Anti-Thy-1 antibody-induced neurite outgrowth in cultured dorsal root ganglionic neurons is mediated by the c-Src-MEK signaling pathway.

Our previous study has shown that anti-Thy-1 antibody promotes neurite outgrowth of cultured dorsal root ganglion( DRG) neurons in a protein kinase A (PKA)-dependent manner. The present study provided another intracellular signaling pathway for the neurotrophic effect of anti-Thy-1 antibody. In DMSO-treated control cells, Thy-1 was enriched in microdomain -like structures on cell membranes by immunofluorescence observation. Treatment of DRG neurons with anti-Thy-1 antibody not only stimulated neurite outgrowth, but also increased the branching complexity of the neurites in both small and large neurons. We have previously shown that anti-Thy-1 antibody causes a time- dependent activation of mitogen- activated protein kinase ( MEK) and of cyclic AMP response-element binding protein ( CREB). Here, anti-Thy-1 antibody elicited a transient activation of c-Src kinase, and the activation of c-Src kinase appeared occurring upstream of the activation of MEK and CREB, since pretreatment with the Src kinase inhibitor, PP2, effectively abolished the anti-Thy-1 antibody-induced neurite outgrowth and the phosphorylation of MEK and CREB . CREB phosphorylation might result in upregulation of certain neurite outgrowth-related proteins. We therefore conclude that anti-Thy-1 antibody activates the c-Src kinase-MEK-CREB cascade and overcomes the inhibitory effect of Thy-1 on neurite outgrowth in DRG neurons

The renal system

The chapter reviews the alterations that occur in the body during the stress of acute exercise, including the decrease in renal blood flow, glomerular filtration rate, excretion of water and sodium/chloride, the release of renin-angiotensin and norepinephrine, increase in the excretion of proteins and other macromolecules, and changes in metabolic functions. Exercise alters renal hemodynamics, excretory function, and hormone release. Many of these changes can affect exercise performance. Renal function during exercise is usually not considered to be essential or critical in terms of limiting or determining exercise capacity. It is extremely difficult to assess the renal system during exercise. Changes in cardiovascular and thermoregulatory function with aging, point toward the alterations in kidney function with age. The problem of exercise or exercise and dehydration induce acute renal failure, which remains an issue. The role of the kidneys as an endocrine organ, not only for the release of renin-angiotensin but also norepinephrine, has profound implications, explaining the effects of chronic exercise on certain disease states. © 2003 American Physiological Society Published by Elsevier Ltd All rights reserved.SCOPUS: ch.binfo:eu-repo/semantics/publishe