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1

The role of genetic factors apoptosisi and 14-3-3 protein in the induction of some atopic diseases

100%
Jagiello E., Krasnowska M., Gacko M., Rucinska M., Skrzydlewski Z.
Postępy Higieny i Medycyny Doświadczalnej
|
1997
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vol. 51
|
issue 4
385-398
EN
In this review we try to summarize some of the new informations about the genetic base of bronchial asthma. We also mention apoptosis (programmed cell death) as the process modulating cell proliferation, differentiation and death. According to the latest reports, the disorders of the regulation of apoptosis may play an important role an the pathogenesis of autoimmunologic and atopic diseases (including bronchial asthma), AIDS and neoplasmatic diseases. There is a linkage between the induction of apoptosis and signal transduction disorders. We describe the Raf/MECK/ERK/MAP signal transduction pathway and 14-3-3 protein - the peptide which possibly might participate in the initiation of the programmed cell death.
2
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Effects of neurosteroids on neuronal survival: Molecular basis and clinical perspectives

80%
Leskiewicz M., Budziszewska B., Basta-Kaim A., Zajac A., Kacinski M., Lason W.
Acta Neurobiologiae Experimentalis
|
2006
|
vol. 66
|
issue 4
359-367
EN
Neurosteroids have long been known to act as important modulators of central nervous system functions. The concept of their mechanism of action, however, have essentially undergone an evolution. Previously, these compounds were postulated to regulate neuronal function mainly via allosteric regulation of some membrane-bound receptors, such as GABAA and NMDA receptors, in a non-genomic way. Recent studies have provided evidence for intracellular targets for neurosteroids, e.g., transcription factors (NFkappa-B, progesterone receptors), protein kinases (phosphatidylinositol 3-kinase, protein kinase C), or microtubule-associated proteins, i.e. factors essential in regulation of neuronal survival and apoptosis. This paper reviews in vitro and in vivo data on neurosteroid involvement in the regulation of neurodegenerative processes with emphasis on new intracellular and genomic mechanisms of their action. Potential utility of neurosteroids in the treatment of some neurodegenerative disorders has been also discussed.
3

Neutrophil recognition of bacterial DNA and Toll-like receptor 9-dependent and independent regulation of neutrophil function

80%
El_ K. D., Jozsef L., Filep J. G.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
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vol. 56
|
issue 1
41-53
EN
Neutrophils are essential for host defense and detect the presence of invading microorganisms through recognition of pathogen-associated molecular patterns. Among these receptors are Toll-like receptors (TLRs). Neutrophils express all known TLRs except for TLR3. TLR9, localized intracellularly, is to date the best characterized sensor for bacterial DNA, containing short sequences of unmethylated CpG motifs, though TLR9-independent intracellular DNA recognition mechanism(s) may also exist. Bacterial DNA has profound impact on neutrophil functions; it promotes neutrophil trafficking in vivo, induces chemokine expression, regulates expression of adhesion molecules, enhances phagocyte activity, and rescues neutrophils from constitutive apoptosis. TLR9 stimulation results in alterations in cellular redox balance, peroxynitrite formation, activation of the mitogen-activated protein kinase, PI3-kinase, and Jun N-terminal kinase pathways and/or nuclear factor ?B and AP-1. These features identify an important role for bacterial DNA and TLR9 signaling in the regulation of neutrophil functions that are critical for optimal expression as well as for resolution of the inflammatory response.
4

