Principal Investigator:
John Castellot, Ph.D.
Professor and Director of the CMDB Graduate Program
Department of Anatomy and Cellular Biology

Department of Anatomy & Cellular Biology
Tufts University 
School of Medicine
136 Harrison Avenue
Boston, Massachusetts 02111

Office Phone:  
(617)636-0303
Lab Phone: 
(617)636-
FAX: 
(617)636-6536

EMail Address:
john.castellot@tufts.edu


Program in Cellular and Molecular Biology

Sackler School

Medical School

Fig. 8 CCN5 inhibits VSMC proliferation. Using an adenovirus construct to over-express CCN5 in VSMC, we observe a dose-dependent inhibition of proliferation when compared to a control adenoviral construct that over-expresses an irrelevant protein, GFP. MOI = multiplicity of infection, i.e., the higher the MOI the higher the level of CCN5 expression in the cell. Virtually identical results were obtained with human fibroid SMC.

Fig. 9 CCN5 inhibits VSMC motility. A confluent monolayer of VSMC is scraped with a small pipette tip to create a wound. Cells not infected with adenovirus migrate into the wound in significant numbers within 30 hr. Cells infected with the control adenovirus containing GFP also migrate rapidly, whereas VSMC over-expressing CCN5 display substantially decreased motility. Hoechst dye is used to stain the nuclei of cells and makes them easy to count. White bars mark the original wound edge. Virtually identical results were obtained with human fibroid SMC.