cell senescence is a state of limited cell proliferation during a stress response or as part of a programmed process. When a senescent cell stops dividing, maintaining metabolic activity contributes to cellular homeostasis maintenance. in this process, the cell cycle is arrested at the G0/G1 phase. p16 inK4a protein is a key regulator of this process via its cyclin-dependent kinase inhibitor (cdKi) function. CDKI 2A (CDKN2A)/p16 gene expression is regulated by dna methylation and histone acetylation. Sirtuins (SirTs) are nicotinamide dinucleotide (nad + )-dependent deacetylases that have properties which prevent diseases and reverse certain aspects of aging (such as immune, metabolic and cardiovascular diseases). By performing quantitative Pcr, Western blot, chiP, and sirnas assays, in this study it was demonstrated that CDKN2A/p16 gene transcriptional activation and repression were accompanied by selective deposition and elimination of histone acetylation during the senescence of MRC5 cells. Specifically, significant H3K9Ac and H3K18Ac enrichment in cells with a senescent phenotype concomitant with CDKN2A/p16 gene overexpression was demonstrated compared with the non-senescent phenotype. Furthermore, the presence of H3K18Ac in deacetyl-transferase SIRT7 knockdown Mrc5 cells allowed CDKN2A/p16 promoter activation. These results suggested that SIRT7 served as a critical component of an epigenetic mechanism involved in senescence mediated by the CDKN2A/p16 gene.

The placenta can be affected by environmental factors, such as exposure to cigarette smoke. This exposure in the fetal context is considered a risk factor for the development of short-term postnatal diseases, such as asthma. Asthma is an inflammatory disease characterized by predominant acquisition of CD4 T lymphocytes (TLs) of the Th2 type. Transcription factors such as GATA binding protein 3 (GATA3) and STAT6 actively participate in the differentiation of virgin TLs towards the Th2 profile, while transcription factors such as STAT1, T-Box transcription factor 21 (T-BET), RUNX1 and RUNX3 participate in their differentiation towards the Th1 profile. The objective of the current study was to evaluate the impact of exposure to cigarette smoke on the gene expression of STAT1, T-BET, GATA3, IL-4, RUNX1 and RUNX3 during the gestation period, and to determine whether the expression levels of these genes are associated with changes in global methylation. STAT1, GATA3, RUNX1 and RUNX3 protein and mRNA expression levels in the placental tissue of women smokers and non-smoking women were determined via immunohistochemistry and quantitative PCR (qPCR) respectively. Additionally, T-BET and IL-4 mRNA expression levels were determined by qPCR. On the other hand, global methylation was determined via ELISA. In the present study, significant increases were observed in RUNX1 transcription factor expression in placentas from women smokers when compared with placentas of non-smoking women. Similarly, significant increases in the expression of GATA3, IL-4 and RUNX3 mRNA were observed. The changes in gene expression were not associated with changes in the global methylation levels. Finally, a higher frequency of low-birth-weight infants were identified in cases of exposure to cigarette smoke during pregnancy when compared with infants not exposed to cigarette smoke during pregnancy. Thus, the data of the present study contributed to the understanding of the genetic and clinical impacts of exposure to cigarette smoke during pregnancy and its importance in maternal and fetal health.

Electronic cigarettes (ECIGs) are electronic devices that heat and vaporize a solution that usually contains a mixture of glycerol, propylene glycol, water, flavors and various concentrations of nicotine. ECIGs have 3 key components: A power source, a cartridge containing an atomizer along with a liquid solution and a mouthpiece. The solution (often known as e-liquid or e-juice) is heated into an aerosol inhaled by the user. Smoking conventional cigarettes is considered a determinant factor in the development of chronic respiratory diseases, cardiovascular diseases, cancers, and reproductive system dysfunctions. Conventional smoking also causes genome damage and alteration of the transcriptome, due to the amounts of noxious substances emitted during the combustion of these products. Recently, cigarette consumers have begun to use ECIGs as a replacement or substitute practice to help them quit smoking. In addition, an increase in the use of ECIGs and similar devices by young individuals has been reported, which is unsurprising due to the unregulated distribution and sale of these products. The present review article describes and discusses the impact and the noxious effects of substances in ECIGs and other nicotine administration systems on DNA structure, gene expression profile, and epigenetic modification, focusing on the respiratory system and embryonic development.

El proceso transición epitelio mesénquima (TEM) permite que una célula epitelial de manera temporal, adquiera un fenotipo mesenquimal como respuesta a un estímulo interno o externo. Este proceso se caracteriza  por la activación y represión de genes involucrados en diferentes vías de señalización asociadas con migración, invasión y apoptosis, entre otros. En este proceso la epigenética cumple un papel fundamental. La epigenética comprende cuatro mecanismos: metilación de ADN, modificación covalente de histonas, ARN no codificantes (ARNnc) y complejos remodeladores de la cromatina, que regulan la expresión de un gen sin alterar su secuencia. En esta revisión de tema los autores describen los principales mecanismos epigenéticos involucrados en la regulación de la expresión de genes que se activan y reprimen concomitantemente en las tres fases del proceso TEM: fase no migratoria, fase premigratoria y fase migratoria.