Endocrinology & Metabolic Syndrome
Open Access

Irina B. Grishina

Biography

Irina Grishina obtained her Ph.D in Biochemistry at Colorado State University based on experimental and theoretical studies in protein spectroscopy and thermodynamics. She continued on to postdoctoral training in molecular genetics of cell cycle with Roger Brent at Harvard Medical School and James Maller at University of Colorado Health Sciences Center. Since 2001, Grishina engaged in studies in organogenesis at New York University, and established a program on urogenital development in mouse models at the Department of Urology. Grishina’s laboratory is interested in defining the roles of developmental signaling factors which, in collaboration with steroid hormones, regulate growth, differentiation and tissue homeostasis of the prostate, urethra and external genitalia. Grishina’s studies are directed to elucidate the etiology of urogenital diseases and malformations, in particular, benign prostate hyperplasia, rectourethral fistulas and hypospadias.

Research Interest

1. Development and disease of the prostate gland. We have shown that developmental ligand of transforming growth factor family, Bone morphogenetic protein 7 (Bmp7), inhibits prostate branching and restricts cells positive for Notch signaling to prostate buds (Grishina et al., http://www.ncbi.nlm.nih.gov/pubmed/16324690). Gain of Notch signaling in the prostate results in abnormal proliferation of the basal and myoblast progenitor cells, which leads to benign prostate hyperplasia (BPH) by 3 months of mouse age (Wu et al., 2011a, http://dx.doi.org/10.1016/j.ydbio.2011.05.659). This disease is mediated by the Notch-dependent downregulation of the tumor-suppressor Pten, improved maintenance of p63-positive basal cells, and cell fate shift favoring myoblast over fibroblast lineages. Loss of Notch signaling during prostate development results in abnormal patterning of basal cells which acquire luminal characteristics similar as in prostate cancer. Our further studies are aimed to elucidate the role of Bmp and Notch signaling in benign prostate disease.
2. Development and malformations of the cloaca and genital appendage. Current models for cloacal septation in mammalian embryo are derived primarily from anatomical observations and many postulates require clarification and experimental proof. Our studies are aimed to clarify the genetic and cellular mechanisms of cloacal and genital development. We found that signaling by Bmp7 is essential for cloaca septation and for formation of the ventral part of the genital appendage (Wu et al., 2009, http://www.ncbi.nlm.nih.gov/pubmed/19159697). Our previous and on-going studies show that cloacal epithelium is the tissue that undergoes extensive remodeling during cloacal septation. We are further investigating the role of Bmp and Wnt signaling in during the early stages of cloacal and genital development.