Biomedical subjects

Magdalena Izdebska

Publications and source records attributed to Magdalena Izdebska.

5 recordsLinked to original sources

PubMed2006

[The cytoskeleton reorganization and differentiation of HL-60 and K-562 human leukemia cell lines].

Microfilaments, microtubules, and intermediate filaments form the cytoskeleton. These substructures play a significant role in cell motility, transport, divisions, differentiation, tumor transformation, and apoptosis. These processes are related with changes in cell shape, in which cytoskeletal proteins take an active part. In non-muscle cells, actin is an essential constituent of microfilaments, tubulin forms microtubules, and vimentin is one of the characteristic proteins of intermediate filaments. The differentiation of cells is associated inseparably with tissue and organ formation, and the induction of malignant cell differentiation can be a method of treatment, especially in hematopoietic steam cell disease therapy. In studies on tumor cell differentiation, agents such as cytokines, retinoids, forbol esters, and vitamin D3 are the most commonly used, and results show these substances may participate in different pathways of signal transduction. Retinoids and vitamin D3 mostly affect gene transcription via nuclear receptors, whereas cytokines act through membrane receptors. The results of studies show actin, tubulin, and vimentin reorganization during the differentiation of leukemia cells, but it remains unknown whether the observed changes are the cause or the result of the differentiation process.

Apoptosis↗

PubMed2006

[Mitochondria and cell death].

In living cells, apoptosis is effected through many different pathways. Programmed cell death (PCD) may proceed with the involvement of membrane receptors, mitochondria, granzyme B, or the endoplasmic reticulum. The mitochondrial pathway is initiated from within the cell as a consequence of changes in reductive potential. It may also be caused by DNA mutation or various disturbances in the cell's metabolism. In some cases, the intrinsic pathway is connected with the extrinsic one, generated by the cell's environment. The central organelle which initiates the intrinsic pathway is the mitochondrion. Changes in the permeability of the mitochondrial outer membrane cause an outflow of cytochrom c, which interacts with cytoplasmic factor Apaf-1 and procaspase 9, in the presence of ATP, and thus triggers the caspase cascade. Apart from cytochrom c, more than 40 regular or executor particles involved in apoptosis might be released from the mitochondrion. These include Smac/DIABLO, Omi/HTR A2, endonuclease G, AIF, and IAP. Moreover, regulatory functions are performed by Bcl-2 family proteins present in the cytoplasm that affect mitochondrial membrane permeability and by heat shock proteins (HSPs), both of these regulating caspase function. The phenomenon of programmed cell death is the main subject of research for many groups of scientists. There are still many aspects which need to be elucidated.

Animals↗

PubMed2005

[The role of actin in Alzheimer's disease].

Alzheimer's disease is associated with the formation of extracellular senile plaques and intracellular neurofibrillary tangles. In the neurons of patients, all the morphological features of apoptosis, e.g. blebbing, formation of apoptotic bodies, and chromatin condensation, as well as cytoskeleton reorganization were observed. Actin filaments interact with proteins characteristic of Alzheimer's disease, such as apolipoprotein E, amyloid precursor protein, pressenilin, and tau protein. The degeneration of neurons is associated with the formation of Hirano bodies, which contain actin, cofilin, tubulin, tau protein, and proteins of the MAP family and APP. Actin rods are also observed in postmortal brains of patients with Alzheimer's disease. These 'rods' have been shown to play a role in Hirano body precursors.

Actin Depolymerizing Factors↗

PubMed2005

[The involvement of transglutaminase 2 in autoimmunological diseases].

Transglutaminase 2 (TG-ase 2) is one of the enzymes which catalyzes the deamination and transacylation of proteins. The transfer of a glutamine acyl residue to a lysine amine group of the acceptor protein is one of the posttranslational covalent modifications regulating some polypeptide activities. The control of protein oligomerization by TG-ase 2 is a cause of the formation of detergent-insoluble macromolecular aggregates. These inclusions are present in degenerating cells during, for example, Alzheimer's and Parkinson's disease. Overexpression of TG-ase 2 has been noted in apoptotic cells. Protein reserves in cereals are rich in glutamine, a substrate of TG-ase 2. Deamination of glutamine is the most important reaction for the initiation of the inflammatory process during gluten-dependent disease of the gut (celiac disease). Grains that contain gliadin are a cause of inflammatory reaction in children with intolerance to glutene. Interactions of the TG-ase product-glutamate with antigens of the major histocompatibility complex type II (MHC II, or HLA DQ) cause autoimmunological reaction by CD4+ T lymphocytes. Knowledge of the kinetic and molecular character of TG-ase 2 has contributed to finding peptides to replace gliadin. These molecules do not evoke immunological events.

Animals↗

PubMed2003

Histological and morphometrical examinations of suprarenal glands in rats after experimental administration of atorvastatin and ethanol.

The experiment was carried out on Wistar rat males weighting about 250 g. Animals from control group I received water and standard granulated fodder ad libitum. Animals from control group II received 20% ethanol instead of water. Animals from experimental group I received Atorvastatin in the dose of 0.28 mg/24h, animals from experimental group II received Atorvastatin in the dose of 2.8 mg/24h, animals from experimental group III received 20% ethanol + Atorvastatin in the dose of 0.28 mg. After 6 weeks the animals were decapitated. H+E staining, PAS method for detection of neutral mucopolysaccharides and Thomas's reaction for detection of lipids were made on 6 micron thick sections. The surface areas of the nuclei sections were assessed in the zona fasciculata. It was stated that ethanol causes strong hyperemia of suprarenal cortex, the high dose of atorvastatin--2.8 mg/24h and small dose of atorvastatin--0.28 mg/24h administered with ethanol cause the decrease of lipid amount in the whole suprarenal cortex and degenerative changes in many cells of the zona fasciculata.

Adrenal Glands↗