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Rajeev tajhya baylor college of medicine email
Rajeev tajhya baylor college of medicine email








rajeev tajhya baylor college of medicine email rajeev tajhya baylor college of medicine email rajeev tajhya baylor college of medicine email

Treatment with a KCa1.1 channel blocker at the onset of clinical signs stopped disease progression in the PIA and CIA models, reduced joint and bone damage, and inhibited FLS invasiveness and proliferation. Inhibiting the function or expression of KCa1.1 ex vivo reduced proliferation and invasive properties of, as well as protease production by, PIA FLS, whereas opening native KCa1.1 or overexpressing the channel enhanced the invasiveness of both FLS from rats with PIA and FLS from healthy rats. In contrast, FLS from healthy rats expressed fewer of these channels. We found that PIA FLS expressed the KCa1.1 channel as their major potassium channel, as has been found in FLS from patients with RA. Finally, we determined the effectiveness of modulating KCa1.1 in 2 rat models of RA, moderate PIA and severe collagen-induced arthritis (CIA). We then used ex vivo functional assays combined with small interfering RNA–induced knockdown, overexpression, and functional modulation of KCa1.1 in PIA FLS. We compared KCa1.1 expression levels in FLS from rats with pristane-induced arthritis (PIA) and in FLS from healthy rats. 1 (the lack of Ca2 in the Baylor College of Medicine institutional animal. The purpose of this study was to define the importance of KCa1.1 (BK, Maxi-K, Slo1, KCNMA1) channel expression and function in FLS and to establish these channels as potential new targets for RA therapy. Rodrguez de la Vega, Gustavo Pedraza-Alva, Rajeev B. Department of Molecular Physiology and Biophysics, Mail Stop BCM335, Room S409A, Baylor College of Medicine, Houston, TX, 77030, USA Zoltán Peth, Mark R. Female Lewis rats were purchased from Taconic (Germantown, NY, USA) and housed in autoclaved setup with food and water ad libitum in an Association for Assessment and Accreditation of Laboratory. His summer project was entitled 'Synthesis, Stability, and Cytotoxicity of the Glutathione-Sulfonium Metabolite of the Anti-Cancer Drug, Busulfan'. Baylor College of Medicine follows the requirements of the Guide for the Care and Use of Laboratory Animals (National Research Council, 8th edition). Fibroblast-like synoviocytes (FLS) participate in joint inflammation and damage in rheumatoid arthritis (RA) and its animal models. CANDIDATE AT BAYLOR MEDICAL COLLEGE While a student at Salem International University, Rajeev Tajhya was a WV-INBRE summer intern in 2006 in the lab of Dr.










Rajeev tajhya baylor college of medicine email