FIND ARTICLE

HIPOCRETINS (OREXINS) AND THEIR RECEPTORS: STRUCTURE, LOCALIZATION AND MOLECULAR MECHANISMS OF ACTIONS

Hypocretins, also known as orexins, are hypothalamic peptides that have been implicated in a variety of behaviors, e.g. food-seeking and feeding, arousal and sleep, reaction to stress. Disturbances in the central hypocretin neurotransmission are believed to underlie narcolepsy. It has also been postulated that hypocretins play an important role in the regulation of hypothalamus-pituitary-adrenal (HPA) axis, energy homeostasis, acquisition and learning of reward system-stimulating signals.

APOPTOSIS AND AUTOPHAGY - MECHANISMS AND DETECTION METHODS

For a long time apoptosis has been considered the only type of programmed cell death responsible for the maintenance of homeostasis in the organism. However, the results of studies, which have been carried out for the last years, prove that depending on its type, the cell can be guided in different directions, which can result either in its survival or death. According to the NCCD Committee, apoptosis and autophagy are ranked as two types of cell death.

STRUCTURE AND BIOLOGICAL FUNCTIONS OF GALECTIN-3. PART II

Gal-3 shares several significant structural properties with Bcl-2 family. Both proteins contain anti-death motif, critical for their anti-apoptotic function but the mechanism by which gal-3 exhibits antiapoptotic activity cannot be explained solely on it. Depending on the type, state and condition of the cell as well as depending on the type of stimulus gal-3 can show pro- or anti-apoptotic activity.

MECHANISMS OF a-AMANITIN HEPATOTOXICITY AND COMPARATIVE ANTIDOTAL EFFICACY OF SUBSTANCES USED IN AMANITA PHALLOIDES INTOXICATION A REVIEW OF EXPERIMENTS ON PRIMARY HEPATOCYTE CULTURES

The course of a-amanitin (a-AMA) toxicity in cultured canine and human hepatocytes is divided into 2 phases. The first phase comprises mainly functional cell impairments expressed by inhibition of protein and urea synthesis. The second stage is lethal and is characterized by ongoing necrosis and/ or apoptosis. a-AMA-induced apoptosis in human heptocyte cultures is p53- and caspase-3-dependent. Moreover, a-AMA causes increase in SOD activity, reduction of CAT activity and a significant increase in lipid peroxidation in cells, which may contribute to its severe hepatotoxicity.

APOPTOSIS – TARGETED ANTICANCER THERAPY

Apoptosis is the major form of cell suicide. Most conventional anticancer agents induce apoptosis indirectly. Although chemiotherapeutic drugs should selectively kill only tumor cells, normal cells are often susceptible to cytotoxic or cytostatic effects of these agents. This is a reason of potentially harmful side effects including inflammation and damage to the surrounding normal tissue. A new therapeu- tic approach in cancer treatment is the use of substances that stimulate cytokine production, angiogenesis inhibitors, gene therapies, antisense oligonucleotides and monoclonal antibodies.

DISTURBANCES OF THE ASYMMETRY OF PHOSPHATIDYLSERINE IN THE CELL MEMBRANE – THE LATEST DATA

The maintenance of transbilayer lipid asymmetry is essential for normal cell membrane func- tion and homeostasis of organisms. Even though many articles appeared about loss of transmembrane phospholipid asymmetry, constantly come out new data about this interesting occurrence. The most noteworthy are studies about phosphatidylserine (PS) externalization in apoptosis. This article present the latest data about the redistribution of PS on the surface of the cells.

STAT3 EXPRESSION IN NORMAL AND MALIGNANTLY TRANSFORMED B-LYMPHOCYTES

The human proto-oncogene STAT3 encodes transcriptional factor that is essential for embryo- genesis, proliferation and differentiation of many cell types, in addition to organ regeneration and involu- tion. It also regulates innate and adaptive immune mechanisms, including B cell maturation. Augmented STAT3 activation has been found in both irreversibly committed B cell lineage precursors and plasmacy- tes. Abnormal STAT3-mediated signal transduction has been observed in a large number of neoplasms, in which it induces anti-apoptotic and cell cycle progression mediating genes transcription.

APOPTOSIS MARKERS IN BLOOD PLATELETS

Blood platelets, enucleate cells derived from megakaryocytes, play an essential role in haemo- stasis and thrombosis. They may be involved probably in platelet activation and programmed death. The experimental evidences discussed in this review indicate that during aging and activation platelets express apoptotic markers similar to those found in nucleated cells.

MITOCHONDRIA - AN APOPTOSIS INTEGRATORS

Supernumerary, old or damaged cells of multicellular organisms are eliminated by apoptosis – programmed cell death. Apoptosis is accompanied by series of characteristic morphological and biochemi- cal events. The cell activates a cascade of cysteine proteases – caspases, that digest target proteins. Nucleases are also activated, which together leads to irreversible cell damage within few hours. Mitochon- dria are the cell compartment that integrates signals from different apoptotic pathways activated by ischemia, heat shock or growth hormones depletion.

APOPTOSIS IN SKELETAL MUSCLES AND KIDNEY AFTER ACUTE AND CHRONIC EXERCISE

Apoptosis in adult organism plays a role in removing of unnecessary, damaged or potentially dangerous cells. Apoptosis inducing factors include DNA damaging factors, such as oxidative stress or partial ischemia. Physical exercise may lead to disturbance and damage in many organs, especially in untrained organisms. It has been demonstrated that an intense exercise could finally lead to apoptosis in skeletal muscles, however apoptotic changes were restricted to single myonuclei.

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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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