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Email

sheikh@bcm.edu

Positions

Professor

Medicine-Nephrology
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Houston, TX US

Education

B.Sc. from Hebrew University Of Jerusalem

01/1976 - Jerusalem, Israel

M.D. from Hadassah Medical School

01/1981 - Jerusalem, Israel

Advanced Training from University Of California, Los Angeles

01/1984 - Los Angeles, CA United States

Advanced Training from National Institutes Of Health

01/1991 - Bethesda, MD United States

Certifications

ABIM-Medicine

#115454

ABIM

Valid indefinitely

ABIM-Nephrology

#115454

ABIM

Re-certified 2002

Honors & Awards

Fulbright & Jaworski L. L. P. Faculty Excellence Award

Recipient of ����������� Fulbright & Jaworski L. L. P. Faculty Excellence Award for Teaching and Evaluation (8/2007).

����������� (08/2007)

Award for Excellence in Teaching

Award for Excellence in Teaching (2001-2002): Department of Medicine, �����������.

BCM (07/2002)

Elected Member, Leadership Committee of KCVD

Member at-Large (Elected): Leadership Committee of the Council on the Kidney in Cardiovascular Disease (KCVD); AHA, 7/2005 - 2010.

AHA (07/2005)

Member, Nominating Committee, KCVD

Member: Nominating Committee of the AHA Council on Kidney in Cardiovascular Disease (KCVVD), 2004-2010.

AHA (07/2004 - 06/2010)

Member of the Academy of Distinguished Educators

Member of the Academy of Distinguished Educators, ����������� (8/2007)

BCM (07/2007)

Professional Interests

• Riverside Clinic
• Kidney Protection via Metabolic Sensors

Websites

Professional Development

Renal Grand Rounds

Conference (Organizer, 2009)

Sponsor: BCM/Methodist Hospital

Weekly conference presented by national and international nephrology leaders, and features state-of-the-art lectures and new advances in nephrology.

Selected Publications

• "http://www-ncbi-nlm-nih-gov.ezproxyhost.library.tmc.edu/pubmed/?term=sheikh-hamad." ;
• Christensen BM, Marples D, Jensen UB, Frokiaer J, Sheikh-Hamad D, Knepper M, Nielsen S "." Am. J. Physiol.. 1998 Aug;275(2):F285-97. Pubmed PMID:
• Morduchowicz GA, Sheikh-Hamad D, Dwyer BE, Stern N, Jo OD, Yanagawa N "." J. Membr. Biol.. 1991 May;122(1):43-53. Pubmed PMID:
• Huang L, Garcia G, Lou Y, Zhou Q, Truong LD, DiMattia G, Lan XR, Lan HY, Wang Y, Sheikh-Hamad D "." Am. J. Pathol.. 2009 Apr;174(4):1368-78. Pubmed PMID:

Funding

Stanniocalcin-1: New paradigms for cytoprotection and anti-inflammation - #I01BX002006

$600,000.00 (04/01/2014 - 09/30/2018)

Grant funding from Veteran Administration

Reactive oxygen species (ROS), endothelial injury and macrophages play critical roles in ischemia/reperfusion (I/R) kidney injury. Our data show stanniocalcin-1 (STC1) diminishes superoxide generation in macrophages, through induction of uncoupling protein-2 (UCP2), decreases the response of macrophages to chemoattractants- and migration across an endothelial monolayer. In cultured endothelial cells, STC1 preserve barrier function. STC1: diminishes superoxide generation; inhibits cytokine-induced activation of Jun-N-terminal kinase (JNK) and loss of tight junction proteins expression. STC1 transgenic mice, which exhibit elevated serum levels and preferential expression of STC1 in macrophages and endothelium, display resistance to I/R kidney injury. Overall hypothesis: STC1 protects from I/R kidney injury through: suppression of superoxide generation; maintenance of normal endothelial barrier function following I/R kidney injury; and inhibition of macrophages. In Objective I, we will determine the role of superoxide and Daxx in STC1-mediated inhibition of JNK in endothelial cells. In Objective II, we will determine the effect of STC1 on hypoxia/reoxygenation (H/RO)-induced changes in the expression and assembly of tight junction proteins in cultured primary kidney endothelial cells. In the context of I/R kidney injury, Objective III will examine endothelial leakage to macromolecules, kidney inflammation and function after kidney endothelium-specific or macrophage-specific overexpression or deletion of STC1. Few therapeutic options are currently available for acute kidney injury (AKI). Our data identify STC1 as a potential therapeutic target for ischemic injury in the kidney and other organs, and our proposed studies will further elucidate STC1 mechanisms of action.

Stanniocalcin-1, a novel anti-inflammatory protein - #R01DK080306

$1,738,389.00 (08/01/2009 - 07/31/2015)

Grant funding from NIH

Macrophages are important mediators of inflammation. Our data show stanniocalcin-1 (STC1) decreases macrophage response to chemoattractants and migration across an endothelial monolayer. STC1 also diminishes superoxide generation in macrophages, by inducing uncoupling protein-2 (UCP2), and inhibits the NF-B pathway. In cultured endothelial cells, STC1 inhibits cytokine-induced changes in permeability and tight junction protein expression. STC1 transgenic mice, which exhibit elevated serum levels and preferential expression of STC1 in macrophages and endothelium, display less inflammatory macrophages in the glomeruli during anti-glomerular basement membrane (GBM) disease, resulting in kidney protection. Overall hypothesis: STC1 suppresses inflammation through inhibition of macrophage recruitment and function, and cytokine-induced increase in endothelial permeability. In Specific Aim I, we will determine mechanisms of UCP2 upregulation by STC1 and the role of superoxide in STC1-mediated inhibition of NF-B in macrophages. In Specific Aim II, we will determine the effect of STC1 on cytokine–induced changes in expression and assembly of tight junction proteins in cultured primary kidney endothelial cells. In Specific Aim III, in the context of anti-GBM disease, we will examine endothelial permeability of native kidney vessels, as well as kidney inflammation and function, after kidney endothelium-specific or macrophage-specific overexpression or deletion of STC1.

Languages

Hebrew, Arabic