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1.
Cell Mol Biol (Noisy-le-grand) ; 62(3): 100-4, 2016 Mar 31.
Article in English | MEDLINE | ID: mdl-27064881

ABSTRACT

The number of smokers is increasing specially in pregnant mothers and millions of children with health problems are born from the smoker mothers. Nicotine as a toxic substance crosses from placenta and accumulates in the developing organs of fetus. In this study, the effects of maternal nicotine exposure on expression levels of kidney laminin α5 in newborn mice were examined. Timed pregnant mice were injected subcutaneously with nicotine at a dose of 2 mg/kg/day from day 7 of gestation to the last day of the pregnancy (Group 1) and from day 7 until the two weeks of postnatal (Group 2). Sham control groups were injected with saline. After the last injection, all the newborn mice were anesthetized; their kidneys were removed and prepared for analysis of mRNA and protein expression of laminin α5 using Real-Time PCR and immunohistochemical techniques, respectively. Our results showed that mRNA levels of kidney laminin α5 in newborn mice were increased in group 1 when compared to sham control group and also group 2. Immunohistochemical analysis demonstrated that the protein levels of laminin α5 in the glomerulus have significantly increased in group 1 when compared to group 2. In the proximal convoluted tubules, the parameter had a high significant increase in group 1 in comparison to control and also group 2. According to the results, it seems that maternal nicotine exposure may induce abnormal laminin α5 expression which may cause defects in kidney function during life time.


Subject(s)
Gene Expression Regulation, Developmental , Kidney/abnormalities , Laminin/genetics , Maternal Exposure/adverse effects , Nicotine/adverse effects , Animals , Animals, Newborn , Female , Kidney/metabolism , Kidney/ultrastructure , Laminin/analysis , Mice , Mice, Inbred BALB C , Pregnancy , RNA, Messenger/genetics
2.
Cell Mol Biol (Noisy-le-grand) ; 62(1): 16-23, 2016 Jan 11.
Article in English | MEDLINE | ID: mdl-26828981

ABSTRACT

Ovarian cancer is the sixth most prevalent cancer in women and is considered the most lethal gynecological malignancy. It can be inherited as a familial disease but also has a strong spontaneous occurrence. Although the disease is associated with genome instability brought on by genetics and environmental factors there is evidence that mutations in the gene encoding for the breast cancer type 1 susceptibility protein (BRCA1) or its down-regulation are involved in its development. Down-regulation of BRCA1 expression by hypermethylation of its promoter may account for some cases of ovarian cancer but this does not explain the cause of the majority of the disease. This review explores the role of BRCA1 promoter hypermethylation and micro-RNAs (miRNA) involved in the regulation of BRCA1 and their role in ovarian cancer development as well as some of the exciting discoveries which could lead to targeting miRNA with a view to restoring BRCA1 expression in diseased tissues.


Subject(s)
BRCA1 Protein/genetics , DNA Methylation/genetics , MicroRNAs/genetics , Ovarian Neoplasms/genetics , Animals , Down-Regulation/genetics , Female , Gene Expression Regulation, Neoplastic/genetics , Humans , Mutation/genetics , Promoter Regions, Genetic/genetics
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