Funk, J. L. (2018). From bedside to bench and back again: investigating medicinal effects of turmeric on bone.. Entorno UDLAP.
Hutchison, J., Cohen, Z., Onyeagucha, B. C., Funk, J., & Nelson, M. A. (2013). How microRNAs influence both hereditary and inflammatory-mediated colon cancers. CANCER GENETICS, 206(9-10), 309-316.
Funk, J. L., Wei, H., Downey, K. J., Yocum, D., Benjamin, J. B., & Carley, W. (2002). Expression of PTHrP and its cognate receptor in the rheumatoid synovial microcirculation. Biochemical and biophysical research communications, 297(4), 890-7.
Parathyroid hormone-related protein (PTHrP), a multifunctional peptide that acts as a vasodilator as well as possible regulator of vascular development, is produced in increased amounts in the rheumatoid synovium. To understand whether PTHrP can contribute to the development and function of the rheumatoid microcirculation, studies were undertaken to identify and compare vascular sites of expression of PTHrP and its cognate receptor in the rheumatoid synovium and/or in cultured rheumatoid synovial endothelial cells. Endothelial cells, including apoptotic cells, as determined by TUNEL staining, were the primary site of vascular PTHrP expression in the rheumatoid synovium, a result confirmed in vitro in rheumatoid synovial microvascular endothelial cells. In contrast, the PTH/PTHrP receptor was primarily located in pericytes and smooth muscle cells within the vasculature. These results are consistent with a possible paracrine pathway for PTHrP action in the synovial microcirculation, wherein PTHrP peptides secreted by the synovial endothelium could act on surrounding PTH1R-positive pericytes and smooth muscle cells.
Funk, J. L., Chen, J., Downey, K. J., & Clark, R. A. (2008). Bone protective effect of simvastatin in experimental arthritis. The Journal of rheumatology, 35(6), 1083-91.
Emerging evidence suggests that clinically important antiinflammatory effects of HMG-CoA reductase inhibition may extend beyond cardiovascular disease to other inflammatory disorders, such as rheumatoid arthritis (RA). Protective bone-specific anabolic and antiresorptive effects of HMG-CoA reductase inhibitors have also been evaluated in normal and osteoporotic bone. The specific effect of statins on inflammation-induced bone loss has not previously been a focus of evaluation. We investigated whether simvastatin, a potent HMG-CoA reductase inhibitor, alters bone turnover in an animal model of RA, thus preventing periarticular bone loss.
Ritter, L., Davidson, L., Henry, M., Davis-Gorman, G., Morrison, H., Frye, J. B., Cohen, Z., Chandler, S., McDonagh, P., & Funk, J. L. (2011). Exaggerated neutrophil-mediated reperfusion injury after ischemic stroke in a rodent model of type 2 diabetes. Microcirculation (New York, N.Y. : 1994), 18(7), 552-61.
We tested the hypothesis that both chronic and acute inflammatory processes contribute to worse reperfusion injury and stroke outcome in an experimental model of T2DM.