Substrain-related dependence of Cu(I)-ATPase activity among prion protein-null mice.

The prion protein (PrP) binds copper and affects copper metabolism, albeit among a poorly understood functional landscape. Much of the data on physiological roles of PrP were obtained in mice of mixed genetic background deficient of the PrP-coding gene Prnp. This strategy is currently under scrutiny due to the flanking gene problem, in particular related with a polymorphism, typical of both the 129Sv and 129Ola mouse substrains, in the Sirpa gene located in the vicinity of Prnp.

CHIP, a carboxy terminus HSP-70 interacting protein, prevents cell death induced by endoplasmic reticulum stress in the central nervous system.

Endoplasmic reticulum (ER) stress and protein misfolding are associated with various neurodegenerative diseases. ER stress activates unfolded protein response (UPR), an adaptative response. However, severe ER stress can induce cell death.

Paracrine interaction between bone marrow-derived stem cells and renal epithelial cells.

Background/aims: Renal tubular cells are the main target of ischemic insult associated with acute renal injury. Low oxygen and nutrient supplies result in ATP depletion, leading to cell death and loss of renal function. A possible mechanism by which bone marrow-derived cells support renal tissue regeneration relies on the capacity of mononuclear cells (BMMC), particularly mesenchymal stem cells (MSC), to secrete paracrine factors that mediate support for kidney regeneration.

Guanine-induced inhibition of renal Na(+)-ATPase activity: evidence for the involvement of the Gi protein-coupled receptor.

There is some evidence to show a possible role of guanosine in the modulation of cellular function, in particular, in the neuronal system. However, nothing is known about the role of guanine in renal function. The aim of the present work was to investigate the role of guanine on modulation of Na+-ATPase activity in isolated basolateral membrane (BLM) of the renal cortex.

Rod photoreceptor cell death is induced by okadaic acid through activation of PKC and L-type voltage-dependent Ca2+ channels and prevented by IGF-1.

Retinal dystrophies involve extensive photoreceptor apoptosis. Neuroprotective effects of insulin-like growth factor (IGF)-1 have been demonstrated in various tissues, including the retina. The aim of this study was to investigate: (i) the action of IGF-1 upon selective photoreceptor death induced by okadaic acid (OA); and (ii) signaling pathways related to both OA-induced cell death and IGF-1 neuroprotective effect.

Interleukin-4 as a neuromodulatory cytokine: roles and signaling in the nervous system.

Although interleukin (IL)-4 is described as a prototypical anti-inflammatory cytokine, in recent years its role as a neuromodulatory cytokine has been extensively discussed. This review highlights the pivotal contributions of IL-4 during the development and normal physiology of neural cells as well as IL-4 connections with the pathophysiology of degenerative or inflammatory processes observed in the central and peripheral nervous system.

Interleukin-4 blocks thapsigargin-induced cell death in rat rod photoreceptors: involvement of cAMP/PKA pathway.

Although the photoreceptors cell death is the main cause of some retinopathies diseases, the mechanisms involved in this process are poorly understood. The neuroprotective effects of interleukin-4 (IL-4) have been shown in several tissues, including retina. We demonstrate that treatment of rat retinal explants with IL-4 completely inhibited the thapsigargin-induced rod photoreceptor cell death after 24 hr in culture.

Adenine-induced inhibition of Na(+)-ATPase activity: Evidence for involvement of the Gi protein-coupled receptor in the cAMP signaling pathway.

In the present work, we demonstrate that adenine reduced Na(+)-ATPase activity in isolated basolateral membrane (BLM) of proximal tubule in a dose-dependent manner. Adenine metabolism was ruled out by TLC analysis of the potential [(3)H]adenine derived-metabolites. Specific binding of [(3)H]adenine to isolated BLM was observed in a dose-dependent manner with K(d) and B(max) of 242.