Biomedical Research Education & Training
Faculty Member

Russell, Shirley Brody, Ph.D.
Research Assistant Professor of Medicine

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Russell, Shirley's picture
Academic history
B.A., University of Rochester
Ph.D., University of Wisconsin, Madison
Postdoc., Harvard Medical School

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3793 TVC 5227

Research Specialty
The pathogenesis of keloids and the genetic basis of this connective tissue disorder

Research Description
Dr. Russell's research is focused on hormonal and cytokine regulation of growth and matrix synthesis in human fibroblasts and characterization of the wound healing response in dermis and gingiva. A long-term goal is to elucidate the molecular basis for the formation of keloids, which are benign dermal tumors that develop during wound healing in genetically predisposed persons. Because the regulators involved in wound healing and their signal transduction pathways are relevant to so many major questions in biology and medicine, these studies may help elucidate the pathogenesis of other diseases involved in abnormal tissue repair, including atherosclerosis, rheumatoid arthritis, uterine fibroma, and gingival hyperplasia. Dr. Russell is Associate Dean for Research, School of Dentistry and the Director of the Regional Research Center for Minority Oral Health.

Meyer LJ, Russell SB, Russell JD, Trupin JS, Egbert BM, Shuster S, Stern R. Reduced hyaluronan in keloid tissue and cultured keloid fibroblasts. J Invest Dermatol., 114(5), 953-959, 2000

Russell SB, Trupin JS, Kennedy RZ, Russell JD, Davidson JM. Glucocorticoid regulation of elastin synthesis in human fibroblasts: down-regulation in fibroblasts from normal dermis but not from keloids. J Invest Dermatol., 104(2), 241-245, 1995

Myles ME, Russell JD, Trupin JS, Smith JC, Russell SB. Keloid fibroblasts are refractory to inhibition of DNA synthesis by phorbol esters. Altered response is accompanied by reduced sensitivity to prostaglandin E2 and altered down-regulation of phorbol ester binding sites. J Biol Chem., 267(13), 9014-9020, 1992

Russell SB, Trupin JS, Myers JC, Broquist AH, Smith JC, Myles ME, Russell JD. Differential glucocorticoid regulation of collagen mRNAs in human dermal fibroblasts. Keloid-derived and fetal fibroblasts are refractory to down-regulation. J Biol Chem., 264(23), 13730-13735, 1989

Russell SB, Trupin KM, Rodriguez-Eaton S, Russell JD, Trupin JS. Reduced growth-factor requirement of keloid-derived fibroblasts may account for tumor growth. Proc Natl Acad Sci U S A, 85(2), 587-591, 1988

Gadson PF, Russell JD, Russell SB. Glucocorticoid receptors in human fibroblasts derived from normal dermis and keloid tissue. J Biol Chem , 259, 11236-11241, 1984

Russell SB, Russell JD, Trupin JS. Hydrocortisone induction of system A amino acid transport in human fibroblasts from normal dermis and keloid. J Biol Chem , 259, 11464-11469, 1984

Trupin JS, Russell SB, Russell JD. Variation in prolyl hydroxylase activity of keloid-derived and normal human fibroblasts in response to hydrocortisone and ascorbic acid. Coll Relat Res , 3, 13-23, 1983

Russell JD, Russell SB, Trupin KM. Fibroblast heterogeneity in glucocorticoid regulation of collagen metabolism: genetic or epigenetic? . In Vitro , 18(6), 557-564, 1982

Russell SB, Russell JD, Trupin JS. Alteration of amino acid transport by hydrocortisone. Different effects in human fibroblasts derived from normal skin and keloid. J Biol Chem , 257, 9525-9531, 1982

Postdoctoral Position Available

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