In this study, a single cell type endothelial cells culture from cardiac microvasculature of rats (MVECs) was established, and endothelilal mesenchymal transition of these cells under hypoxia or TGF?1 was determined. First, the purity of endothelial cell culture was improved. By optimising digestion of collagenase at 45 minutes and early washing after one hour of adhesion, I obtained a purity of 90% MVECs. These cells presented microscopically a cobblestone endothelial-like monolayer, whereas cells with shorter digestion and longer adhesion times appeared fibroblast like spindle-shaped and elongated. Due to cell transformations after every step of sub-culturing, we used just the first passage of cells at a confluence of 95 %. To analyse the influence of hypoxia and reoxygenation on these cells, efficiency of oxygen deprivation was proven by detection of HIF-1?-protein. Transforming growth factor beta (TGF?) as growth factor is mainly involved in cardial transforming processes, termed cardial remodeling. In this study, it could be shown that hypoxia with following reoxygenation activates well-known signaling molecules of TGF?1, named SMAD-proteins. In particular, hypoxia induced the expression of SMAD2 and SMAD1/5. Because both molecules are phosphorylated and activated at the outer membrane via the TGFß-receptor it might be argued that hypoxia induces TGF?1 release from MVECs. A specific TGF?-receptor-inhibitor against ALK5 could block the SMAD2 activation. Furthermore, I could demonstrate that hypoxia provokes endothelial mesenchymal transition (EndoMT). This was detected by the increased expression of mesenchymal markers like ?-SMA and FSP-1. The upregulation could be blocked by specific ALK5-inhibition, thereby showing contribution of TFG?/SMAD2 signaling. Low concentrations of TGF?1 (0,01 ng/ml) revealedvimilar results, whereas high TGF?1 concentrations (1 ng/ml) triggerd an impressive transformation of endothel cells. It can therefore be concluded that a small release of TGF?1 provokes a cardial EndoMT. In our study, hypoxia induced a reduction in cell count, presumable by a diminished proliferation rate, which then contributes to pore formation in the monolayer. Once rhomboid-oval single cells transformed around the pores to spindle-shaped, mainly ?-SMA marked cells. Equally to hypoxia, TGF?1 triggered pore fomations. The endothelial marker CD31 did not show any change in its expression, neither under hypoxia nor by TGF?1. Thus, it can be concluded that the endothelial cell marker still exists after EndoMT. In vivo hypoxic conditions, as they are found in myocardial infarction, may provoke EndoMT. This can contribute to desintegration of the cell layer and may facilitate immigration of endothelial derived mesenchymal cells and the release of TGF?1 into cardiac tissue. These processes can contribute to cardiac fibrosis and heart failure progression after myocardial infarction. As both processes are mediated via TGF?1/SMAD2 signaling, interference with this pathway should be a major aim for prevention of myocardial damage due to infarction.