Publications by authors named "Julie Loiselle"

Introduction: Maternal lifestyle, in particular physical activity (PA), influences many of the physiological adaptations during pregnancy associated with feto-placental development and growth. There is limited to no information on the link between PA during pregnancy and the molecular mechanisms governing placental function. The aim of this study was to investigate the molecular mechanisms through which maternal PA may influence placental function.

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Hydrogen sulfide (H S) is the most recently recognized gasotransmitter, influencing a wide range of physiological processes. As a critical regulator of metabolism, H S has been suggested to be involved in the pathology of many diseases, particularly obesity, diabetes and cardiovascular disorders. Its involvement in liver health has been brought to light more recently, particularly through knockout animal models, which show severe hepatic lipid accumulation upon ablation of H S metabolic pathways.

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Presented herein are RNA expression data linked to the exposure of human lung epithelial cells to either low dose radon-emitting rock, tobacco smoke or cannabis smoke. Two cell lines were used, one representing a 'normal' lung epithelial cell (BEAS-2B, derived from immortilized bronchial epithelial cells from a cadaver) and one representing a 'cancerous' lung epithelial cell (NCI-H1975, derived from a primary lung adenocarcinoma from a non-smoker). Control cells were cultured under standard conditions.

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Radon is the second leading cause of lung cancer, after tobacco smoke. While tobacco smoke-induced carcinogenesis has been studied extensively, far less is known about radon-induced carcinogenesis, particularly in relation to the influence of radon on gene expression. The objectives of the work described herein were to (a) determine if and how exposure to low dose radon-emitting rock influences cells, at the gene expression level, and (b) compare any gene expression changes resulting from the exposure to radon-emitting rock with those induced by exposure to tobacco smoke.

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RBM10 is an RNA binding motif (RBM) protein expressed in most, if not all, human and animal cells. Interest in RBM10 is rapidly increasing and its clinical importance is highlighted by its identification as the causative agent of TARP syndrome, a developmental condition that significantly impacts affected children. RBM10's cellular functions are beginning to be explored, with initial studies demonstrating a tumor suppressor role.

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Background: RBM10 is an RNA binding protein involved in message stabilization and alternative splicing regulation. The objective of the research described herein was to identify novel targets of RBM10-regulated splicing. To accomplish this, we downregulated RBM10 in human cell lines, using small interfering RNAs, then monitored alternative splicing, using a reverse transcription-PCR screening platform.

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Lung cancers are the leading cause of cancer-related deaths worldwide, with small cell lung cancer (SCLC) being the most aggressive type. At the time of diagnosis, SCLC has usually already metastasized, and an astonishing 95% of patients eventually succumb to the disease. This highlights the need for more effective SCLC screening and treatment options.

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Small cell lung cancer (SCLC) is the most aggressive type of lung cancer, with almost 95% of patients succumbing to the disease. Although , a tumor suppressor gene, is downregulated in the majority of lung cancers, its role in SCLC is unknown. Using the GLC20 SCLC cell line, which has a homozygous deletion encompassing the gene locus, we established stable expressing sublines and investigated the effects of re-expression.

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Background: Expression and function of the two RNA binding proteins and regulators of alternative splicing, RBM5 and RBM10, have largely been studied in human tissue and cell lines. The objective of the study described herein was to examine their expression in mouse tissue, in order to lay the framework for comprehensive functional studies using mouse models.

Methods: All RNA variants of Rbm5 and Rbm10 were examined in a range of normal primary mouse tissues.

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We previously examined the expression of Rbm5 during myoblast differentiation and found significantly more protein in the early stages of skeletal myoblast differentiation than during the later stages. We decided to determine if this elevated level was necessary for differentiation. Our hypothesis was that if high levels of Rbm5 protein expression were necessary for the initiation of skeletal myoblast differentiation, then inhibition of expression would prevent differentiation.

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Background: RBM10 is an RNA binding protein involved in the regulation of transcription, alternative splicing and message stabilization. Mutations in RBM10, which maps to the X chromosome, are associated with TARP syndrome, lung and pancreatic cancers. Two predominant isoforms of RBM10 exist, RBM10v1 and RBM10v2.

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RBM5 and RBM10 play an important role in transformed cells. This role includes influencing the alternative splicing and/or expression of factors involved in apoptosis and cell cycle arrest. To date, all apoptosis studies relating to RBM5 and RBM10 have been performed in transformed cell lines, potentially confounding mechanistic interpretation because of the many mutations present in this population.

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Skeletal muscle differentiation occurs during muscle development and regeneration. To initiate and maintain the differentiated state, a multitude of gene expression changes occur. Accurate assessment of these differentiation-related gene expression changes requires good quality template, but more specifically, appropriate internal controls for normalization.

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