural remodeling. Electrocardiograms demonstrate sinus rhythm (SR) in wild type (WT) ( A ) and LKB1 knockout (KO) mice ( B ). LKB1 KO mice develop spontaneous AF ( C) and then heart failure (HF). Cardiac magnetic resonance imaging showed significant right and left atrial enlargement in LKB1 KO mice in AF and HF ( lower panel ). D) ECG analysis demonstrated heart rate was similar in WT and KO mice in SR while ventricular rate was slower in KO in AF and HF. E ). Atrial size significantly increased in AF and HF with progressive right and left atrial enlargement compare to WT mice. F ) Left ventricular ejection fraction was reduced in AF. G, H I ) Disrupted atrial energetics and metabolism was associated with development of atrial remodeling, AF and HF. Atrial myocardial content of nucleotides including ATP ( G ) and ADP ( H ) was significantly lower in LKB1 KO mice in SR and AF compare to WT mice. As shown by high performance liquid chromatography measurement ( G ), ATP was significantly depleted in LKB1 KO atrial myocardium starting in SR and further decrease in AF. Metabolic stress, as reflected in AMP/ATP ratio ( I ), was more significant in LKB1 KO hearts with AF than in WT. Thus, AF is associated with impaired myocardial energetics and metabolism. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P$
Figure Legend Snippet: Atrial Energetics and Mitochondrial Dysfunction in Mouse Model of Atrial Fibrillation with Heart Failure. A, B C) As opposed to wild type (WT) mice, a novel mouse model of atrial fibrillation (AF) shows significant electrical and structural remodeling. Electrocardiograms demonstrate sinus rhythm (SR) in wild type (WT) ( A ) and LKB1 knockout (KO) mice ( B ). LKB1 KO mice develop spontaneous AF ( C) and then heart failure (HF). Cardiac magnetic resonance imaging showed significant right and left atrial enlargement in LKB1 KO mice in AF and HF ( lower panel ). D) ECG analysis demonstrated heart rate was similar in WT and KO mice in SR while ventricular rate was slower in KO in AF and HF. E ). Atrial size significantly increased in AF and HF with progressive right and left atrial enlargement compare to WT mice. F ) Left ventricular ejection fraction was reduced in AF. G, H I ) Disrupted atrial energetics and metabolism was associated with development of atrial remodeling, AF and HF. Atrial myocardial content of nucleotides including ATP ( G ) and ADP ( H ) was significantly lower in LKB1 KO mice in SR and AF compare to WT mice. As shown by high performance liquid chromatography measurement ( G ), ATP was significantly depleted in LKB1 KO atrial myocardium starting in SR and further decrease in AF. Metabolic stress, as reflected in AMP/ATP ratio ( I ), was more significant in LKB1 KO hearts with AF than in WT. Thus, AF is associated with impaired myocardial energetics and metabolism. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Techniques Used: Mouse Assay, Knock-Out, Magnetic Resonance Imaging, High Performance Liquid Chromatography

Mitochondrial Dysfunction in mechanism of Atrial Fibrillation and Heart Failure in Mice Atria. A-F) Mitochondrial electron transport chain, matrix, inner- and outer membrane proteins were significantly impaired in LKB1 knockout (KO) heart atria compared with wild type (WT) atria, particularly in atrial fibrillation (AF) and heart failure (HF) co-existence. In KO atria with AF and HF, succinate dehydrogenase (complex II) ( A ), cytochrome c oxidase (complex IV) ( B ), pyruvate dehydrogenase ( C ), voltage gated anion channel ( D ), prohibitins 1 ( E ) and cytochrome c ( F ) levels were significantly lower compare to WT atria and KO atria in sinus rhythm (SR) without HF. Functional and structural impairment started in SR and then worsen in persAF and HF. G-I) Mitochondrial dysfunction was associated with oxidative stress and mitochondrial DNA (mtDNA) damage. There was significantly higher reactive oxygen species (ROS) generation in AF and HF compared to WT atrial tissue as shown in elevated level of hydrogen peroxide (H 2 O 2 ) that was measured by using 2,7-dichlorofluorescein (DCF) diacetate fluorescence ( G ) and superoxide as shown elevated ROS scavenger, superoxide dismutase (SOD) ( H ). Mitochondrial DNA (mtDNA, long fragment: 8636-bp) was significantly damaged in AF and HF ( I, upper panel ). However, the short fragment of mtDNA was similarly amplified in both groups ( I, lower panel ). Thus, impaired mitochondrial complexes and oxidative stress were associated with mtDNA damage in AF and HF. Insets show western blotting for specific proteins in panels A-F and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Figure Legend Snippet: Mitochondrial Dysfunction in mechanism of Atrial Fibrillation and Heart Failure in Mice Atria. A-F) Mitochondrial electron transport chain, matrix, inner- and outer membrane proteins were significantly impaired in LKB1 knockout (KO) heart atria compared with wild type (WT) atria, particularly in atrial fibrillation (AF) and heart failure (HF) co-existence. In KO atria with AF and HF, succinate dehydrogenase (complex II) ( A ), cytochrome c oxidase (complex IV) ( B ), pyruvate dehydrogenase ( C ), voltage gated anion channel ( D ), prohibitins 1 ( E ) and cytochrome c ( F ) levels were significantly lower compare to WT atria and KO atria in sinus rhythm (SR) without HF. Functional and structural impairment started in SR and then worsen in persAF and HF. G-I) Mitochondrial dysfunction was associated with oxidative stress and mitochondrial DNA (mtDNA) damage. There was significantly higher reactive oxygen species (ROS) generation in AF and HF compared to WT atrial tissue as shown in elevated level of hydrogen peroxide (H 2 O 2 ) that was measured by using 2,7-dichlorofluorescein (DCF) diacetate fluorescence ( G ) and superoxide as shown elevated ROS scavenger, superoxide dismutase (SOD) ( H ). Mitochondrial DNA (mtDNA, long fragment: 8636-bp) was significantly damaged in AF and HF ( I, upper panel ). However, the short fragment of mtDNA was similarly amplified in both groups ( I, lower panel ). Thus, impaired mitochondrial complexes and oxidative stress were associated with mtDNA damage in AF and HF. Insets show western blotting for specific proteins in panels A-F and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Techniques Used: Mouse Assay, Knock-Out, Functional Assay, Fluorescence, Amplification, Western Blot

