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Charles E. Sparks, M.D.

Contact Information

Phone Numbers

Office: (585) 275-8236

Fax: (585) 756-5337

Biography

With a broad base of experience in clinical chemistry, Dr. Sparks serves as Director of the Protein Laboratory, and Associate Director of the Automated Laboratory. His primary research interest is in lipoproteins as a risk factor in the development of cardiovascular disease.

Research

Apo B exists as B48 and B100 produced through a novel posttranscriptive mechanism of apo B mRNA editing producing protein products of differing size with differing metabolisms. The goal of our research is to understand apo B triglyceride-rich lipoprotein (TRL) assembly contrasting B100 and B48 synthetic pathways. McArdle RH-7777 cells (McA) have provided many useful insights into inherent differences in B100 and B48 in TRL biogenesis. Recent studies indicate that B100-TRL assembly occurs by lipidation of conformationally "acceptable" B100. B48 undergoes initial lipidation similar to B100 followed by neutral lipidation of the precursor high density lipoprotein particle (B48-HDL) to form B48-TRL. More than 70% of the triglyceride (TG) fatty acids (FA) arise from cytosolic, stored TG through a process involving lipolysis/reesterification. Lipolyzed FAs, possibly through acylation reactions with PL intermediates, traverse the ER membrane by unknown means prior to fusion with B48-HDL. Unlike B100, that is synthesized and rapidly secreted by rat hepatocytes (RH), there is a kinetically distinct pool of B48 that has a long cellular retention time. We hypothesize that this pool may provide a ready supply of B48-HDL as a precursor for the rapid assembly of TRL via a later assembly step. In cells that make predominantly B48, such as intestine, the cellular pool of B48 allows TRL secretion to occur without a requirement for de novo apo B synthesis. We recently identified a novel protein factor, an apo B secretion enhancer (BSE), whose expression correlates with apo B mRNA abundance in McA cells transfected with BSE. Apo B mRNA abundance, however, does not correspond with a proportional increase in apo B secretion. Studies explore the role of BSE in the observed changes in apo B mRNA stability/transcription. Apo B degradation studies address the non-proportional secretory rate. A phospholipid (PL)-dependent pathway for the stimulation of apo B secretion by BSE is suggested as BSE is homologous with betaine homocysteine methyltransferase (BHMT), a methylation enzyme. An hypothesis explored is that, apart from its ability to stabilize apo B mRNA, an ER form of BSE may provide newly synthesized phosphatidylcholine (PC) via phosphatidylethanolamine (PE) methylation of phosphatidylserine (PS) and increased supply of PL may be a mechanism for the enhancing secretion of apo B.

Importance of the research is related to the role of apo B in lipid transport and as a factor associated with risk of arterial disease. Additional research focuses on the role of apo B as a risk factor in developing heart attacks, strokes, and in recurrent heart attacks in human populations.

Credentials

Faculty Appointments

Specialties

  • Clinical Pathology/Laboratory Medicine - American Board of Pathology

Education

1963
BS | Mass Inst Technology
Biochemistry

1968
MD | Jefferson Medical College
Medicine

Post-doctoral Training & Residency

07/01/1976 - 06/30/1977
Fellowship in Biochemistry at Medical College of Pennsylvania Hospital

07/01/1975 - 06/30/1976
Fellowship in Cardiopulmonary Medicine at University of Pennsylvania

07/01/1975 - 06/30/1976
Fellowship in Cardiopulmonary Medicine at University of Pennsylvania

07/01/1976 - 06/30/1977
Fellowship in Biochemistry at Medical College of Pennsylvania Hospital

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Awards

2002 - 2005
Secretarial Appointee. Department of Veterans Affairs Medical Research Service Merit Review Subcommittee for Endocrinology (Chair: Endocrinology-A Review Board, Fall 2003, Spring & Fall 2004)

1998
Co-Chair. Thrombogenic Factors and Recurrent Coronary Events Symposium, Perugia, Italy

1988
Co-Chair. National Symposium Meeting, American Diabetes Association, Lipoproteins, Diabetes and Atherosclerosis.

1981
Invited Speaker. Gordon Research Conference on Atherosclerosis: "Is intestinal apo B a determinant for lipoprotein recognition?"

1978 - 2004
Conferee. Lipid Metabolism and Atherosclerosis, 1978, '79, '80, '81, '84, '86, '88, '90, '92, '96, '00, '04 Gordon Research Conference, Kimball Union Academy, Meriden, NH

1975 - 1977
Individual Research Service Award Grantee, National Institutes of Health

1974 - 1975
Chief Resident in Pathology, University of Pennsylvania

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Publications

Journal Articles

12/2014
Corsetti JP, Gansevoort RT, Bakker SJ, Sparks CE, Vart P, Dullaart RP. "Apolipoprotein B attenuates albuminuria-associated cardiovascular disease in prevention of renal and vascular endstage disease (PREVEND) participants." Journal of the American Society of Nephrology : JASN.. 2014 Dec 0; 25(12):2906-15. Epub 2014 May 22.

6/2014
Sparks CE, Corsetti JP, Sparks JD. "High-density lipoproteins: taking the good with the bad." Current opinion in lipidology.. 2014 Jun 0; 25(3):230-2.

10/2013
Sparks CE, Sparks JD. "Hepatic postprandial transition and very low-density lipoprotein biogenesis." Current opinion in lipidology.. 2013 Oct 0; 24(5):450-2.

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