Effects of Sphk1 deletion in smooth muscle cells on murine arterial transcriptome in hypertension

The function of the cardiovascular system is regulated by sphingosine-1-phosphate (S1P) signalling. Vascular sphingosine kinase 1 (Sphk1), an S1P-producing enzyme, is upregulated in hypertension (HTN), and mice lacking Sphk1 globally exhibit alleviated angiotensin II (AngII)-induced HTN. Identifying the cellular mechanisms that provide this protection remains challenging due to the pleiotropic action of S1P. To obtain mice lacking Sphk1 in smooth muscle cells (SMCs), Sphk1 f/f (flox/flox) mice were crossed with transgenic mice harboring Cre recombinase gene under control of the mouse smooth muscle protein 22-alpha/transgelin (SM22α/Tagln) promoter. Subsequently, resulting Sphk1f/-Tagln-cre+ offsprings were mated to Sphk1f/f mice to generate mice lacking Sphk1 specifically in SMCs (Sphk1f/fTagln-cre+, later referred to as SMC KO-Sphk1) and control mice (Sphk1f/fTagln-cre-, hereafter referred to as wild type (WTf/f) mice).