Tyrosine phosphorylation is a post-translational modification which governs growth factor-induced vascular cell proliferation, adhesion, transmigration and differentiation. Protein tyrosine phosphatases (PTP) are negative regulators of tyrosine kinases, and therefore, they play a vital role in controlling the magnitude of tyrosine-phosphorylation-dependent signal transduction processes. Aberrant tyrosine phosphorylation frequently caused by the deregulation of protein-tyrosine phosphatases (PTPs) contributes to vascular cell dysfunction leading to different cardiovascular pathologies. The primary underlying mechanisms related to PTP deregulation are the alterations in PTP gene expression or alterations in the mechanisms which control PTP activity. Reactive oxygen species (ROS)-induced reversible oxidation of PTP has been identified to be a major, but less appreciated, mechanism which limits PTP activity in vascular cells. The primary goal of our projects is to identify the mechanistic basis behind the potential deregulation of tyrosine kinase-tyrosine phosphatase signalling axis in contributing to vascular cell dysfunction in various cardiovascular disease conditions.