Mitochondrial Ultrastructural Remodeling in Mechanism of Atrial Fibrillation and Heart Failure. A-F) Mitochondrial ultrastructure was significantly disrupted in atrial fibrillation (AF) and heart failure (HF). Electron microscopy showed that atrial cardiomyocyte with AF and HF has higher number of mitochondria than in wild type (WT) ( A ) and larger mitochondrion-volume ( B ). Mitochondrial matrix edema and disruption of the inner and outer membranes were demonstrated by measurement of crista density that was significantly lower in AF and HF indicating mitochondrial damage ( C ). Electron microscopy images showed significantly impaired mitochondrial ultrastructure in cardiomyocytes with AF compare to WT in SR ( D, E F ). Mitochondrial functional and structural damage were associated with activation of mitochondrial apoptotic cascade (caspase 9) in mice atria ( G ), and human atria ( H ) with HF and AF. Mitochondrial apoptotic cascade, was activated in KO atria in AF compare to WT atria. Insets show western blotting for specific proteins in panels G and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Figure Legend Snippet: Mitochondrial Ultrastructural Remodeling in Mechanism of Atrial Fibrillation and Heart Failure. A-F) Mitochondrial ultrastructure was significantly disrupted in atrial fibrillation (AF) and heart failure (HF). Electron microscopy showed that atrial cardiomyocyte with AF and HF has higher number of mitochondria than in wild type (WT) ( A ) and larger mitochondrion-volume ( B ). Mitochondrial matrix edema and disruption of the inner and outer membranes were demonstrated by measurement of crista density that was significantly lower in AF and HF indicating mitochondrial damage ( C ). Electron microscopy images showed significantly impaired mitochondrial ultrastructure in cardiomyocytes with AF compare to WT in SR ( D, E F ). Mitochondrial functional and structural damage were associated with activation of mitochondrial apoptotic cascade (caspase 9) in mice atria ( G ), and human atria ( H ) with HF and AF. Mitochondrial apoptotic cascade, was activated in KO atria in AF compare to WT atria. Insets show western blotting for specific proteins in panels G and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Techniques Used: Electron Microscopy, Functional Assay, Activation Assay, Mouse Assay, Western Blot

2) Product Images from "Endothelial exosome plays functional role during rickettsial infection"

Article Title: Endothelial exosome plays functional role during rickettsial infection

Journal: bioRxiv

doi: 10.1101/2020.11.16.385740

Recipient cells take up Exos. ( a ) Purified plsExos (5 x 10 10 particles in 50 μL PBS) labeled with PKH26 were administrated to wild-type mice intravenously (n=3). After 4 hrs, organs were dissected for frozen sectioning after euthanasia and perfusion via the right ventricle. Representative immunofluorescent staining of ECs from liver, brain, and lung using an antibody against CD31(an EC marker) is shown. The nuclei were stained with DAPI. Cells with red fluorescence indicate the uptake of PKH26 labeled Exos. Scale bars, 20 µm. ( b ) Purified ECExos were labeled with PKH26 (red) and added to the culture medium of human BMECs (2000 particles per cell) as indicated. Pictures were taken using fluorescence microscopy after 2 hrs of ECExo incubation. Scale bars, 20 µm.