IL-15 and IL-15Ra in CD4+T cell immunity

80%
Van_ B. T., Grooten J.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 2
115-126
EN
The cytokine IL-15 performs numerous functions, such as promotion of growth and survival, on a plethora of cell types from both the lymphoid and non-lymphoid compartments. Therefore, mice genetically engineered to either lack or overexpress functional IL-15 display reduced immunological responses and leukemia, respectively. Surprisingly, IL-15 protein is hardly found in serum or body fluids. Due to the lack of a clear demonstration of its presence as protein, IL-15 was often referred to as a 'ghost cytokine'. Recently, however, membrane-bound IL-15 was detected in both a membrane-anchored form and an IL-15Ralpha-bound form on monocytes. Interestingly, the latter complex can be transpresented to cells expressing the intermediate-affinity IL-2/15Rbeta- gammaC receptor and thereby support the survival and proliferation of T cells. Moreover, overlapping promoter elements indicate a model of co-regulation of IL-15 and IL-15Ralpha by which IL-15 activities are controlled in a cell-contact-dependent manner. In this review, recent reports on IL-15 are combined with previous observations and discussed in terms of their functional consequences for CD4+ T cell responses.
5

A role of NF-B and the proteasome in autoimmunity

80%
Hayashi T., Faustman D.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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vol. 48
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issue 5
353-365
EN
Type 1 diabetes (also known as insulin-dependent diabetes mellitus or juvenile-onset diabetes) is usually caused by T cell-mediated autoimmunity, with a prediabetic state characterized by the production of autoantibodies specific for proteins expressed by pancreatic beta cells. The non-obese diabetic (NOD) mouse is a spontaneous model of type 1 diabetes with a strong genetic component that maps to the major histocompatibility complex (MHC) region of the genome. A specific proteasome defect has been identified in NOD mouse lymphocytes that results from down-regulation of expression of the proteasome subunit LMP2, which is encoded by a gene in the MHC genomic region. This defect both prevents the proteolytic processing required for the production and activation of the transcription factor nuclear facktor-kappaB (NF-kappaB), which plays important roles in immune and inflammatory responses, as well as increases the susceptibility of the affected cells to apoptosis induced by tumor necrosis factor alpha (TNF-alpha). The proteasome dysfunction is both tissue and developmental stage specific and likely contributes to disease pathogenesis and tissue targeting.
6
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Postnatal development of the rat striatum - a study using in situ DNA end labeling technique

80%
Maciejewska B., Lipowska M., Kowianski P., Domaradzka-Pytel B., Morys J.
Acta Neurobiologiae Experimentalis
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1998
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vol. 58
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issue 1
23-28
EN
We have examined the development of rat striatum for evidence of cells dying in the process of physiological cell death. In present study we have indicated apoptotic cells in sections stained with cresyl violet (cell death characterized by pyknosis) or with DNA end labeling assay (TUNEL method). Our results demonstrated that cell loss during maturation of the rat striatum had the characteristics of apoptosis rather than necrosis. The greatest number of TUNEL - positive and pyknotic cells in the striatum were found during the first postnatal days; after 7th day of postnatal life a rapid decrease of its number was observed. After the second postnatal week no TUNEL-positive cells were observed in the striatum. Our analysis suggests that apoptotic cell death occurring during the development of striatal neuronal population takes place during the first week of postnatal life.
7

Rewinding the DISC

80%
Chaigne-Delalande b., Moreau J.-F., Legembre P.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 1
9-14
EN
Fas (CD95/APO-1) belongs to the tumor necrosis factor receptor family and its signaling pathway has been extensively studied over the past 15 years. Blockade of the Fas-mediated apoptotic signal leads to abusive lymphoproliferation, auto-immunity, and an increased risk of developing lymphoma and leukemia. Fas engagement drives the formation of a complex termed DISC (death-inducing signaling complex), which contains the adaptor molecule Fas-associated protein, two members of the caspase family caspase-8 and -10, and a pseudo-caspase termed c-FLIP. According to different authors, DISC formation relies either on the redistribution of Fas into the lipid rafts or the recruitment of the actin cytoskeleton and receptor endocytosis or the production of ceramide. However, the accurate molecular ordering upstream from the formation of DISC remains very puzzling and is highly debated. Herein we review some of the factors that would potentially facilitate or limit the formation of DISC.
8

