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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Prime Recipient Report

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

Reporting Information

Award Type*: Grant

Award Number*: 3R00ES016723-03S1

Final Report*: Recipient responsible for this data

Award Recipient Information

Recipient DUNS Number*: 030811269

Recipient Account Number: Recipient responsible for this data

Recipient Congressional District*: 8

Award Information

Funding Agency Code*: 7529

Awarding Agency Code*:7529

Award Date*: 07-30-2009

Amount of Award*: $ 251,022

Program Source (TAS)*: 750863

CFDA Number*: 93.701

Sub Account Number for Program Source (TAS)*: Recipient responsible for this data

Total Number of Sub Awards to Individuals*: Recipient responsible for this data

Total Amount of Sub Awards to Individuals*: Recipient responsible for this data

Total Number of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Amount of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Number of Sub Awards less than $25,000/award*: Recipient responsible for this data

Total Amount of Sub Awards less than $25,000/award*: 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*: TECHNOLOGY AND ENDOTHELIAL BIOLOGY OF KIDNEY INJURY MOLECULE-1

Project Status*: Recipient responsible for this data

Total Federal Amount of ARRA Funds Received/Invoiced*: Recipient responsible for this data

Number of Jobs*: Recipient responsible for this data

Description of Jobs Created*: Recipient responsible for this data

Quarterly Activities/Project Description*: Recipient responsible for this data

Activity Code (NAICS or NTEE-NPC)*: Recipient responsible for this data

Total Federal Amount of ARRA Expenditure* (Enter the cumulative total amount of Recovery Funds received that were expended to projects or activities. Refer to the Data Model for details on how to calculate this amount.): Recipient responsible for this data

Total Federal ARRA Infrastructure Expenditure Recipient responsible for this data

Infrastructure Contact Name: Recipient responsible for this data

Infrastructure Contact Email: Recipient responsible for this data

Infrastructure Contact Phone: Recipient responsible for this data

Infrastructure Contact Phone Ext: Recipient responsible for this data

Infrastructure Contact Street Address 1: 10 VINING STREET

Infrastructure Contact Street Address 2: Not Available

Infrastructure Contact Street Address 3: Recipient responsible for this data

Infrastructure City: BOSTON

Infrastructure State: MA

Infrastructure ZIP Code+4: 02115-6114

Infrastructure Purpose and Rationale (If applicable, enter an explanation about how the infrastructure investment will contribute to one or more purposes of the Recovery Act. Refer to the Data Model for details on what to report. 4000 characters or less.): Recipient responsible for this data

Primary Place of Performance

Street Address 1: RESEARCH ADMINISTRATION75 FRANCIS ST

Street Address 2: BOSTON

City*: BOSTON

State*: MA

ZIP Code+4*: 2115

Congressional District*: 8

Country*: US

Recipient Highly Compensated Officers

Prime Recipient Indication of Reporting Applicability*: Recipient responsible for this data

1. Officer Name and Compensation: Recipient responsible for this data
2. Officer Name and Compensation: Recipient responsible for this data
3. Officer Name and Compensation: Recipient responsible for this data
4. Officer Name and Compensation: Recipient responsible for this data
5. Officer Name and Compensation: Recipient responsible for this data

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