Figure Legend Snippet: Recipient cells take up Exos. ( a ) Purified plsExos (5 x 10 10 particles in 50 μL PBS) labeled with PKH26 were administrated to wild-type mice intravenously (n=3). After 4 hrs, organs were dissected for frozen sectioning after euthanasia and perfusion via the right ventricle. Representative immunofluorescent staining of ECs from liver, brain, and lung using an antibody against CD31(an EC marker) is shown. The nuclei were stained with DAPI. Cells with red fluorescence indicate the uptake of PKH26 labeled Exos. Scale bars, 20 µm. ( b ) Purified ECExos were labeled with PKH26 (red) and added to the culture medium of human BMECs (2000 particles per cell) as indicated. Pictures were taken using fluorescence microscopy after 2 hrs of ECExo incubation. Scale bars, 20 µm.

Techniques Used: Purification, Labeling, Mouse Assay, Staining, Marker, Fluorescence, Microscopy, Incubation

Knock-Out:

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION
Article Snippet: .. Cardiac specific liver kinase B1 (LKB1) knockout (KO) mice ( C57BL/6 ) were generated by crossing LKB1 flox/flox mice with transgenic mice expressing Cre-recombinase from the myosin heavy chain promoter., , LKB1 KO mice were born in SR and then developed spontaneous AF which followed with HF in persAF as we and others reported previously., , Wild-type (WT) mice were of the same strain as the corresponding transgenic mice (Jackson Lab). ..

Article Title: The Absence of Indoleamine 2,3-Dioxygenase Inhibits Retinal Capillary Degeneration in Diabetic Mice
Article Snippet: .. IDO knockout (IDO−/− ) and wild-type (WT) mice (all on C57BL/6J background) were obtained from Jackson Laboratories (Bar Harbor, ME, USA). .. Male IDO−/− and WT mice at 3 months of age were administered five sequential intraperitoneal injections of streptozotocin (MP Biomedicals, Solon, OH, USA) solution freshly prepared in citrate buffer (pH 4.5) at a dose of 55 mg/kg body weight on 5 consecutive days (to animals fasted for 6 hours) to induce diabetes.

Article Title: α-Linolenic acid but not linolenic acid protects against hypertension: critical role of SIRT3 and autophagic flux
Article Snippet: .. SIRT3 knock-out (SIRT3KO) and wild-type (WT) mice were obtained from Jackson Laboratory (Bar Harbor, Maine, USA), and hypertension was also induced by AngII infusion (0.4 mg/kg/d, 2 weeks). ..

Mouse Assay:

Article Title: IκB-kinase-ε in the tumor microenvironment is essential for the progression of gastric cancer
Article Snippet: .. Assessment of melanoma lung metastasis After confluence of culture in ordinary DMEM, B16-F10 were delivered to IKKε null mice and wild-type (WT) mice (purchased from The Jackson Laboratory) by tail-vein injection (2×105 cells/mouse). ..

Article Title: Endothelial exosome plays functional role during rickettsial infection
Article Snippet: .. Wild-type (WT) mice (C57BL/6J) were obtained from Jackson Laboratory (Bar Harbor, ME). .. C57BL/6J mice are highly susceptible to R. australis .

Article Title: The volatile anesthetic sevoflurane reduces neutrophil apoptosis via Fas death domain–Fas-associated death domain interaction
Article Snippet: .. Wild-type (WT) mice on the C57BL/6 background were purchased from The Jackson Laboratory (Bar Harbor, ME, USA) and inbred in our animal facility. ..

Article Title: Activation of TLR4 is necessary for trauma hemorrhagic shock-induced gut injury and PMN priming
Article Snippet: .. Male 10-12 week old outbred cesarean-derived (CD-1) mice, TLR4-mutated (C3H/HeJ) mice and their wild-type (WT) mice (C3H/HeOuJ), TRIF deficient and their wild type (C57BL/6J) littermates were obtained from The Jackson Laboratory. .. Mice on the C57BL/6J background with a specific deletion of the MyD88 gene (MyD88-/- mice) were kindly provided by Dr. Samuel J. Leibovich (UMDNJ-New Jersey Medical School, Newark, N.J).

Article Title: TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice
Article Snippet: .. All breeding pairs of the wild-type (WT) laboratory mice of the C57BL/6J strain were purchased from The Jackson Laboratory, and breeding pairs of mice with targeted deletion of TREM-1/3 and RIPK3 genes on a C57BL/6J background were obtained from Genentech. ..