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Winthrop University Hospital

Jodi F. Evans, PhD

Winthrop Titles/Positions

Assistant Scientist Winthrop University Hospital Research Institute

Academic Faculty Appointments

Assistant Professor, Molloy College


Suite 623 222 Station Plaza North Mineola, NY 11501


Suite 623 222 Station Plaza North Mineola, NY 11501




Brief Resume

Dr. Evans first joined the Winthrop Research Team in 1996, working under the direction of Dr. James K. Yeh. She spent many years with Dr. Yeh successfully investigating many aspects of bone and cartilage biology. In 2006, Dr. Evans earned her Ph.D. from St. John's University, after which she joined the laboratory of Dr. Louis Ragolia, the director of the Biomedical Research Core, as a post-doctoral researcher. Dr. Evans is a recent recipient of the NIH Pathway to Independence Award (K99/R00) and is developing an independent research path that bridges bone and cartilage biology with cardiovascular pathology.

Description of Research Interests/Activities

Dr. Evans hopes to find a link between increased exposure to stress hormones and calcified atherosclerotic lesion development. Increased stress, manifested by increased activity of the hypothalamic-pituitary-adrenal (HPA) axis has long been linked to increased risk for atherosclerosis. Populations at increased risk for the development of calcified atherosclerotic lesions; the obese, diabetics and the aging, also have hyperactive HPA axes. Recent studies have identified chondrocyte-like cells undergoing endochondral differentiation as an initiating factor in the formation of calcified regions within atherosclerotic lesions. HPA hormones facilitate chondrogenic differentiation of cultured multipotential mesenchymal cells and accelerate the differentiation of chondroprogenitors along the endochondral pathway. Dr. Evans’ project is designed to investigate the contribution of HPA axis hyperactivity on pre-mature cartilage metaplasia and ultimate calcification of atherosclerotic lesions of the diabetic mouse. She is also examining the chondrogenic potential of mesenchymal stem cells of the aorta and their response to HPA hormone exposure.

Areas of Experience

Bone & Mineral Metabolism


Selected Publications

1: Evans JF, Lee JH, Ragolia L. Ang-II-induced Ca(2+) influx is mediated by the
1/4/5 subgroup of the transient receptor potential proteins in cultured aortic
smooth muscle cells from diabetic Goto-Kakizaki rats. Mol Cell Endocrinol. 2009
Apr 10;302(1):49-57. Epub 2008 Dec 24. PubMed PMID: 19135126.

2: Yeh JK, Evans JF, Niu QT, Aloia JF. A possible role for melanocortin peptides
in longitudinal growth. J Endocrinol. 2006 Dec;191(3):677-86. PubMed PMID:

3: Evans JF, Shen CL, Pollack S, Aloia JF, Yeh JK. Adrenocorticotropin evokes
transient elevations in intracellular free calcium ([Ca2+]i) and increases basal
[Ca2+]i in resting chondrocytes through a phospholipase C-dependent mechanism.
Endocrinology. 2005 Jul;146(7):3123-32. Epub 2005 Mar 31. PubMed PMID: 15802497.

4: Evans JF, Niu QT, Canas JA, Shen CL, Aloia JF, Yeh JK. ACTH enhances
chondrogenesis in multipotential progenitor cells and matrix production in
chondrocytes. Bone. 2004 Jul;35(1):96-107. PubMed PMID: 15207745.
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