A morte celular por apoptose é caracterizada por alterações bioquímicas e moleculares específicas, incluindo a exposição de diversos ligantes, responsáveis pelo seu reconhecimento imediato por fagócitos. Em situações não patológicas, a remoção eficiente da célula apoptótica é assegurada pela redundância do sistema, onde ocorre a interação dos diversos ligantes por ela expostos com as moléculas receptoras presentes na superfície da célula fagocítica. A presente revisão enfatisará as interações moleculares operantes em sistemas celulares de mamíferos e não mamíferos, assim como as consequências do seu reconhecimento e sinalização. Além disso, serão discutidos alguns modelos celulares nos quais a exposição do fosfolipídeo fosfatidilserina (PS), característica do fenótipo apotótico, não é obrigatoriamente seguida da morte celular.

Cell death by apoptosis is characterized by specific biochemical changes, including the exposure of multiple ligands, expected to tag the dying cell for prompt recognition by phagocytes. In non-pathological conditions, an efficient clearance is assured by the redundant interaction between apoptotic cell ligands and multiple receptor molecules present on the engulfing cell surface. This review concentrates on the molecular interactions operating in mammalian and non-mammalian systems for apoptotic cell recognition, as well as on the consequences of their signaling. Furthermore, some cellular models where the exposure of the phosphatidylserine (PS) phospholipid, a classical hallmark of the apoptotic phenotype, is not followed by cell death will be discussed.

Many studies have been developed trying to understand the complex molecular mechanisms involved in oncogenesis and progression of prostate cancer (PCa). Current biotechnological methodologies, especially genomic studies, are adding important aspects to this area. The construction of extensive DNA sequence data and gene expression profiles have been intensively explored to search for candidate biomarkers to evaluate PCa. The use of DNA micro-array robotic systems constitutes a powerful approach to simultaneously monitor the expression of a great number of genes. The resulting gene expressing profiles can be used to specifically describe tumor staging and response to cancer therapies. Also, it is possible to follow PCa pathological properties and to identify genes that anticipate the behavior of clinical disease. The molecular pathogenesis of PCa involves many contributing factors, such as alterations in signal transduction pathways, angiogenesis, adhesion molecules expression and cell cycle control. Also, molecular studies are making clear that many genes, scattered through several different chromosomal regions probably cause predisposition to PCa. The discovery of new molecular markers for PCa is another relevant advance resulting from molecular biology studies of prostate tumors. Interesting tissue and serum markers have been reported, resulting in many cases in useful novelties to diagnostic and prognostic approaches to follow-up PCa. Finally, gene therapy comes as an important approach for therapeutic intervention in PCa. Clinical trials for PCa have been demonstrating that gene therapy is relatively safe and well tolerated, although some improvements are yet to be developed.

A morte celular programada (PCD) ou apoptose, um processo ativo de morte celular, desempenha um papel fundamental no desenvolvimento tecidual normal e na organogênese, assim como na patogênese de diferentes doenças. Embora este processo ocorra em uma gama variada de diferentes células e tecidos, sob a influência dos mais diversos agentes indutores, a resultante morfológica e bioquímica do processo é extremamente monótona, sugerindo que um mecanismo único opere em todas as situações. Era consensualmente aceito que um programa de morte programada não poderia ser vantajoso para organismos unicelulares e que a PCD teria surgido na evolução para servir às necessidades organizacionais dos seres multicelulares. No entanto, a descrição de PCD em três diferentes espécies de tripanosomatídeos patogênicos indica que a origem da PCD é anterior à da multicelularidade. A hipótese colocada neste trabalho é a de que uma população de tripanosomatídeos tem uma organização social e que esta é necessária ao cumprimento das exigências biológicas de um parasita heterôxênico. A proposta inclui possíveis papéis biológicos para a PCD no desenvolvimento do parasita no inseto vetor e/ou no hospedeiro mamífero e sugere abordagens experimentais para se localizar a origem evolutiva da PCD entre os cinetoplastídeos.

Programmed cell death (PCD) or apoptosis, an active process of cell death, plays a central role in normal tissue development and organogenesis, as well as in the pathogenesis of different diseases. Although it occurs in diverse cells and tissues under the influence of a remarkable variety of inducing agents, the resultant ultrastructural and biochemical changes are extremely monotonous, indicating the existence of a common biological mechanism underlying its occurrence. It is generally accepted that a developmental program leading to cell death cannot be advantageous to unicellular organisms and that PCD appeared in evolution to fulfill the organizational needs of multicellular life. However, the recent description of apoptotic death occurring in three different species of pathogenic kinetoplastids suggests that the evolutionary origin of PCD precedes the appearence of multicellular organisms. The present study proposes that a population of pathogenic Trypanosomatids is socially organized and that PCD is a prerequisite for this organization and for the fulfillment of the demands of a heteroxenic lifestyle. This proposal includes possible roles for PCD in the development of the parasite in the insect vector and/or in its mammalian host and suggests experimental strategies to localize the evolutionary origin of PCD within the kinetoplastids.