FIND ARTICLE

THE ROLE OF APOPTOSIS IN THE OVARIAN CELLS

Apoptosis is a natural process at reproductive age in women. It concerns granulosa and thecal cells. This process influences on the amount of ovarian follicles, luteal corpus sufficiency and on steroidogenesis and menopause. Apoptosis cause normal function and homeostasis of ovarian cells. Knowing the mechanism of apoptosis in human ovary to optimalize the management in endocrinologia disorders and neoplasmus.

STRESS PROTEINS IN EXERCISE ADAPTATION

Intracellular protein destroying and impairment of their synthesis result in disturbance of cell homeostasis and can lead to cell death. Counteracting these changes the cell induces synthesis of stress proteins among others. Physical exercise has stress attributes, especially if it is a long-lasting and intensive one. It can be assumed that this will bring about an intensification of stress protein expression what was experimentally confirmed. However the significance of this reaction is not fully clear taking into account the variety of functions the stress protein act in the organism.

NITRIC OXIDE AS A BIOREGULATOR OF APOPTOSIS

Nitric oxide (NO), synthesized from L-arginine by NO synthases, is a small, diffusible, highly reactive molecule with dichotomous regulatory roles under physiological and pathological con- ditions. Apoptosis plays an important role in the development of the organism but also under various pathological conditions. NO can exert both pro- and anti-apoptotic effects, depending on the conditions and cell type.

THE ROLE OF APOPTOSIS IN RESPONSIVENESS TO ALLOGRAFT: TOLERANCE AND GRAFT REJECTION

Studies of a few last years give evidence for a role of apoptosis not only in graft rejection but also in induction of transplantation tolerance. Apoptosis – programmed cell death is an active process which refers to superflous and defective cells. For a responsiveness to allograft the most important are two mechanisms of apoptosis: AICD (activation induced cell death) which involves Fas/FasL engage- ment and PCD (passive cell death) – caused by cytokine withdrawal. Graft rejection is caused by genetic differences between a donor and a recipient.

APOPTOSIS IN HUMAN ERYTHROCYTES

Until very recently, erythrocytes have been considered unable to undergo apoptosis, as they lack mitochondria and nuclei, key organelles in the apoptotic machinery of other cells. However, in most recent observations it does not seem to be the truth.The major spinning point in this research was finding caspases (cysteine proteases), that play the major role in programmed cell death, in humans mature erythrocytes. This article shows the progress of apoptosis in different stadia of humans erythro- cytes development as well as in several pathological stadia.

INDUCTION OF APOPTOSIS AS A TARGET OF CANCER GENE THERAPY

Cell death, commonly recognized as necrosis or apoptosis, is thought to be a one of biological processes describing cell life. The phenomena of cell recycling during human life is known for a various types of cells and the resistance of cancer cells to apoptosis is also well described. Proapoptotic gene therapy is one of the method of cancer therapy. The main rationales are focused on induction of apopto- sis of cancer cells and therefore inhibition its growth. Mostly, gene therapy trials are concerned on genes encoding well known proteins of apoptotic signaling as BAX, P53, TNF, caspases.

Autophagy the tool of cancer cell survival or death?

In the last decade a progress has been achieved in understanding the mechanisms which control the cell death. Accumulating evidence suggest that apoptosis is not the only one type of pro- grammed cell death (PCD). Cells use different pathways to active self-destruction process. There are three types of programmed cell death (PCD): condensation prominent, type I or apoptosis, dependent on the activity of caspases, type II – autophagy prominent and type III occurring through disintegration of cells into fragments without condensation and involvement of lysosomal system.

Apoptosis and tumors

General characteristics of apoptosis and mechanisms leading to activation of caspases and endonucleases, the main executors of apoptosis is described. The crucial role in these processes of mitochondria and the proteins released from them procaspase 9, cytochrom c and AIF factor is also shown. Information is also presented about membrane receptors, their ligands as well as various regulatory proteins, those from BCL-2/BAX and IAPs families included. It is pointed out that changes in the level of expression and/or properties of regulatory proteins characterize various tumor cells.

Various aspects of protein kinases action in apoptosis

Apoptosis is a complex process requiring collaboration of several intracellular and extracellular factors. It is known that some intracellular agents controlling cell proliferation and differentiation could modulate apoptosis. Among others, the protein kinases could be involved in control of apoptosis, because it is well known that protein phosphorylation plays important role in this process. Although it is clear that protein kinases may take part in apoptosis but still their role is not obvious.

Glycoprotein 120-mediated cytopathic effects in HIV-1 infection

In this article the mode of infection with HIV-1 virus and the role of glycoprotein 120 (gp120) in this process were described. The gp120 is responsible for a number of phenomena resulting from HIV-1 infection. Against the epitopes of gp120 humoral and cellular responses develop. However, because of a high variability of this protein, caused by mutations, in the process of infection these responses become ineffective. Moreover, gp120, as revealed from numerous studies, causes a decrease in the number of peripheral blood CD4+ T lymphocytes, both infected and uninfected.

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The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

Editorial address:
Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email: mnowicki@ump.edu.pl

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