scholarly journals Distribution and Severity of Neuropathology in β-Mannosidase-Deficient Mice is Strain Dependent

2013 ◽  
pp. 73-81 ◽  
Author(s):  
Kathryn L. Lovell ◽  
Mei Zhu ◽  
Meghan C. Drummond ◽  
Robert C. Switzer ◽  
Karen H. Friderici
Keyword(s):  
Strain Dependent ◽  
Deficient Mice ◽  
Is Strain

scholarly journals Mouse model of panic disorder: Vulnerability to early environmental instability is strain‐dependent

2021 ◽  
Author(s):  
Alessandra Luchetti ◽  
Matteo Di Segni ◽  
Diego Andolina ◽  
Rossella Ventura ◽  
Marco Battaglia ◽  
...  
Keyword(s):  
Panic Disorder ◽  
Mouse Model ◽  
Environmental Instability ◽  
Strain Dependent ◽  
Is Strain

Intensity of Halothane- and Hypercapnia-Induced Cerebral Hyperemia Is Strain-Dependent in Rats

1996 ◽  
Vol 83 (2) ◽  
pp. 359-365 ◽  
Author(s):  
Hiroshi Takahashi ◽  
Jeffrey R. Kirsch ◽  
Toshiki Okada ◽  
Richard J. Traystman
Keyword(s):  
Strain Dependent ◽  
Is Strain

scholarly journals Tensin2 is important for podocyte-glomerular basement membrane interaction and integrity of the glomerular filtration barrier

2020 ◽  
Vol 318 (6) ◽  
pp. F1520-F1530
Author(s):  
Kozue Uchio-Yamada ◽  
Keiko Yasuda ◽  
Yoko Monobe ◽  
Ken-ichi Akagi ◽  
Osamu Suzuki ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Filtration ◽  
Glomerular Basement Membrane ◽  
Dependent Manner ◽  
Glomerular Filtration Barrier ◽  
Filtration Barrier ◽  
Gbm Thickening ◽  
Strain Dependent ◽  
Deficient Mice

Tensin2 (Tns2), an integrin-linked protein, is enriched in podocytes within the glomerulus. Previous studies have revealed that Tns2-deficient mice exhibit defects of the glomerular basement membrane (GBM) soon after birth in a strain-dependent manner. However, the mechanisms for the onset of defects caused by Tns2 deficiency remains unidentified. Here, we aimed to determine the role of Tns2 using newborn Tns2-deficient mice and murine primary podocytes. Ultrastructural analysis revealed that developing glomeruli during postnatal nephrogenesis exhibited abnormal GBM processing due to ectopic laminin-α2 accumulation followed by GBM thickening. In addition, analysis of primary podocytes revealed that Tns2 deficiency led to impaired podocyte-GBM interaction and massive expression of laminin-α2 in podocytes. Our study suggests that weakened podocyte-GBM interaction due to Tns2 deficiency causes increased mechanical stress on podocytes by continuous daily filtration after birth, resulting in stressed podocytes ectopically producing laminin-α2, which interrupts GBM processing. We conclude that Tns2 plays important roles in the podocyte-GBM interaction and maintenance of the glomerular filtration barrier.

scholarly journals Microglial—Macrophage Synthesis of Tumor Necrosis Factor after Focal Cerebral Ischemia in Mice is Strain Dependent

2002 ◽  
Vol 22 (7) ◽  
pp. 785-797 ◽  
Author(s):  
Kate Lykke Lambertsen ◽  
Rikke Gregersen ◽  
Bente Finsen
Keyword(s):  
Cerebral Ischemia ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Border Zone ◽  
Mouse Strains ◽  
Strain Dependent ◽  
Necrosis Factor ◽  
Is Strain

Commonly used inbred mouse strains display substantial differences in sensitivity to focal cerebral ischemia. Such differences can often be ascribed to differences in vascular anatomy. The authors investigated whether a contributing factor could be strain-related differences in cellular synthesis of the pleiotropic and potential neurotoxic cytokine tumor necrosis factor (TNF) in the border zone of and within the focal cerebral infarct. In all mouse strains investigated they found that TNF was synthesized by infarct and periinfarct infiltrating Mac-1 immunopositive microglia—macrophages. BALB/c mice, which developed the largest infarcts, contained significantly fewer TNF-producing microglia—macrophages compared with SJL and C57BL/6 mice at both 12 and 24 hours after permanent occlusion of the distal part of the middle cerebral artery. SJL mice developed larger infarcts than C57BL/6 mice, whereas the number of TNF-producing microglia—macrophages per infarct volume unit was comparable. Western blotting data confirmed the increased TNF levels in SJL mice compared with BALB/c and C57BL/6 mice. Furthermore, mice with 12-hour postischemic survival consistently contained two-to threefold more TNF-producing microglia—macrophages than mice with 24-hour survival. The data show that the magnitude of the cellular TNF response to cerebral ischemia is strain dependent, while the time-profile and the cellular sources of TNF are similar irrespective of genetic background. Furthermore, the lack of correlation between infarct size and cellular TNF response suggests that the functionally important TNF is produced in the very early phase (minutes to a few hours) after induction of ischemia, just as it raises the possibility that different mouse strains display different sensitivities to TNF.

The involvement of prostaglandin E2 in interleukin-1β evoked anorexia is strain dependent

2017 ◽  
Vol 60 ◽  
pp. 27-31 ◽  
Author(s):  
Anna Nilsson ◽  
Louise Elander ◽  
Martin Hallbeck ◽  
Unn Örtegren Kugelberg ◽  
David Engblom ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Interleukin 1Β ◽  
Strain Dependent ◽  
Is Strain

Inflammation-induced airway smooth muscle responsiveness is strain dependent in mice

2011 ◽  
Vol 24 (4) ◽  
pp. 361-366 ◽  
Author(s):  
Jesper Säfholm ◽  
Cecilia Lövdahl ◽  
Linda Swedin ◽  
Piet J.M. Boels ◽  
Sven-Erik Dahlén ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Strain Dependent ◽  
Is Strain
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