Here we aim to describe each factor that leads to skin aging and describe their mechanisms. A PubMed database searches (from January 2004 to March 2014) using aging and skin as searched terms. There are substantial evidences showing that aging is associated with damage from free radicals represented by various reactive oxygen species (ROS). Mitochondria are producers and also targets of oxidative stress. The cycle of mitochondrial dysfunction can trigger the aging process. In the cellular senescence and telomeres theory, the diploid cells exhibit a limited proliferation potential. After a finite number of divisions, they enter a state of senescence with a stop replication in cell proliferation. It is suggested that aging is associated mainly with hyper-regulation of apoptosis. Obesity presumably accelerates the process of aging, which is aggravated by smoking. And the influence of the environment, called solar UV irradiation is of considerable importance to skin aging. There are several mechanisms that trigger the natural aging process and contribute to age-related changes, including oxidative stress theory of free radicals, the mitochondrial dysfunction, telomere shortening, UV radiation and other mechanisms that taken together or alone may or not accelerate the change in skin.

Introduction. We evaluated the association between components of the renin-angiotensin system and the development of breast cancer in a case-control study by means of angiotensinconverting enzyme (ACE) insertion/deletion (I/D) and angiotensin II type 1 (AT 1 )-receptor A1166C polymorphisms. Methods. Genotyping was performed by PCR-RFLP (restriction fragment length polymorphism) or PCR (polymerase chain reaction) using genomic DNA extracted from buccal cells of subjects with (101 cases) or without (307 controls) breast cancer. Results. The frequencies of genotypes for ACE were: DD, ID and II (in %: cases: 60; 20; 20; controls: 46; 37; 17; p=0.019, χ 2 ); and for AT 1 -receptor were: AA, AC and CC (in %: cases: 65; 30; 5; controls: 51; 44; 5; p=0.114, χ 2 ). The results suggested that the A1166C polymorphism was not associated with breast cancer risk. On the other hand, for the ACE (I/D), there seemed to be different risks for cancer between cases and controls. Conclusions. The ID genotype was less frequently associated with the disease than were the DD or II; that is, women with the ID genotype were 3.1 times less likely to develop breast cancer than those with the other genotypes. The ID genotype might be protective against breast cancer and the ACE (I/D) polymorphism a possible target for developing genetic markers for breast cancer.

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Kobayashi NCC et al. 86rev assoC Med bras 2015; 61(1):86-93

Associations have been found between the angiotensin-converting enzyme insertion deletion (I/D) polymorphism (ACE I/D) and endometrial and epithelial ovarian cancer (EC and EOC, respectively). In this study, the following frequencies for each of three ACE polymorphisms, DD, ID, and II, respectively, were observed: in the EC group, 55, 24, and 21% versus the control group 39, 40, and 21% (p = 0.033*); in the EOC group 49, 36, and 15% versus the control group 49, 33, and 18% (p = 0.82). According to these allelic distributions, DD carriers are 2.0 times more likely than individuals carrying the ID or II genotypes to develop EC; therefore, the DD genotype seems to be protective against EC. In contrast, no association was observed between ACE (I/D) polymorphism with EOC. The ACE (I/D) polymorphism might play a role in the pathogenesis of EC and it should be considered when identifying genetic markers for EC.

. Conception, design, intellectual and scientific content of the study; analysis and interpretation of data; manuscript writing; critical revision. ABSTRACT PURPOSE:Evaluate the expression profile of genes related to Innate and Adaptive Immune System (IAIS) of human Primary Epidermal keratinocytes (hPEKP) of patients with severe burns. METHODS:After obtaining viable fragments of skin with and without burning, culture hKEP was initiated by the enzymatic method using Dispase (Sigma-Aldrich). These cells were treated with Trizol® (Life Technologies) for extraction of total RNA. This was quantified and analyzed for purity for obtaining cDNA for the analysis of gene expression using specific IAIS PCR Arrays plates (SA Biosciences). RESULTS:After the analysis of gene expression we found that 63% of these genes were differentially expressed, of which 77% were repressed and 23% were hyper-regulated. Among these, the following genes (fold increase or decrease): IL8 (41), IL6 (32), TNF (-92), HLA-E (-86), LYS (-74), CCR6 (-73), CD86 (-41) and HLA-A (-35).CONCLUSIONS: This study contributes to the understanding of the molecular mechanisms underlying wound infection caused by the burn. Furthermore, it may provide new strategies to restore normal expression of these genes and thereby change the healing process and improve clinical outcome.

PURPOSE:To evaluate the effect of keratinocyte growth factor (KGF) treatment on the expression of wound-healing-related genes in cultured keratinocytes from burn patients. METHODS:Keratinocytes were cultured and divided into 4 groups (n=4 in each group): TKB (KGF-treated keratinocytes from burn patients), UKB (untreated keratinocytes from burn patients), TKC (KGF-treated keratinocytes from controls), and UKC (untreated keratinocytes from controls). Gene expression analysis using quantitative polymerase chain reaction (qPCR) array was performed to compare (1) TKC versus UKC, (2) UKB versus UKC, (3) TKB versus UKC, (4) TKB versus UKB, (5) TKB versus TKC, and (6) UKB versus TKC. RESULTS:Comparison 1 showed one down-regulated and one up-regulated gene; comparisons 2 and 3 resulted in the same five downregulated genes; comparison 4 had no significant difference in relative gene expression; comparison 5 showed 26 down-regulated and 7 up-regulated genes; and comparison 6 showed 25 down-regulated and 11 up-regulated genes. CONCLUSION:There was no differential expression of wound-healing-related genes in cultured primary keratinocytes from burn patients treated with keratinocyte growth factor.