scholarly journals P47 phox -deficient NADPH oxidase defect in neutrophils of diabetic mouse strains, C57BL/6J-m db/db and db /+

2000 ◽  
Vol 67 (2) ◽  
pp. 210-215 ◽  
Author(s):  
Chi-Kuang Huang ◽  
Lijun Zhan ◽  
Michael O. Hannigan ◽  
Youxi Ai ◽  
Thomas L. Leto
2020 ◽  
Vol 128 (11) ◽  
pp. 117009
Author(s):  
James G. Wagner ◽  
Christina E. Barkauskas ◽  
Aaron Vose ◽  
Ryan P. Lewandowski ◽  
Jack R. Harkema ◽  
...  

Diabetologia ◽  
1993 ◽  
Vol 36 (8) ◽  
pp. 727-733 ◽  
Author(s):  
T. Lund ◽  
S. Shaikh ◽  
E. Kendall ◽  
R. D. Campbell ◽  
M. Hattori ◽  
...  

2014 ◽  
Vol 306 (11) ◽  
pp. F1348-F1356 ◽  
Author(s):  
Shuaishuai Zhu ◽  
Yelin Yang ◽  
Jin Hu ◽  
Lingling Qian ◽  
Yuchen Jiang ◽  
...  

Diabetic nephropathy (DN) is the leading cause of end-stage kidney disease worldwide. The purpose of this study is to investigate whether the WldS (slow Wallerian degeneration; also known as Wld) gene plays a renoprotective role during the progression of DN. Diabetes was induced in 8-wk-old male wild-type (WT) and C57BL/WldS mice by streptozotocin (STZ) injection. Blood and urinary variables including blood glucose, glycated hemoglobin (GHb), insulin, urea nitrogen, and albumin/creatinine ratio were assessed 4, 7, and 14 wk after STZ injection. Periodic acid-Schiff staining, Masson staining, and silver staining were performed for renal pathological analyses. In addition, the renal ultrastructure was observed by electron microscope. The activities of p38 and ERK signaling in renal cortical tissues were evaluated by Western blotting. NAD+/NADH ratio and NADPH oxidase activity were also measured. Moreover, the expressions of TNF-α, IL-1, and IL-6 were examined. We provide experimental evidence demonstrating that the WldS gene is expressed in kidney cells and protects against the early stage of diabetes-induced renal dysfunction and extracellular matrix accumulation through delaying the reduction of the NAD+/NADH ratio, inhibiting the activation of p38 and ERK signaling, and suppressing oxidative stress as evidenced by the decreased NADPH oxidase activity and lower expression of TNF-α, IL-1, and IL-6.


1996 ◽  
Vol 10 (1) ◽  
pp. 73-75 ◽  
Author(s):  
M.G. Humphreys-Beher

Numerous models of exocrine tissue pathology related to autoimmune initiation of disease have been described, primarily by either immunohistology or histopathology. These model systems include inbred mouse strains that develop systemic lupus erythematosus, rheumatoid arthritis, graft vs. host disease, and diabetes. Commonly observed features of these mice include organized lymphocytic foci, composed of CD4+ and CD8+ T-cells, in both the salivary and the lacrimal glands. However, only the diabetic mouse model (NOD) undergoes a corresponding loss in exocrine gland function related to the presence of lymphocytic infiltrates. As we define the underlying pathophysiology of Sjögren's syndrome, the future of animal models for this disease will involve genetic exploration of candidate genes for development of autoimmune exocrinopathy.


Author(s):  
L. Vacca-Galloway ◽  
Y.Q. Zhang ◽  
P. Bose ◽  
S.H. Zhang

The Wobbler mouse (wr) has been studied as a model for inherited human motoneuron diseases (MNDs). Using behavioral tests for forelimb power, walking, climbing, and the “clasp-like reflex” response, the progress of the MND can be categorized into early (Stage 1, age 21 days) and late (Stage 4, age 3 months) stages. Age-and sex-matched normal phenotype littermates (NFR/wr) were used as controls (Stage 0), as well as mice from two related wild-type mouse strains: NFR/N and a C57BI/6N. Using behavioral tests, we also detected pre-symptomatic Wobblers at postnatal ages 7 and 14 days. The mice were anesthetized and perfusion-fixed for immunocytochemical (ICC) of CGRP and ChAT in the spinal cord (C3 to C5).Using computerized morphomety (Vidas, Zeiss), the numbers of IR-CGRP labelled motoneurons were significantly lower in 14 day old Wobbler specimens compared with the controls (Fig. 1). The same trend was observed at 21 days (Stage 1) and 3 months (Stage 4). The IR-CGRP-containing motoneurons in the Wobbler specimens declined progressively with age.


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