Susan Berry, M.D.

Professor
Department of Pediatrics
Ph: (612) 624-7144
4-150 MoosTower
e-mail: berry002@umn.edu

Research Interests

The major priority in Dr. Berry's laboratory is defining the molecular actions of growth hormone. She uses the model of the rat serpin multigene family, as several rat serpins are growth hormone responsive and developmentally expressed. As such, they are useful for investigation of the role(s) that hormones have in influencing the program of orderly gene expression in development. She developed the rat Spi 2.1 locus as a model system for the study of growth hormone response: this gene is now the most frequently used and best characterized model for the study of growth hormone action. Current projects include definition of the cis DNA element binding the GH inducible nuclear factor (GHINF) complex and determining the additional components of the GHINF complex, having demonstrated the participation of Stat5 in this signal transduction pathway.

In addition, the serpins respond to acute phase stimuli (inflammation). Several lines of evidence suggest there may be an interaction between this normal physiologic response to stress and growth regulation. Investigation of this interaction may provide new insights into the the modulation of growth and the role of serpins in this modulation. In the rat Spi 2 locus there are both negative and positive acute phase reactants, while the promoters for these genes remain highly homologous. This permits a detailed examination of the interaction of both cis and trans factors in the coordinate regulation of the positive and negative responses to inflammation. Her current project in this area is defining the role of STAT proteins in the response to inflammation, using the rat Spi 2 gene model.

An additional area of investigation in the lab is to define molecular mechanisms by which gene expression can be altered during maturation, and to evaluate the participation of hormonal signals in development. Prenatal growth may be mediated by different hormonal stimuli than growth after birth. Work is ongoing to define the participation of GH in perinatal growth and gene expression, currently investigating a relative resistance to growth hormone action in perinatal life.

Recent Publications

• Berry SA, Bergad PL, Stolz AM, Towle HC, and Schwarzenberg SJ: Regulation of Spi 2.1 and 2.2 gene expression after turpentine inflammation: discordant responses to IL-6. Amer J Physiol 276 (Cell Physiol):C1374-C1382, 1999
• Bergad PL, Towle HC, and Berry SA: Definition of a high affinity growth hormone DNA response element. Mol Cell Endocrinol 150:151-159, 1999
• Humbert JT, Bergad PL, Masha O, Stolz A, Kaul S, Berry SA: Growth hormone action in hypothyroid infant rats. Pediatr Res, 47(2):250-255, 2000
• Bergad PL, Towle HC, Berry SA. YY1 and glucocorticoid receptor participate in the Stat5-mediated growth hormone response of the Spi 2.1 gene J Biol Chem 275(11):8114-8120, 2000
• Bergad PL, Schwarzenberg SJ, Amarasinghe S, Humbert JT, Towle HC, Berry SA. Inhibition of growth hormone action in models of inflammation. Am J Physiol, 279:C1906-C1917, 2000