Department of Pathology
  Brigham and Women's Hospital
  A teaching Affliate of Harvard Medical School
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Guillermo Garcia-Cardena, Ph.D.

Associate Professor of Pathology, Harvard Medical School

Academic Activities:
Our laboratory is using cellular, molecular, bioengineering, and computational biology tools to understand how mechanical forces generated by the flow of blood act on blood vessels to activate signaling pathways critical for cellular specification during developmental processes, and for flow-mediated vasoprotection in the context of human cardiovascular disease. BIOMECHANICAL CONTROL OF EMBRYONIC DEVELOPMENTAL PROCESSES When the heart starts beating and blood flow is first established during vertebrate development endothelial cells lining nascent blood vessels are first expose to hemodynamic forces. The effects this critical developmental transition has on the developing vascular system remain poorly characterized. We are currently studying two processes related to this transition namely, arterial specification and the induction of embryonic hematopoiesis via the flow-mediated specification of the hemogenic endothelium. BIOMECHANICAL CONTROL OF ENDOTHELIAL VASOPROTECTION In experiments design to probe the transcriptional machinery responsible for the endothelial vasoprotective phenotype present in regions of the human vasculature resistant to atherosclerosis, we revealed that the transcription factor Kruppel-like factor 2 (KLF2) acts as an integrator of the flow-mediated endothelial vasoprotective phenotype. Importantly, we demonstrated that Statins, one of the most widely used class of drugs for cardiovascular disease, increase the expression of KLF2, explaining in part, the well-described non-lipid lowering, vasoprotective effects of this class of drugs. These observations have led us to initiate high-throughput screens to identify small molecules and siRNAs capable of regulating KLF2 expression. These experiments should enable us to dissect mechanistically how flow leads to the expression of KLF2, and could aid in the identification of new molecules capable of acting as “pharmacomimetics of flow-dependent vasoprotection”.
77 Avenue Louis Pasteur
Boston,MA 02115
Education and Training:

Graduate School - : Yale University Ph.D.

Clinical Specialties: Research Interests: Publication:
  1. Parmar KM, Larman HB, Dai G, Zhang Y, Wang ET, Moorthy SN, Kratz JR, Lin Z, Jain MK, Gimbrone MA, Garcia-Cardena G. Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2. J. Clin. Invest. 2006; 116: 49-58.
  2. Parmar KM, Nambudiri V, Dai G, Larman HB, Gimbrone MA Jr, Garcia-Cardena G. Statins exert endothelial atheroprotective effects via the KLF2 transcription factor. J. Biol. Chem. 2005; 280: 26714-26719
  3. Kwei S, Stavarakis G, Takahas M, Taylor G, Folkman J, Gimbrone MA Jr, García-Cardeña G. Early Adaptive Resposnes of the Vascular Wall during Venous Arterialization in Mice. Am. J. Pathol. 2004; 164: 81-89.
  4. Comander J, Weber G, Gimbrone, MA Jr, García-Cardeña G. ARGUS - a new database system for web-based analysis of multiple microarray datasets. Genome Research 2001; 11:1603-1610.
  5. García-Cardeña G, Comander J, Anderson KR, Blackman BR, Gimbrone, MA Jr. Biomechanical activation of vascular endothelium as a determinant of its functional phenotype. Proc. Natl. Acad. Sci. USA. 2001; 98:4478-4485.
  6. Shin D*, García-Cardeña G*, Hayashi SI, Gerety S, Asahara T, Stavrakis G, Isner J, Folkman J, Gimbrone MA Jr, Anderson DJ. Expression of EphrinB2 identifies a stable genetic difference between arterial and venous vascular smooth muscle as well as endothelial cells, and marks subsets of microvessels at sites of adult neovascularization. Dev. Biol. 2001; 230:139-150. *Denotes equal contribution by these authors.
  7. García-Cardeña G, Fan R, Shah V, Sorrentino R, Cirino G, Papapetropoulos A, Sessa WC. Dynamic activation of endothelial nitric oxide synthase by Hsp90. Nature 1998; 392:821-824.
<September 2019>

<Sunday, September 15, 2019>
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