Current Issue : April - June Volume : 2015 Issue Number : 2 Articles : 6 Articles
The remodeling of Ca2+ signaling is a common finding in cancer pathophysiology serving the purpose of facilitating proliferation,\nmigration, or survival of cancer cells subjected to stressful conditions. One particular facet of these adaptive changes is the alteration\nof Ca2+ fluxes through the plasma membrane, as described in several studies. In this review, we summarize the current knowledge\nabout the expression of different Ca2+ channels in the plasma membrane of melanoma cells and its impact on oncogenic Ca2+\nsignaling. In the last few years, new molecular components of Ca2+ influx pathways have been identified in melanoma cells. In\naddition, new links between Ca2+ homeostasis and specific cell processes important in melanoma tumor progression have been\nunveiled.Thus, not only do Ca2+ channels appear to have a potential as prognostic markers, but their pharmacological blockade or\ngene silencing is hinted as interesting therapeutic approaches....
Transient receptor potential (TRP) receptor expressed by primary sensory neurons mediate thermo sensitivity and may play a role in sensory pathophysiology. Nociceptors with peripheral and central projections express temperature sensitive transient receptor potential (TRP) ion channels, also called thermo TRP’s. Chemo sensitivity of thermo TRP’s to certain natural compounds eliciting pain or expediting thermal properties has proven to be good tool in characterising these receptors. Capsaicin, a pungent chemical in hot peppers, has assisted in the cloning of the first thermo TRP, TRPV1. The transient receptor potential vanilloid-1(TRPV1) cation channel is a receptor that is activated by heat (>42°C), acidosis (pH<6) and a variety of chemicals among which capsaicin is the best known. The activity of TRPV1 is controlled by multitude of regulatory mechanism that either causes sensitization or desensitization of the channel. As many proalgesic pathways converge on TRPV1 and the nocisensor is up regulated and sensitized by inflammation and injury, TRPV1 is thought to be a central transducer of hyperalgesia and prime target for the pharmacological control of pain. In addition to endogenous agonists, a wide variety of chemical agonists and antagonists have been discovered to activate and inhibit TRPV1. Efforts are underway to determine conditions under which agonist mediated desensitization of TRPV1 or inhibition by antagonist can produce analgesia. The search for a role of TRPV2 in pain remains dormant due to lack of suitable experimental models. However TRPV3 and TRPV4 encoding for detection of warm temperature and expressed in nociceptors can’t be excluded. This review will discuss current knowledge on the role of capsaicin receptor in nociception....
MicroRNAs (miRNAs) are small, endogenous noncoding RNAs that regulate a variety of biological processes such as differentiation,\ndevelopment, and survival. Recent studies suggest that miRNAs are dysregulated in cancer and play critical roles in cancer\ninitiation, progression, and chemoresistance. Therefore, exploitation of miRNAs as targets for cancer prevention and therapy\ncould be a promising approach. Extensive evidence suggests that many naturally occurring phytochemicals regulate the expression\nof numerous miRNAs involved in the pathobiology of cancer. Therefore, an understanding of the regulation of miRNAs by\nphytochemicals in cancer, their underlying molecular mechanisms, and functional consequences on tumor pathophysiology may\nbe useful in formulating novel strategies to combat this devastating disease.These aspects are discussed in this review paper with\nan objective of highlighting the significance of these observations from the translational standpoint....
Experimental models of diabetic retinopathy (DR) have had a crucial role in the comprehension of the pathophysiology of the\ndisease and the identification of new therapeutic strategies. Most of these studies have been conducted in vivo, in animal models.\nHowever, a significant contribution has also been provided by studies on retinal cultures, especially regarding the effects of the\npotentially toxic components of the diabetic milieu on retinal cell homeostasis, the characterization of themechanisms on the basis\nof retinal damage, and the identification of potentially protective molecules. In this review, we highlight the contribution given by\nprimary retinal cultures to the study of DR, focusing on early neuroglial impairment. We also speculate on possible themes into\nwhich studies based on retinal cell cultures could provide deeper insight....
Methamphetamine (METH) is a sympathomimetic amine that belongs to phenethylamine and amphetamine class of psychoactive\ndrugs, which are widely abused for their stimulant, euphoric, empathogenic, and hallucinogenic properties. Many of these effects\nresult from acute increases in dopamine and serotonin neurotransmission. Subsequent to these acute effects, METH produces\npersistent damage to dopamine and serotonin release in nerve terminals, gliosis, and apoptosis. This review summarized the\nnumerous interdependent mechanisms including excessive dopamine, ubiquitin-proteasome system dysfunction, protein nitration,\nendoplasmic reticulum stress, p53 expression, inflammatory molecular, D3 receptor, microtubule deacetylation, and HIV-1 Tat\nprotein that have been demonstrated to contribute to this damage. In addition, the feasible therapeutic strategies according to\nrecent studies were also summarized ranging from drug and protein to gene level....
Suicidal erythrocyte death or eryptosis is characterized by erythrocyte shrinkage, cell membrane blebbing, and cell membrane\nscrambling with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include Ca2+ entry, ceramide\nformation, stimulation of caspases, calpain activation, energy depletion, oxidative stress, and dysregulation of several kinases.\nEryptosis is triggered by a wide variety of xenobiotics. It is inhibited by several xenobiotics and endogenous molecules including\nNO and erythropoietin. The susceptibility of erythrocytes to eryptosis increases with erythrocyte age. Phosphatidylserine\nexposing erythrocytes adhere to the vascular wall by binding to endothelial CXC-Motiv-Chemokin-16/Scavenger-receptor\nfor phosphatidylserine and oxidized low density lipoprotein (CXCL16). Phosphatidylserine exposing erythrocytes are further\nengulfed by phagocytosing cells and are thus rapidly cleared from circulating blood. Eryptosis eliminates infected or defective\nerythrocytes thus counteracting parasitemia in malaria and preventing detrimental hemolysis of defective cells. Excessive eryptosis,\nhowever, may lead to anemia and may interfere with microcirculation. Enhanced eryptosis contributes to the pathophysiology\nof several clinical disorders including metabolic syndrome and diabetes, malignancy, cardiac and renal insufficiency, hemolytic\nuremic syndrome, sepsis, mycoplasma infection, malaria, iron deficiency, sickle cell anemia, thalassemia, glucose 6-phosphate\ndehydrogenase deficiency, andWilson�s disease. Facilitating or inhibiting eryptosis may be a therapeutic option in those disorders....
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