Acetylglucosamine

Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

Glucosamine represents one of the most commonly used drugs to treat osteoarthritis. However, mechanisms of its antiarthritic activities are still poorly understood. The present study identifies a novel mechanism of glucosamine-mediated anti-inflammatory activity. It is shown that both glucosamine and N-acetylglucosamine inhibit IL-1beta- and TNF-alpha-induced NO production in normal human articular chondrocytes.

Author(s): 
Shikhman, A. R.
Kuhn, K.
Alaaeddine, N.
Lotz, M.
Publication Title: 
Annals of the Rheumatic Diseases

OBJECTIVE: To examine the therapeutic efficacy of N-acetylglucosamine (GlcNAc) in rabbits with experimental osteoarthritis (OA). METHODS: Experimental OA was induced in rabbits by anterior cruciate ligament transection (ACLT). In the first study, rabbits (six in each group) received intramuscular injections of GlcNAc or normal saline three times a week starting 1 week postoperatively. In the second study, rabbits (eight in each group) were injected intra-articularly with GlcNAc (either once or twice a week) or normal saline.

Author(s): 
Shikhman, A. R.
Amiel, D.
D'Lima, D.
Hwang, S.-B.
Hu, C.
Xu, A.
Hashimoto, S.
Kobayashi, K.
Sasho, T.
Lotz, M. K.
Publication Title: 
Journal of Immunology (Baltimore, Md.: 1950)

T cell recruitment into inflamed skin is dependent on skin-homing receptor binding to endothelial (E)- and platelet (P)-selectin. These T cell receptors, or E- and P-selectin ligands, can be targeted by the metabolic fluorosugar inhibitor, 4-F-GlcNAc, to blunt cutaneous inflammation. Compelling new data indicate that, in addition to T cells, NK cells are also recruited to inflamed skin in allergic contact hypersensitivity (CHS) contingent on E- and P-selectin-binding.

Author(s): 
Gainers, Madeliene E.
Descheny, Leyla
Barthel, Steven R.
Liu, Luzheng
Wurbel, Marc-André
Dimitroff, Charles J.
Publication Title: 
Endocrinology

We recently found that plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP(2))-regulated filamentous actin (F-actin) polymerization was diminished in hyperinsulinemic cell culture models of insulin resistance. Here we delineated whether increased glucose flux through the hexosamine biosynthesis pathway (HBP) causes the PIP(2)/F-actin dysregulation and insulin resistance induced by hyperinsulinemia.

Author(s): 
Bhonagiri, Padma
Pattar, Guruprasad R.
Horvath, Emily M.
Habegger, Kirk M.
McCarthy, Alicia M.
Elmendorf, Jeffrey S.
Publication Title: 
The Journal of Biological Chemistry

Prior studies have shown that treatment with the peracetylated 4-fluorinated analog of glucosamine (4-F-GlcNAc) elicits anti-skin inflammatory activity by ablating N-acetyllactosamine (LacNAc), sialyl Lewis X (sLe(X)), and related lectin ligands on effector leukocytes. Based on anti-sLe(X) antibody and lectin probing experiments on 4-F-GlcNAc-treated leukocytes, it was hypothesized that 4-F-GlcNAc inhibited sLe(X) formation by incorporating into LacNAc and blocking the addition of galactose or fucose at the carbon 4-position of 4-F-GlcNAc.

Author(s): 
Barthel, Steven R.
Antonopoulos, Aristotelis
Cedeno-Laurent, Filiberto
Schaffer, Lana
Hernandez, Gilberto
Patil, Shilpa A.
North, Simon J.
Dell, Anne
Matta, Khushi L.
Neelamegham, Sriram
Haslam, Stuart M.
Dimitroff, Charles J.
Publication Title: 
The Journal of Investigative Dermatology

Galectin-1 (Gal-1) has been shown to play a major role in tumor immune escape by inducing apoptosis of effector leukocytes and correlating with tumor aggressiveness and disease progression. Thus, targeting the Gal-1/Gal-1 ligand axis represents a promising cancer therapeutic approach.

Author(s): 
Cedeno-Laurent, Filiberto
Opperman, Matthew J.
Barthel, Steven R.
Hays, Danielle
Schatton, Tobias
Zhan, Qian
He, Xiaoying
Matta, Khushi L.
Supko, Jeffrey G.
Frank, Markus H.
Murphy, George F.
Dimitroff, Charles J.
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