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AGE SIGNALING IN DIABETIC RENAL DISEASE

Award Number: F32DK062680
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/01/2002
PERIOD OF PERFORMANCE END DATE: 08/31/2005

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AGE SIGNALING IN DIABETIC RENAL DISEASE - DESCRIPTION (provided by applicant): Nephropathy is one of the major complications of both type 1 and type 2 diabetes mellitus. Thus approximately 40% of individuals with diabetes will develop kidney disease, and renal failure accounts for a significant proportion of the mortality attributable to diabetes. The progression to diabetic kidney disease is a complex and poorly understood process. Elevated plasma glucose triggers the secretion of transforming growth factor-beta (TGF-Beta) which, in turn, stimulates the pathologically excessive deposition of extracellular matrix-a process mediated by glomerular mesangial cells. Elevated blood glucose also stimulates mesangial cell hyperplasia and hypertrophy. These processes eventually culminate in renal failure. While a direct signaling role for glucose has been proposed, glucose itself is a weak mesangial cell agonist. Advanced glycation endproducts (AGEs), formed by the nonenzymatic glycation of proteins and lipids, are present in excess in diabetes and are thought to be important early in the development of diabetic renal disease. AGEs exert their effects by interacting with the receptor for advanced glycation endproducts (RAGE). RAGE expression is elevated in diabetes. Blockade of RAGE has been shown to suppress vascular hyperpermeabiity and accelerated atherosclerosis in diabetic rats. These results, suggest that AGEs/RAGE play a central role in triggering the early pathophysiologic changes associated with diabetic nephropathy. Accordingly, investigating RAGE intracellular signaling mechanisms and cellular effects is important to furthering our understanding of diabetic renal disease. We propose two broad areas of study: dissection of the signaling pathways coupling mesangial cell RAGE to ERK and PI-3-kinase and identification of signaling elements recruited by RAGE that are important to pathophysiologic changes of mesangial cells associated with diabetes.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2004 ( Subtotal = $52,492 )
2004	2004	NEW ENGLAND MEDICAL CENTER HOSPITALS, INC	750 WASHINGTON STREET	BOSTON	MA	02111	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	4	7/21/2004	NON-COMPETING CONTINUATION	$52,492
														Subtotal = $52,492

Issue Date FY: 2003 ( Subtotal = $49,864 )
2003	2003	NEW ENGLAND MEDICAL CENTER HOSPITALS, INC	750 WASHINGTON STREET	BOSTON	MA	02111	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	3	8/25/2003	NON-COMPETING CONTINUATION	$49,864
														Subtotal = $49,864

Issue Date FY: 2002 ( Subtotal = $46,192 )
2002	2002	NEW ENGLAND MEDICAL CENTER HOSPITALS	171 HARRISON AVENUE, BOX 453	BOSTON	MA	02111	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	2	9/25/2002	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$46,192
2002	2002	MASSACHUSETTS GENERAL HOSPITAL	32 FRUIT STREET	BOSTON	MA	02114	SUFFOLK	USA	Kidney Diseases, Urology and Hematology Research	000	1	9/25/2002	NEW	$0
														Subtotal = $46,192

Grand Total All Awards = $148,548

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AGE SIGNALING IN DIABETIC RENAL DISEASE

Award Number: F32DK062680

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/01/2002

PERIOD OF PERFORMANCE END DATE: 08/31/2005

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