An overview of the apoptosis mechanism in endothelial cells

Abstract EN

Tissue factor (TF) has a non-coagulant role in cell proliferation, migration and metastasis.

An overexpression of TF leads to a variety of diseases, such as thrombosis in cancer, metastasis and angiogenesis.

In contrast, TF can induce apoptosis in endothelial cells via the mechanism of inhibiting formation of the TF–β1 integrin complex.

The cell undergoes apoptosis due to loss of cell attachment (Anoikis), resulting in reduced Src activity in the cell.

The β1 integrin affects Src activity during TF signalling.

The mechanism involves the activation of a protein 38 (P38) mitogen-activated protein kinase (MAPK) and caspases coupled with P53 activation.

Prolonged overexpression of TF inside the cell induces cell signaling for apoptosis.

This pathway involves activating Src to stimulate cell proliferation.

The result reveals a significant effect of β1 integrin inhibition on the level of Src phosphorylation indicating the relationship between the β1 integrin and Src during cell apoptosis.

Amutation in the TF 253 sequence is capable of inducing apoptosis in endothelial cells.

The β1-integrin inhibition and the mutant-TF Ala 253 are both major factors in inducing apoptosis.