6 research outputs found

    Comparison of specific expression profile in two in�vitro hypoxia models

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    Abstract. The microenvironment plays a fundamental role in carcinogenesis: Acidity and hypoxia are actively involved in this process. It is important to have in vitro models to study these mechanisms. The models that are most commonly referred to are the hypoxia chamber and the chemical induction [Cobalt (II) chloride]. It is not yet defined if these models are interchangeable if the metabolic effect is the same, and if the results may be compared in these models. In the present study, the response to the effect of stress (hypoxia and acidity) in both models was evaluated. The results indicated that in the chemical model, the effect of hypoxia appeared in an early form at 6 h; whereas in the gas chamber the effect was slow and gradual and at 72 h there was an overexpression of erythropoietin (EPO), vascular endothelial growth factor (VEGF), carbonic anhydrase 9 (CA9) and hypoxia-inducible factor 1α (HIF1α). In addition to the genes analyzed by reverse transcription-quantitative polymerase chain reaction, the global expression analysis between both models revealed the 9 most affected genes in common. The present study additionally identified 3 potential genes (lysyl oxidase, ankyrin repeat domain 37, B-cell lymphoma 2 interacting protein 3 like) previously identified in other studies, which may be considered as universal hypoxia genes along with HIF1α, EPO, VEGF, glucose transporter 1 (GLUT1), CA9, and LDH. To the best of the author's knowledge, this is the first time that both hypoxia models have been compared, and it was demonstrated that the effect of hypoxia induction was time sensitive in each model. These observations must be considered prior to selecting one of these models to identify selective hypoxia genes and their effects in cancer

    Evaluation of the Expression of Genes Associated with Inflammation and Apoptosis in Androgenetic Alopecia by Targeted RNA-Seq

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    Abstract Androgenetic alopecia (AGA) or male pattern baldness is the most common form of hair loss in humans. Despite being a very frequent dermatological entity, molecular pathophysiology remains unclear. Several authors relate the presentation of AGA with a premature apoptotic process during the anagen phase and with an inflammatory microenvironment in the hair follicle. We evaluated a panel of 30 genes associated with inflammation and apoptosis in 5 AGA patients by targeted RNA-Seq. WNT7A gene was highly expressed in patients in stages 3V to 5 on the Hamilton-Norwood scale compared to patients with 5A stage. CASP7 and TNF genes were overexpressed in stages 3V and 4 compared to stages 5 and 5A. Overexpression of these genes detected only at early stages of AGA proves the role of WNT pathway, apoptosis, and inflammation in the development of this disorder

    Odor memory stability after reinnervation of the olfactory bulb.

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    The olfactory system, particularly the olfactory epithelium, presents a unique opportunity to study the regenerative capabilities of the brain, because of its ability to recover after damage. In this study, we ablated olfactory sensory neurons with methimazole and followed the anatomical and functional recovery of circuits expressing genetic markers for I7 and M72 receptors (M72-IRES-tau-LacZ and I7-IRES-tau-GFP). Our results show that 45 days after methimazole-induced lesion, axonal projections to the bulb of M72 and I7 populations are largely reestablished. Furthermore, regenerated glomeruli are re-formed within the same areas as those of control, unexposed mice. This anatomical regeneration correlates with functional recovery of a previously learned odorant-discrimination task, dependent on the cognate ligands for M72 and I7. Following regeneration, mice also recover innate responsiveness to TMT and urine. Our findings show that regeneration of neuronal circuits in the olfactory system can be achieved with remarkable precision and underscore the importance of glomerular organization to evoke memory traces stored in the brain
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