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Michael C. Seeds, Ph.D.

 

Assistant Professor, Internal Medicine-Molecular Medicine; Pulmonary, Critical Care, Allergy and Immunologic Diseases

 

Email: mseeds@wfubmc.edu

 

 

Education:

Wake Forest University, Department of Medicine, Section on Infectious Diseases, fellowship, 1987-1988

Wake Forest University, Department of Biochemistry (then Bowman Gray School of Medicine), Ph.D., 1987

University of Virginia, Department of Biology, M.S. 1981

University of Virginia, Department of Biology, B.A.  1976

 

Research Interests: The regulation of granulocyte

secretory phospholipases A2 and their contribution to inflammation and host defense.


  Current Research:

The research focus of the laboratory is the function and regulation of granulocyte secretory phospholipases A2 (sPLA2).  The sPLA2s are small (~14 kD) enzymes that hydrolyze predominantly extracellular phospholipids. The combined biochemistry of sPLA2s provides a diversity of function through their and their free fatty acid and lysophospholipid products. These functions including release of inflammatory lipid mediators; microbicidal activity; membrane remodeling during cell activation, growth, and cell death; and membrane phospholipid digestion following phagocytosis. Over-activation of sPLA2 and the subsequent unregulated hydrolysis of host tissue phospholipids can contribute to several human pathologies. Primary cells (human neutrophils and eosinophils), cell lines, and mouse models are utilized to study the regulation of sPLA2s during inflammation.  These laboratory studies utilize a variety of techniques, including molecular biology, microscopy, biochemistry, and cell physiology to understand the function and regulation of these enzymes.  Collaborations include investigations of surfactant injury during asthma, granulocyte apoptosis, innate immunity, and genetic variations in sPLA2 genes which impact on pulmonary diseases. 

 

Publications:

Sivertson KL, Seeds MC, Long DL, Peachman KK, Bass DA. The differential effect of dexamethasone on granulocyte apoptosis involves stabilization of Mcl-1L in neutrophils but not in eosinophils. Cell Immunol. 2007 Jun 13.

 

El Mezayen R, El Gazzar M, Seeds MC, McCall CE, Dreskin SC, Nicolls MR. Endogenous signals released from necrotic cells augment inflammatory responses to bacterial endotoxin. Immunol Lett. 2007 Jul 31;111(1):36-44. Epub 2007 May 25.

 

 

Hite RD, Seeds MC, Jacinto RB, Grier BL, Waite BM, Bass DA. Lysophospholipid and fatty acid inhibition of pulmonary surfactant: non-enzymatic models of phospholipase A2 surfactant hydrolysis. Biochim Biophys Acta. 2005 Dec 30;1720(1-2):14-21.

 

Pascual RM, Carr EM, Seeds MC, Guo M, Panettieri RA Jr, Peters SP, Penn RB. Regulatory features of interleukin-1beta-mediated prostaglandin E2 synthesis in airway smooth muscle. Am J Physiol Lung Cell Mol Physiol. 2006 Mar;290(3):L501-8.

 

Hite RD, Seeds MC, Safta AM, Jacinto RB, Gyves JI, Bass DA, Waite BM. Lysophospholipid generation and phosphatidylglycerol depletion in phospholipase A(2)-mediated surfactant dysfunction. Am J Physiol Lung Cell Mol Physiol. 2005 Apr;288(4):L618-24.

 

Publications:
For a listing of additional publications, refer to PubMed, a service provided by the National Library of Medicine