We discuss the clinical and experimental evidence that supports the notion that the microcirculation, specifically cell-to-cell communication, likely contributes to the development of VaD. Through exploration of the concept of the NVU, we elucidate

the extensive cerebrovascular communication that exists and highlight models that may help test the contribution(s) of cell-to-cell communication at the microvascular level to the development and progression of VaD. Lastly, we explore the possibility that some dementia, generally considered to be find more purely neurodegenerative, may actually have a vascular component at the neurovascular level. Conclusion:  This latter recognition potentially broadens the critical involvement of microvascular events that contribute to the numerous dementias affecting an increasingly larger sector of the adult population. “
“Cell–cell adhesion complexes are increasingly recognized as an important cell-signaling site, similar to integrin-extracellular matrix FA. Furthermore, cell–cell adhesions are involved in the regulation

of multi-cellular/tissue organization and organ, tissue, and cellular level functional behavior. Although N-cadherin is the major cell–cell adhesion molecule in VSM, only limited studies have been undertaken to understand its function in VSM. Nutlin-3a cell line In contrast, N-cadherin signaling and functions have been extensively studied in neurons, fibroblasts, and myocytes, as well as in the context

of epithelial-mesenchymal-transitions. Increasing evidence has indicated Sulfite dehydrogenase that N-cadherin-mediated cell–cell adhesions are important for tissue integrity and cell proliferation. Relevant to VSM, N-cadherin’s role in actin cytoskeleton organization and contraction, as well as its role in regulation of Rho family GTPases are of particular interest. This article briefly reviews the fundamentals of N-cadherin biology that help shape our current understanding of its function and signaling mechanisms. In particular, attention is given to applications of this knowledge to VSM. The review points to the need for more research effort that is directed at understanding the role of N-cadherins in the regulation of vascular function. “
“Please cite this paper as: Wang, Hein, Zhang, Zawieja, Liao and Kuo (2011). Oxidized Low-Density Lipoprotein Inhibits Nitric Oxide-Mediated Coronary Arteriolar Dilation by Up-regulating Endothelial Arginase I. Microcirculation18(1), 36–45. Oxidized low-density lipoprotein (OxLDL) causes impairment of endothelium-dependent, nitric oxide (NO)-mediated vasodilation involving l-arginine deficiency. However, the underlying mechanism remains elusive. Since arginase and endothelial NO synthase (eNOS) share the substrate l-arginine, we hypothesized that OxLDL may reduce l-arginine availability to eNOS for NO production, and thus vasodilation, by up-regulating arginase.