p62 may serve as a proteotoxic stress sensor, promote segregation

p62 may serve as a proteotoxic stress sensor, promote segregation and degradation of misfolded proteins by autophagy, and mediate the cross talk between the ubiquitin-proteasome system and autophagy. (Trends Cardiovasc Med 2011; 21:224-228) (C) 2011 Elsevier inc. All rights reserved.”
“Pain was reported by 60-90% of patients with depression, and chronic pain states are often linked to depression. Animal models of pain/depression are generally lacking for the identification of centrally active drugs. In the present

study, pain sensitivity was assessed in a mouse model of anxiety/depression on the basis of chronic corticosterone click here (CORT) administration through the drinking water (CORT model). We measured thermal hyperalgesia as shown by a decrease

in the latency to hind paw licking in the hot plate test and cold allodynia reflected by a decrease in the time spent on the plate set at 20 degrees C in the thermal preference plate test. Subsequently, we determined the effect of chronic administration of the selective serotonin reuptake inhibitor fluoxetine (an antidepressant known to reverse anxiety/depressive-like state in CORT-treated Epacadostat supplier mice) on pain relief. Fluoxetine administration reduced both heat hyperalgesia and cold allodynia, thus unveiling a putative link between mood and nociception in the CORT model. This hypothesis is consistent with previous clinical studies reporting the analgesic efficacy of fluoxetine in depressed patients suffering from pain disorders. Together, these results suggest that the CORT model, with pain/anxiety/depressive-like state, is a good candidate for translational research. NeuroReport 23:525-529 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Graft arteriosclerosis (GA), the major cause of late cardiac allograft failure, is characterized by a diffuse, concentric arterial intimal hyperplasia composed of infiltrating host T cells, macrophages, and predominantly graft-derived smooth muscle-like cells that proliferate and elaborate extracellular matrix, resulting in luminal obstruction and allograft ischemia. Interferon-gamma (IFN-gamma),

a proinflammatory cytokine produced by effector T cells, is a critical mediator for smooth muscle-like cell proliferation. We have exploited Carbachol the power of mouse genetics to examine the function of AIP1, a signaling adaptor molecule involved in vascular inflammation, in two newly established IFN-gamma-mediated models of GA. Our data suggest that AIP1 inhibits intimal formation in GA by downregulating IFN-gamma-activated migratory and proliferative signaling pathways in smooth muscle-like cells. (Trends Cardiovasc Med 2011;21:229-233) (C) 2011 Elsevier Inc. All rights reserved.”
“In women, pain symptoms and nociceptive thresholds vary with the reproductive cycle, suggesting the role of estrogen receptors (ERs) in modulating nociception.

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