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Recent News and Articles on the Keywords: kidney disease + gene protects + gene  Related to the article below (Last Update: 5/12/2008)

Alcoholic Lung Disease
RedOrbit, TX - Apr 30, 2008
2005), and at least one clinical study suggests that people who do not express the ACE gene variant associated with increased enzyme activity are at lower ...
Source: Google News

Gene therapy by skeletal muscle expression of decorin prevents fibrotic disease in rat kidney -
Y Isaka, DK Brees, K Ikegaya, Y Kaneda, E Imai, NA … - Nature Medicine, 1996 - nature.com
... protects against scarring in experimental kidney disease. Nature 360, 361-364
(1992). | Article | PubMed | ISI | ChemPort |; Blau, HM & Springer, ML Gene ...

Human adrenomedullin gene delivery protects against cardiovascular remodeling and renal injury. -
J Chao, K Kato, JJ Zhang, E Dobrzynski, C Wang, J … - Peptides, 1911 - ncbi.nlm.nih.gov
Peptides. 2001 Nov;22(11):1731-7. Click here to read Human adrenomedullin gene delivery
protects against cardiovascular remodeling and renal injury. ...

A specific endothelin subtype A receptor antagonist protects against injury in renal disease … -
A Benigni, C Zoja, D Corna, S Orisio, L Longaretti … - Kidney Int, 1993 - nature.com
... subtype A receptor antagonist protects against injury in renal disease progression.
We have recently reported that renal preproendothelin-1 gene is up ...

Targeted disruption of Bcl-2 alpha beta in mice: occurrence of gray hair, polycystic kidney disease, … -
K Nakayama, K Nakayama, I Negishi, K Kuida, H Sawa … - Proceedings of the National Academy of Sciences of the …, 1994 - pubmedcentral.nih.gov
... at 4-5 weeks of age, and polycystic kidney disease-like change of renal tubules. ...
Caenorhabditis elegans gene ced-9 protects cells from programmed cell ...

TGF-[beta] in kidney fibrosis: A target for gene therapy. -
WA Border, NA Noble - Kidney International, 1997 - pt.wkhealth.com
... of transforming growth factor-? protects against scarring in experimental kidney
disease.Nature 360 ... G, Jani A, Felgner PL: Direct gene transfer into ...

[CITATION] Does the A118G Polymorphism at the-opioid Receptor Gene Protect against Morphine-6-Glucuronide … -
J L?tsch, M Zimmermann, J Darimont, C Marx, R … - Anesthesiology, 2002
... dl) caused by glomerulonephritis, failed kidney transplant, peripheral ... Neither disease
state nor concomitant medications (table 2 ... in the OPRM1-gene (coding the ...

Increased tumor necrosis factor and IL-1 beta gene expression in the kidneys of mice with lupus … -
JM Boswell - The Journal of Immunology, 1988 - Am Assoc Immnol
... likely source of increased gene expression for ... Recombinant Complement C3 Inhibitor
Protects Against Renal ... IFN-{gamma}-Dependent Autoimmune Kidney Disease in MRL ...

Human Adrenomedullin Gene Delivery Protects against Cardiac Hypertrophy, Fibrosis, and Renal Damage … -
JJ Zhang, H Yoshida, L Chao, J Chao - Human Gene Therapy, 2000 - liebertonline.com
... These results indicate that human AM gene delivery protects against salt ... in therapeutic
applications to salt-related cardiovascular and renal diseases. ...

A gene for high urinary kallikrein may protect against hypertension in Utah kindreds -
TD Berry, SJ Hasstedt, SC Hunt, LL Wu, JB Smith, … - Hypertension, 1989 - Am Heart Assoc
... high urinary kallikrein may protect against hypertension ... of Human Plasma Kallikrein
Gene Polymorphisms and ... Role in End-Stage Renal Disease Hypertension, April 1 ...

Adenovirus-mediated kallikrein gene delivery attenuates hypertension and protects against renal … -
E Dobrzynski, H Yoshida, J Chao, L Chao - Immunopharmacology, 1999 - Elsevier
... The ability of kallikrein gene transfer to protect against renal ... of the
kallikrein?kinin system in volume-dependent hypertension and renal diseases. ...

Source: Google Scholar

A Gene That Protects From Kidney Disease
A combination of mice and patient studies sheds light on cause and possible new therapies of kidney diseases

Researchers from the European Molecular Biology Laboratory (EMBL) and the University of Michigan have discovered a gene that protects us against a serious kidney disease. In the current online issue of Nature Genetics they report that mutations in the gene cause nephronopthisis (NPHP) in humans and mice. NPHP is a disease marked by kidney degeneration during childhood that leads to kidney failure requiring organ transplantation. The insights might help develop effective, noninvasive therapies.
The kidneys are the organs that help our body dispose of potentially harmful waste. Diseases that affect this fundamental function are very serious but so far only poorly understood. NPHP is such a disease; it causes the kidneys to degenerate and shrink starting early on in childhood often leading to renal failure before the age of 30. So far, kidney transplantation in early age has been the only way to save patients suffering from NPHP. With a new mouse model Mathias Treier and his group at EMBL have shed new light on the molecular mechanisms underlying NPHP opening up novel ways to treat the disease.

"Our mice show striking similarities with NPHP patients," says Mathias Treier, group leader at EMBL. "Very early on in their lives their kidney cells start to die and the mice develop all the characteristic disease symptoms. It is the first time that a mouse model reveals increased cell death as the mechanism underpinning kidney degeneration in NPHP. The genetic cause is a mutation in a gene called GLIS2."

GLIS2 normally prevents cell death in the adult kidney. It does so by shutting down genes that initiate cell death and that are only required during the development of the organ. A mutation interfering with GLIS2 function reactivates these harmful genes the result being that large numbers of kidney cells die. The organ shrinks and changes in its architecture occur which affect normal kidney function.

To find out if GLIS2 has the same effect in humans Friedhelm Hildebrandt and his team at the University of Michigan carried out a genetic screen of patients suffering from NPHP. They found that like the mouse model some patients carried mutations in the same GLIS2 gene, confirming that GLIS2 is a crucial player in NPHP also in humans.
This is an excellent example of how combining basic research with clinical studies can help uncovering mechanisms of human disease," says Henriette Uhlenhaut who carried out the research in Treier's lab. "The next step will be to translate the insights gained into new therapeutic approaches to develop alternatives to kidney transplantations. With GLIS2 we have already identified one promising candidate drug target and our mouse model will help us find many others."

European Molecular Biology Laboratory (EMBL)
http://www.embl-heidelberg.de
 
 
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