The effects of CTHRC1 on endothelial cell proliferation
Document Type
Oral Presentation
Department
Biological Sciences
Abstract
During wound healing fibroblasts produce the protein CTHRC1. This protein is associated with wound healing and angiogenesis, which signals endothelial cells to form around the new blood vessels. In this study we looked at how CTHRC1 affects mouse cardiac endothelial cells (MCEC1) in vitro both with the cleaved and non-cleaved from of the protein. To study the effects of CTHRC1 on endothelial cells we introduced treatment media to MCEC1 cells which contained cleaved (VVD) and full length (FL) forms of the protein and tested them against a control (C) and a vector (V). We grew the cells on 12 well plates. At time points of 24, 48, and 72 hours we took 3 samples from each treatment and counted them with a cell counter under a microscope. Further studies included using a further time point of 96 hours, staining to count cell density, using flow cytometry on cells marked for ki67 presence, and using flow cytometry to count cells. We noticed that the VVD and FL treatments introduced higher rates of proliferation and higher total number of cells at confluency. Pictures of cells at the 72 hour time points also show that treated cells have a smaller morphology compared to their control counterparts. This is corroborated by higher cell densities. Further, flow cytometry shows that there is no significant difference in the concentrations of ki67 between the different treatments. In conclusion, this protein seems to increase the proliferation rates and morphology of the endothelial cells, but does not increase time in the cellular proliferation phase.
The effects of CTHRC1 on endothelial cell proliferation
During wound healing fibroblasts produce the protein CTHRC1. This protein is associated with wound healing and angiogenesis, which signals endothelial cells to form around the new blood vessels. In this study we looked at how CTHRC1 affects mouse cardiac endothelial cells (MCEC1) in vitro both with the cleaved and non-cleaved from of the protein. To study the effects of CTHRC1 on endothelial cells we introduced treatment media to MCEC1 cells which contained cleaved (VVD) and full length (FL) forms of the protein and tested them against a control (C) and a vector (V). We grew the cells on 12 well plates. At time points of 24, 48, and 72 hours we took 3 samples from each treatment and counted them with a cell counter under a microscope. Further studies included using a further time point of 96 hours, staining to count cell density, using flow cytometry on cells marked for ki67 presence, and using flow cytometry to count cells. We noticed that the VVD and FL treatments introduced higher rates of proliferation and higher total number of cells at confluency. Pictures of cells at the 72 hour time points also show that treated cells have a smaller morphology compared to their control counterparts. This is corroborated by higher cell densities. Further, flow cytometry shows that there is no significant difference in the concentrations of ki67 between the different treatments. In conclusion, this protein seems to increase the proliferation rates and morphology of the endothelial cells, but does not increase time in the cellular proliferation phase.
