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Rheumatic diseases

Senior Researchers:

Professor Hans Carlsten

Centre for Bone and Arthritis Research

Postmenopausal RA is characterized by dramatic bone loss due to systemic inflammation and loss of endogenous estrogen. ER activation can ameliorate arthritis and preserve bone. The long-term goal of this module is to establish ER-specific ligands that reproduce these beneficial effects of natural estrogens but not their adverse side effects. Such ligands have significant clinical therapeutic potential.

Preclinical research
Recent studies show that certain populations of immune cells affect bone mass regulation. Drs. Carlsten and Tarkowski will determine which immune mechanisms are important for SS modulation of bone. Administration of corticosteroids increases the risk of osteoporosis and arteriosclerosis. To test the hypothesis that natural and synthetic estrogens could protect against these side effects, they will establish a murine model of corticosteroid-induced osteoporosis.

These investigators will continue to dissect the beneficial testosterone-mediated effect of ethanol on inflammatory responses, focusing on joint inflammation and destruction. Specifically, they will (1) further characterize intracellular transcription pathways that mediate the anti-inflammatory properties of ethanol (NF-kB, AP-1, MAP-kinases, and IKAROS transcription factors); (2) determine if increased testosterone levels affect the sensitization phase or the effector phase of the in vivo inflammatory process; (3) assess the effect of ethanol analogues lacking euphoric properties on SS production; and (4) determine if ethanol influences the release of testosterone at the hypothalamic, pineal gland, or gonadal level.

Genetic epidemiology
In other studies, Dr. Carlsten will look for human gene polymorphisms at the ERa and ERb locus. A polymorphism is a plausible molecular mechanism for individual differences in the sensitivity of the immune system to estrogen.

Page Manager: Marie Lagerquist|Last update: 12/10/2010

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