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LENS BASEMENT MEMBRANE IN SPARC-NULL CATARACTOGENESIS

Award Number: R01EY014150
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 09/30/2002
PERIOD OF PERFORMANCE END DATE: 07/31/2006

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LENS BASEMENT MEMBRANE IN SPARC-NULL CATARACTOGENESIS - DESCRIPTION (provided by applicant): SPARC (secreted protein acidic and rich in cysteine), also termed osteonectin and BM-40, is a matricellular glycoprotein which has been shown to regulate cell functions such as cell cycle, cell shape change, migration, adhesion, gene expression and ECM production. SPARC-null mice are viable but exhibit cataract with 100% penetrance. Lens capsule, a highly-developed lens basement membrane (BM), is a specialized ECM structure which functions to regulate cell behavior and differentiation of the lens epithelial cells. SPARC, as a major cell-matrix regulator that is localized in the lens capsule and lens epithelium, may play a pivotal role in the lens BM structure, matrix organization and its connections to intracellular pathways, and lens cell-ECM interactions, defects in which can have significant pathological consequences, such as cataract formation. We will test the hypothesis that the absence of SPARC contributes to a loss of the structural and functional integrity of the lens BM, and leads to alteration of lens cell-ECM interactions, that contribute to the generation of cataracts. Based on our understanding of SPARC structure and function, we propose three aims to test our hypotheses: 1) SPARC plays a pivotal role in structural stability and organization of the lens BM. Mice lacking SPARC will exhibit alterations of lens BM components and compromised lens capsule structure; 2) SPARC modulates lens epithelial cell adhesion through its regulation of the production of the adhesive proteins laminin 1 and fibronectin, and by its interaction with them; 3) Lens capsule permeability is compromised in SPARC-null lens, which contributes, in part, to the cataract formation in this model. The experiments proposed in this application will provide an understanding of the role of SPARC in the organization of ECM components, in cell-ECM interactions during lens development, and in the generation of cataracts in SPARC-null mice.


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: 2005 ( Subtotal = $273,750 )
2005	2005	BENAROYA RESEARCH INSTITUTE AT VIRGINIA MASON	1201 NINTH AVENUE	SEATTLE	WA	98101	KING	USA	Vision Research	000	5	7/25/2005	NON-COMPETING CONTINUATION	$273,750
														Subtotal = $273,750

Issue Date FY: 2004 ( Subtotal = $273,750 )
2004	2004	BENAROYA RESEARCH INSTITUTE AT VIRGINIA MASON	1201 NINTH AVENUE	SEATTLE	WA	98101	KING	USA	Vision Research	000	4	7/15/2004	NON-COMPETING CONTINUATION	$273,750
														Subtotal = $273,750

Issue Date FY: 2003 ( Subtotal = $273,750 )
2003	2003	THE HOPE HEART INSTITUTE	556 18TH AVENUE	SEATTLE	WA	98122	KING	USA	Vision Research	000	2	8/11/2003	NON-COMPETING CONTINUATION	$273,750
														Subtotal = $273,750

Issue Date FY: 2002 ( Subtotal = $273,750 )
2002	2002	THE HOPE HEART INSTITUTE	556 18TH AVENUE	SEATTLE	WA	98122	KING	USA	Vision Research	000	1	9/16/2002	NEW	$273,750
														Subtotal = $273,750

Grand Total All Awards = $1,095,000

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LENS BASEMENT MEMBRANE IN SPARC-NULL CATARACTOGENESIS

Award Number: R01EY014150

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 09/30/2002

PERIOD OF PERFORMANCE END DATE: 07/31/2006

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