A Mouse Model for Carney Complex

2004 ◽  
Vol 30 (4) ◽  
pp. 903-911 ◽  
Author(s):  
Kurt J. Griffin ◽  
Lawrence S. Kirschner ◽  
Ludmila Matyakhina ◽  
Sotirios Stergiopoulos ◽  
Audrey Robinson‐White ◽  
...  
Keyword(s):  
Mouse Model ◽  
Carney Complex

A Mouse Model for the Carney Complex Tumor Syndrome Develops Neoplasia in Cyclic AMP–Responsive Tissues

2005 ◽  
Vol 65 (11) ◽  
pp. 4506-4514 ◽  
Author(s):  
Lawrence S. Kirschner ◽  
Donna F. Kusewitt ◽  
Ludmila Matyakhina ◽  
William H. Towns ◽  
J. Aidan Carney ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Mouse Model ◽  
Carney Complex

scholarly journals Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia

2015 ◽  
Vol 23 (1) ◽  
pp. 15-25 ◽  
Author(s):  
Sisi Liu ◽  
Emmanouil Saloustros ◽  
Annabel Berthon ◽  
Matthew F Starost ◽  
Isabelle Sahut-Barnola ◽  
...  
Keyword(s):  
Mouse Model ◽  
Carney Complex ◽  
Regulatory Subunit ◽  
Adrenocortical Cells ◽  
Gene Coding ◽  
Bilateral Adrenal Hyperplasia ◽  
Dependent Protein ◽  
And Control

Primary pigmented nodular adrenocortical disease (PPNAD), whether in the context of Carney complex (CNC) or isolated, leads to ACTH-independent Cushing's syndrome (CS). CNC and PPNAD are caused typically by inactivating mutations of PRKAR1A, a gene coding for the type 1a regulatory subunit (R1α) of cAMP-dependent protein kinase (PKA). Mice lacking Prkar1a, specifically in the adrenal cortex (AdKO) developed CS caused by bilateral adrenal hyperplasia (BAH), which is formed from the abnormal proliferation of fetal-like adrenocortical cells. Celecoxib is a cyclooxygenase 2 (COX2) inhibitor. In bone, Prkar1a inhibition is associated with COX2 activation and prostaglandin E2 (PGE2) production that, in turn, activates proliferation of bone stromal cells. We hypothesized that COX2 inhibition may have an effect in PPNAD. In vitro treatment of human cell lines, including one from a patient with PPNAD, with celecoxib resulted in decreased cell viability. We then treated AdKO and control mice with 1500 mg/kg celecoxib or vehicle. Celecoxib treatment led to decreased PGE2 and corticosterone levels, reduced proliferation and increased apoptosis of adrenocortical cells, and decreased steroidogenic gene expression. We conclude that, in vitro and in vivo, celecoxib led to decreased steroidogenesis. In a mouse model of PPNAD, celecoxib caused histological changes that, at least in part, reversed BAH and this was associated with a reduction of corticosterone levels.

Regenerating myofibers in tibialis anterior muscles of young ‘MDX’ mice

1987 ◽  
Vol 45 ◽  
pp. 726-727
Author(s):  
H. D. Geissinge ◽  
L.D. Rhodes
Keyword(s):  
Muscular Dystrophy ◽  
Mouse Model ◽  
Tibialis Anterior ◽  
Physiological Activity ◽  
Mdx Mice ◽  
Mode Of Inheritance

A recently discovered mouse model (‘mdx’) for muscular dystrophy in man may be of considerable interest, since the disease in ‘mdx’ mice is inherited by the same mode of inheritance (X-linked) as the human Duchenne (DMD) muscular dystrophy. Unlike DMD, which results in a situation in which the continual muscle destruction cannot keep up with abortive regenerative attempts of the musculature, and the sufferers of the disease die early, the disease in ‘mdx’ mice appears to be transient, and the mice do not die as a result of it. In fact, it has been reported that the severely damaged Tibialis anterior (TA) muscles of ‘mdx’ mice seem to display exceptionally good regenerative powers at 4-6 weeks, so much so, that these muscles are able to regenerate spontaneously up to their previous levels of physiological activity.

Mouse model of gastric infection with cytotoxin-expressing strain of Helicobacter pylori in studying of pathogenesis of chronic gastric ulcer

1998 ◽  
Vol 13 (11-s4) ◽  
pp. S178-S184 ◽  
Author(s):  
PETER KONTUREK ◽  
TOMASZ BRZOZOWSKI ◽  
STANISLAW KONTUREK ◽  
ELZBIETA KARCZEWSKA ◽  
ROBERT PAJDO ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Mouse Model ◽  
Chronic Gastric Ulcer
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