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Faculty Detail Faculty Entry   
Name ROSA A SERRA  
Campus Address MCLM 660 Zip 0005
Phone 205-934-0842
E-mail rserra@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:rserra@uab.edu">rserra@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Pathology   Cell Adhesion & Matrix Research Center Professor
Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor

Biographical Sketch 
Rosa Serra, Professor of Cell Biology, received her B.S. degree in Biology from St. Louis University in 1986 and her Ph.D. degree in Molecular and Cellular Biology from The Pennsylvania State University, College of Medicine in 1992. Dr. Serra pursued her postdoctoral fellowship in the laboratory of Dr. Harold Moses at Vanderbilt University then continued at Vanderbilt as a Research Assistant Professor in Cell Biology. In 1999, Dr. Serra was appointed to the faculty of Molecular and Cellular Physiology at the University of Cincinnati, College of Medicine. Dr. Serra joined the UAB faculty in 2002.

Society Memberships
Organization Name Position Held Org Link
No records
 

Research/Clinical Interest
Title
Mechanism of TGF-ß Action in Developmental and Disease Processes
Description
The TGF-ß family of polypeptides consists of multifunctional factors involved in the development of many organ systems and in the progression of disease. One of the main functions of TGF-ß is to mediate signaling between cell types during the formation of various organ systems. The overall goal of the laboratory is to understand the role and mechanism of TGF-ß signaling in embryonic and post-natal development and to apply this knowledge to the understanding and treatment of human degenerative and neoplastic disease.

We are using several molecular and genetic tools to address these issues, including transgenic mice, mouse organ cultures, primary cell cultures, adenovirus expression systems, as well as subtractive libraries and gene arrays. One of our objectives is to investigate the role of TGF-ß signaling in stromal epithelial interactions during normal mammary gland development and tumor progression. The overall hypothesis of this study is that TGF-ß signaling in the mammary stroma affects branching morphogenesis and tumor development by regulating the expression of specific genes in mammary gland fibroblasts. Data from transgenic mouse studies suggest that TGF-ß signaling in the stroma normally acts to limit branching. We are currently elucidating the mechanism of TGF-ß action in the mammary gland through a variety of in vitro and in vivo techniques.

Another objective is to provide insight into mechanisms of chondroprotection through an understanding of the signals involved in the formation of articular cartilage. To this end, we generated transgenic mice that express a dominant-negative mutation of the TGF-ß type II receptor (MT-DNIIR). The phenotype of these mice suggest that endogenous TGF-ßs act as chondroprotective agents, however, the mechanism of TGF-ß’s chondroprotective effects are not known. One of the ways to address this issue is through a global analysis of gene expression. Interesting biological pathways are starting to emerge from this analysis. How TGF-ß regulates these biological processes and their role in the chondrocyte phenotype will now be determined. We are also using an embryonic mouse metatarsal organ culture model and a cre/lox transgenic mouse strategy to study the molecular pathways that regulate endochondral bone formation. These models facilitate determination of how different growth factors and cell types interact to regulate chondrocyte proliferation and differentiation.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Sohn P, Cox M, Chen D, Serra R. Molecular profiling of the developing mouse axial skeleton: a role for Tgfbr2 in the development of the intervertebral disc. BMC Dev Biol. 2010  20214815 
Loss of TGF-ß or Wnt5a results in an increase in Wnt/ ß-catenin activity and redirects mammary tumor phenotype. Breast Cancer Research 11: R19 2009.  19344510 
Haycraft CJ and Serra R. Cilia involvement in patterning and maintenance of the skeleton. Curr Top Dev Biol 85:303-332, 2008.
 		 19147010  
Seo H-S, Serra R Deletion of Tgfbr2 in Prx1-cre expressing limb mesenchyme results in defects in the development of the long bone and joints. Developmental Biology 310:304-316, 2007.  17822689 
Roarty K and Serra R. Wnt5a is required for proper mammary gland development and TGF-ß mediated inhibition of ductal growth. Development 134:3929-3939, 2007.  17898001 
Song B, Haycraft CJ, Yoder B, Serra R, Intraflagellar transport proteins are required for post-natal development of the growth plate. Developmental Biology 305:202-216, 2007.  17359961 
Serra R, Crowley MR. Mouse models of TGF-ß signaling in breast development and disease. Endocrine-related Cancer, 12:721-747 2005.  16322320 
Baffi, MO, Slattery E, Sohn P, Moses HL, Chytil A, Serra R ,: Conditional Deletion of the TGF-b Type II Receptor in Col2a Expressing Cells Results in Defects in the Axial Skeleton Without Alterations in Chondrocyte Differentiation or Embryonic Development of Long Bones. Developmental Biology, 276:124-142, 2004   15531369 
Alvarez J, Sohn P, Zeng X, Doetchman T, Robbins D, Serra R: TGF-ß2 mediates the effects of Hedgehog on Hypertrophic Differentiation and PTHrP Expression. Development 129:1913-1924, 2002.   11934857 
Serra R, Johnson M, Filvaroff E, Laborde J, Sheehan D, Derynck R, Moses HL: Expression of a truncated kinase defective TGF-ß type II receptor in mouse skeletal tissue results in defects in chondrocyte differentiation and an osteoarthritis-like phenotype. Journal of Cell Biology 139:541-552, 1997.   9334355 
 

Keywords
breast cancer, stromal-epithelial interactions, osteoarthrits, endochondral bone formation, developmental biology

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