The field is confused by a lack of standardization in definitions and methodology, and emphasis should be on investigating the underlying mechanisms behind peripheral blood flow changes with local cold exposure. “
“Please cite this paper as: Taylor MS, Francis M, Qian X, Solodushko V. Dynamic Ca2+ signal modalities in the vascular endothelium. Microcirculation 19: 423–429, 2012. The endothelium is vital to normal vasoregulation. Although acute vasodilation associated with broad endothelial Ca2+ elevation is well known, the control and targeting of Ca2+-dependent signals in the endothelium are poorly understood. Recent studies have revealed localized GDC0199 IP3-motivated

Ca2+ events occurring basally along the intima that may provide the fundamental basis for various endothelial influences. Here, we provide an overview of dynamic endothelial Ca2+ signals and discuss the potential role of these signals in constant endothelial control of arterial tone and the titration of functional responses in vivo. In particular, we focus on the

functional architecture contributing to the properties and ultimate impact of these signals, check details and explore new avenues in evaluating their prevalence and specific modalities in intact tissue. Finally, we discuss spatial and temporal effector recruitment through modification of these inherent signals. It is suggested that endothelial Ca2+ signaling is a continuum in which the specific framework of store-release components and cellular targets along the endothelium allows for differential modes of Ca2+ signal expansion and distinctive profiles of effector recruitment. The precise composition and distribution of these inherent components may underlie dynamic endothelial control and specialized functions of different vascular beds. “
“Please cite this paper as: Clark, Jensen, Kluger, Morelock, Hanidu, Qi, Tatake, Pober (2011). MEK5 is Activated by Shear Stress, Activates ERK5 and Induces KLF4 to Modulate TNF Responses

in Human Dermal Microvascular Endothelial Cells. Microcirculation18(2), 102–117. Objective:  ECs lining arteries respond to LSS by suppressing pro-inflammatory changes, in part through the activation of MEK5, ERK5 Niclosamide and induction of KLF4. We examined if this anti-inflammatory pathway operates in human ECs lining microvessels, the principal site of inflammatory responses. Methods:  We used immunofluorescence microscopy of human skin to assess ERK5 activation and KLF4 expression in HDMECs in situ. We applied LSS to or overexpressed MEK5/CA in cultured HDMECs and assessed gene expression by microarrays and qRT-PCR and protein expression by Western blotting. We assessed effects of MEK5/CA on TNF responses using qRT-PCR, FACS and measurements of HDMEC monolayer electrical resistance. We used siRNA knockdown to assess the role of ERK5 and KLF4 in these responses. Results:  ERK5 phosphorylation and KLF4 expression is observed in HDMECs in situ. LSS activates ERK5 and induces KLF4 in cultured HDMECs.