Hong Shi

TL;DR: It is shown that endothelial KLF4 is an essential determinant of atherogenesis and thrombosis andMechanistically, it is demonstrated that KLF 4 differentially regulated pertinent endothelial targets via competition for the coactivator p300, and cogent evidence is provided implicated as essential in vivo regulators of vascular function in the adult animal.

TL;DR: Evidence that hemizygous deficiency of KLF2 increased diet-induced atherosclerosis in apolipoprotein E–deficient mice is provided and novel observations establish that KLF 2 is an atheroprotective factor.

TL;DR: It is shown that endothelial KLF2 and KLF4 control a large segment of the endothelial transcriptome, thereby affecting virtually all key endothelial functions, and establishing an absolute requirement for KLF 2/4 for maintenance of endothelial and vascular integrity in the adult animal.

TL;DR: In this paper, the authors identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo, and demonstrate that exposure to either hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxyia inducible factor 1α (HIF-1α), findings that were recapitulated in human septic patients.

TL;DR: These studies indicate that KLF2 confers barrier-protection via differential effects on the expression of key junction protein occludin and modification of a signaling molecule (myosin light chain) that regulate endothelial barrier integrity.