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HHS Recovery Act Recipient Reporting Readiness Tool

Step 4. Review and Copy the Grant Awards Data

TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.

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Award Detail for: TECHNOLOGY AND ENDOTHELIAL BIOLOGY OF KIDNEY INJURY MOLECULE-1
BRIGHAM & WOMEN`S HOSPITAL
DUNS Number: 030811269
10 VINING STREET
BOSTON, MA 02115-6114
Recipient Report: Grant or Loan
Prime Recipient

Reporting Information
Award Type Award Number Final Report
Grant 3R00ES016723-03S1 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
030811269 Recipient responsible for this data 8

Award Information
Funding Agency Code Awarding Agency Code Award Date
7529 7529 07-30-2009
Amount of Award Sub Account Number for Program Source (TAS)  
$ 251,022 Recipient responsible for this data
Program Source (TAS)* CFDA Number 
750863 93.701
Total Number of Sub Awards to Individuals Total Amount of Sub Awards to Individuals
Recipient responsible for this data Recipient responsible for this data
Total Number of Payments to Vendors less than $25,000/award Total Amount of Payments to Vendors less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Total Number of Sub Awards less than $25,000/award Total Amount of Sub Awards less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Award Description
Kidney Injury Molecule-1 (KIM-1) is a type 1 transmembrane protein that is not detectable in normal kidney tissue but is expressed at very high levels in dedifferentiated proximal tubule epithelial cells in human and rodent kidneys after ischemic or toxic injury. The extracellular domain of KIM-1 is cleaved and can be quantitated, by an ELISA assay, in the urine of rodents and patients with kidney injury or renal cell carcinoma. An important feature common to repair of the tissue after injury (e.g. acute kidney injury, AKI) or growth of cancer (e.g. renal cell carcinoma, RCC) is adequate supply of oxygen through formation of blood vessels. This led us to hypothesize that the function of KIM-1 ectdomain is to activate the endothelial cells by paracrine mechanisms and stimulate angiogenesis. In the preliminary results we found that KIM-1 ectodomain binds to endothelial cells and stimulates migration in a chemotactic and chemoattractant manner. Furthermore, KIM-1 also induced a 2-fold increase in the number of new blood vessels in the in vivo matrigel plug assay indicating its role in neovascularization. The objective of this proposal is to investigate the mechanisms involved in endothelial repair stimulated by KIM-1 following kidney toxicity due to drugs or environmental toxicants. In the first specific aim the expression of soluble KIM-1 will be characterized in relation with other biomarkers involved in endothelial repair process after kidney injury using various in vivo preclinical and clinical models of kidney toxicity. The second aim of this proposal is to investigate the mechanism of angiogenesis by KIM-1 in the context of endothelial cell regeneration by conducting structure function studies to identify the critical domain of KIM-1 responsible for endothelial cell survival, migration, tube formation and new blood vessel growth. We will also investigate if KIM-1 stimulates migration by inducing candidate gene expression further activating Rho and Integrin linked kinase pathways to cause chemotaxis. We will determine the critical role of KIM-1 in angiogenesis and endothelial resurtucturing by "Knock-in" and "Knockout" strategies using Kim-1 transgenic mice that overexpresses KIM-1 selectively on the epithelial cells of the embryonic and adult kidney proximal tubules and investigate if these mice have faster and more effective endothelial regeneration and recovery from kidney toxicity. Consequently, we will also use the KIM-1 knockout mice to determine if they are more susceptible to nephrotoxicity owing to the lack of repair. Since kidney is a major target for toxicity due to chemical annd physical agents, unraveling the mechanisms of how KIM-1 regulates growth of blood vessels would offer treatment paradigms to promote (in AKI) or inhibit (in kidney cancer) angiogenesis to ameliorate or perhaps even cure disorders that are leading causes of mortality today.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
TECHNOLOGY AND ENDOTHELIAL BIOLOGY OF KIDNEY INJURY MOLECULE-1 Recipient responsible for this data Recipient responsible for this data
Number of Jobs Description of Jobs Created
Recipient responsible for this data Recipient responsible for this data
Quarterly Activities/Project Description
Recipient responsible for this data
 
Activity Code (NAICS or NTEE-NPC)
1Recipient responsible for this data2Recipient responsible for this data
3Recipient responsible for this data4Recipient responsible for this data
5Recipient responsible for this data6Recipient responsible for this data
7Recipient responsible for this data8Recipient responsible for this data
9Recipient responsible for this data10Recipient responsible for this data
Total Federal Amount of ARRA
Expenditure
Total Federal ARRA
Infrastructure Expenditure
Infrastructure Contact Name
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Email Infrastructure Contact Phone Infrastructure Contact Phone Ext.
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Street Address 1 Infrastructure Contact Street Address 2 Infrastructure Contact Street Address 3
10 VINING STREET Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
BOSTON MA 02115-6114
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
RESEARCH ADMINISTRATION75 FRANCIS ST Recipient responsible for this data BOSTON
State Zip Code+4 Congressional District
MA 2115 8
Country  
US

Recipient Highly Compensated Officers
Prime Recipient Indication of Reporting Applicability # Officer Name Officer Compensation
Recipient responsible for this data 1 Recipient responsible for this data Recipient responsible for this data
2 Recipient responsible for this data Recipient responsible for this data
3 Recipient responsible for this data Recipient responsible for this data
4 Recipient responsible for this data Recipient responsible for this data
5 Recipient responsible for this data Recipient responsible for this data

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The information provided by this tool is baseline data that the Recipient should include in the Recipient Report that must be submitted to FederalReporting.gov beginning October 1, 2009. The data from this tool can be cut and pasted directly into the Recipient Report.