Cam Patterson, M.D.



  • B.A., Vanderbilt University, 1985
  • M.D., Emory University School of Medicine, 1989
  • Resident and Chief Resident, Internal Medicine, Emory University Affiliated Hospitals, 1989-1993
  • Research Fellow, Cardiovascular Biology Laboratory, Harvard School of Public Health, 1993-1996
  • Clinical Fellow, Cardiology, The University of Texas Medical Branch at Galveston, 1997-1999

Funding Sources

  • National Institutes of Health
  • Cystic Fibrosis Foundation
  • Foundation Milena Carvajal-Pro Kartagener

Research Interests

The Patterson laboratory has two major ongoing efforts. The first is to understand the transcriptional programs regulating endothelial cell differentiation and cell type-specific gene expression. We postulate a two-step transcriptional response that mediates endothelial cell differentiation. The first step would involve a transcriptional program that activates expression of genes required for determination of the endothelial cell lineage. The second step would determine expression of genes characteristic of, but not necessarily specific for, the endothelial cell lineage. To determine the factors involved in early steps in endothelial cell differentiation, we are using the KDR/flk-1 promoter as a model. Using a combination of transient transfection assays, DNA-protein and protein-protein interaction experiments, and transgenic models, we have identified important cis-acting elements in the 5' flanking sequence and 1st intron of this gene, and we are in the process of determined the unique transcription factors interacting with this sequence. In an attempt to identify factors comprising the second step in the endothelial cell transcriptional response, we have been searching for transcription factors in endothelial cells that are inducible by the potent angiogenic factor VEGF. Our ultimate goal is to define the cascade of transcription factors involved in the endothelial cell differentiation process, based on the assumption that these same factors will participate in endothelial cell phenotypic expression in cardiovascular disease.

In a second project, our laboratory is exploring the interface between mechanisms of protein folding and protein degradation, particularly as these processes relate to modulation of the stress reponse in tissues such as the ischemic myocardium and in transformed cell types. As a model, we have examined the function of a novel, highly conserved protein identified in our laboratory that we call CHIP. Our most recent experiments have demonstrated that CHIP itself is a ubiquitylation factor that determines the ubiquitylation and degradation of proteins that interact with the molecular chaperones Hsc70 and Hsp90, and thus provides protection to cells under conditions of stress. Consistent with this hypothesis, we have generated mice that are deficient in CHIP (CHIP -/-), and find that cells in these mice are susceptible to stress-induced apoptosis. Our major goals for the future will be to determine how CHIP mediates its antiapoptotic effects and to determine how this effect modifies cardiac responses to ischemia and hypertrophy.

Selected Publications

PubMed 1

  • Kedar V, McDonough H, Arya R, Li H-H, Willis M, Rockman HA, Patterson C. Muscle-specific Ring Finger 1 is a bona fide ubiquitin ligase that degrades cardiac troponin I. Proceedings of the National Academy of Sciences USA, (2005).
  • Li H-H, Kedar V, Zhang C, McDonough H, Arya R, Wang D-Z, Patterson C. Atrogin-1 inhibits calcineurin-dependent cardiac hypertrophy by participating in an SCF ubiquitin ligase complex. Journal of Clinical Investigation, 114: 1058-1071 (2004).
  • Arya R, Kedar V, Hwang JR, McDonough H, Li H-H, Taylor J, Patterson C. Muscle ring finger protein-1 inhibits PKC? activation and prevents cardiomyocyte hypertrophy. Journal of Cell Biology, 164: (2004).
  • Aitsebaomo J, Wennerberg K, Der CJ, Zhang C, Kedar V, Kingsley-Kallesen ML, Zeng G.-Q, Patterson C. p68RacGAP is a novel GTPase-activating protein that interacts with Vezf1 and modulates endothelial cell capillary formation. Journal of Biological Chemistry, 279:17963-17972 (2004).
  • Dai Q, Zhang C, Wu Y, McDonough H, Whaley RA, Godfrey V, Li H-H, Madamanchi N, Xu W, Neckers L, Cyr D, Patterson C. CHIP activates HSF1 and confers protection against apoptosis and cellular stress. EMBO Journal, 22: 5446-5458 (2003).
  • Moser M, Binder O, Wu Y, Aitsebaomo J, Ren R, Bode C, Bautch VL, Conlon FL, Patterson C. BMPER, a novel endothelial cell precursor-derived protein, antagonizes BMP signaling and endothelial differentiation. Molecular and Cellular Biology, 23:5664-5679 (2003).
  • Wu Y, Moser M, Bautch VL, Patterson C. HoxB5 is an upstream transcriptional switch for differentiation of vascular endothelium from precursor cells. Molecular and Cellular Biology, 23:5680-5691 (2003).
  • Connell P, Ballinger CA, Jiang J, Wu Y, Höhfeld J, Patterson C. Regulation of heat shock protein-mediated protein triage decisions by the co-chaperone CHIP. Nature Cell Biology, 3: 93-96 (2001).
  • Meacham GC, Patterson C, Zhang W, Younger JM, Cyr DM. The Hsc70 co-chaperone CHIP targets immature CFTR for proteasomal degradation. Nature Cell Biology, 3:100-105 (2001).
  • Moon S-K, Thompson LJ, Madamanchi N, Ballinger SW, Runge MS. Patterson C. Aging, oxidative responses and proliferative capacity in cultured mouse aortic smooth muscle cells. American Journal of Physiology, 280: H2779-H2789 (2001).
  • Madamanchi NR, Li S, Patterson C, Runge MS. Reactive oxygen species regulate heat shock protein 70 via the JAK-STAT pathway. Arteriosclerosis, Thrombosis, and Vascular Biology, 21: 321-326 (2001).
  • Sriram V and Patterson C. The cell cycle in vasculoproliferative diseases: Potential interventions and routes of delivery. Circulation, 103:2414-2419 (2001).
  • Patterson C, Stouffer GA, Madamanchi NR, Runge MS. New tricks for old dogs: Thrombin, vascular smooth muscle cells, and atherogenesis. Circulation Research, 88:987-997 (2001).
  • Patterson C. Current topics in vascular biology: An update for the 21st century. Spanish Journal of Cardiology, 54:635-642 (2001).