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SUNY Downstate Medical Center

Department of Cell Biology

photo of Xian-cheng Jiand

Xian-cheng Jiang, PhD

Professor

Department of Cell Biology

Tel: (718) 270-6701 • Fax: (718) 270-3732

e-mail: xjiang@downstate.edu

Lipid Metabolism and Metabolic Diseases:

Research Interests: The primary interest of my laboratory is to investigate the effect of lipid metabolism and metabolic diseases, such as atherosclerosis, metabolic syndrome, obesity, and liver steatosis. We are particularly interested in understanding how phospholipid metabolism influences plasma lipoprotein metabolism, cell membrane lipid composition and function, and the development of metabolic diseases. 

We have three on-going specific aspects:

  1. Sphingomyelin biosynthesis. Sphingomyelin is one of the major phospholipids on the cell membrane and in the circulation. The biochemical synthesis of sphingomylin occurs through the actions of serine palmitoyl-CoA transferase (SPT), 3-ketosphinganine reductase, ceramide synthase, dihydroceramide desaturase and sphingomyelin synthase (SMS). We are studying the impact of SPT and SMS activity on lipid metabolism and disease development, using systemic gene knockout or overexpression, and tissue specific gene knockout or overexpression approaches.
  2. Phosphotidycholine (PC) remodeling. PC is the major lipid on cell membrane and all plasma lipoproteins. PCs are first synthesized from glycerol-3-phosphate in the de novo pathway, and undergo maturation in the remodeling pathway, as reported by Lands (Lands’ cycle). The remodeling process, which concerns the turnover of about half of the PC molecules, involves the deacylation of PC to lysophosphatidylcholine (lysoPC), followed by reacylation of lysoPC to PC. The deacylation is catalyzed by calcium independent phospholipase A2 (iPLA2) and the reacylation is catalyzed by lysophosphatidylcholine acyltransferase (LPCAT). We are studying LPCAT function, using systemic or tissue specific gene knock out mouse models. 
  3. Phospholipid transfer protein (PLTP). PLTP is an independent risk factor for human coronary artery diseases. In mouse models, it has been shown that systemic PLTP deficiency reduces atherosclerosis,  while its overexpression demonstrates the opposite effect. Therefore, PLTP is considered a promising target for pharmacological intervention in atherosclerosis. However, the mechanisms involved in these reactions are not entirely clear. For better understanding of them, we are evaluating the effect of PLTP on lipoprotein production, using mouse models (systemic or tissue specific knockout) available in our laboratory.

List of Publications (Pub Med)