Dynamic control of B lymphocyte development in the bursa of Fabricius

80%
Funk P. E., Palmer J. L.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 6
389-398
EN
The chicken is a foundational model for immunology research and continues to be a valuable animal for insights into immune function. In particular, the bursa of Fabricius can provide a useful experimental model of the development of B lymphocytes. Furthermore, an understanding of avian immunity has direct practical application since chickens are a vital food source. Recent work has revealed some of the molecular interactions necessary to allow proper repertoire diversification in the bursa while enforcing quality control of the lymphocytes produced, ensuring that functional cells without self-reactive Ig receptors populate the peripheral immune organs. Our laboratory has focused on the function of chB6, a novel molecule capable of inducing rapid apoptosis in bursal B cells. Our recent work on chB6 will be presented and placed in the context of other recent studies of B cell development in the bursa.
9

Viral strategies in modulation of NF-kappaB activity

80%
Lisowska K., Witkowski J. M.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 6
367-375
EN
Activation of nuclear factor (NF)-kappaB transcription factors family in response to different stimuli such as inflammatory cytokines, stress inducers or pathogens? products results in host innate and adaptive immunity. NF-kappaB plays a central role in promoting the expression of genes involved in inflammatory, immune and apoptotic processes, including those encoding cytokines, chemokines, cytokine receptors or proteins involved in antigen presentation. Although the main function of NF-kappaB is to activate specific genes in the cells of the immune system, its role in controlling the host cell cycle makes NF-kappaB an interesting target for pathogenic viruses. Some viruses take advantage of anti-apoptotic properties of NF-kappaB to escape host defence mechanisms, other use apoptosis to spread. This review describes the role of NF-kappaB family in immune responses, mechanism of NF-kappaB activation and different strategies that viruses have developed to modulate NF-kappaB pathway in order to facilitate and enhance viral replication and avoid host immune responses.
10
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Sphingosylphosphorylcholine induces mitochondria-mediated apoptosis in neuro 2a cells: Involvement of protein kinase C

80%
Miguel B. G., Fernandez I., Toboso I., Agudo-Lopez A., Catalan E., Martinez A. M.
Acta Neurobiologiae Experimentalis
|
2008
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vol. 68
|
issue 4
443-452
EN
We demonstrate that sphingosylphosphorylcholine-mediated cell death involves the activation of different protein kinase C isozymes in different manners. Treating cells with sphingosylphosphorylcholine resulted in activation of protein kinase C delta, which is necessary, together with elevation of Ca2+, for sphingosylphosphorylcholine-induced apoptosis. A rapid translocation from cytosol to membrane, and a proteolytic protein kinase C delta cleavage was found, probably due to activation of caspase-3, to give a catalytically active fragment involved in cellular apoptosis. Moreover, sphingosylphosphorylcholine also induced translocation of protein kinase C zeta, resulting in an anti-apoptotic effect. To explore whether a mitochondrial pathway is involved in sphingosylphosphorylcholine-induced apoptosis, we analyzed the effect of sphingosylphosphorylcholine on cytochrome c release and caspase-3 activity. We must point out that the sphingolipid caused an increase of cytochrome c release from mitochondria to cytosol concomitantly with an increase of caspase-3 activity. Furthermore, a translocation of Bax was found, after sphingosylphosphorylcholine treatment.
11
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Cell death and neuronal arborization upon quercetin treatment in rat neurons

80%
Jakubowicz-Gil J., Rzeski W., Zdzisinska B., Dobrowolski P., Gawron A.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 2
139-146
EN
Quercetin, one of the major flavonoids, exhibits many beneficial effects on human organism as antihistamine, antioxidant, anti-inflammatory, anticancer and antiviral drug. It is recommended as suplement of healthy diet but still the knowledge of its beneficial effect on normal cells is not satisfactory. We decided to examine the effect of flavonoid on neurons morphology and their susceptibility to cell death. Fractal analysis of rat neurons revealed that 24 hours long incubation with quercetin diminished neuronal arborisation in cortical neurons. Neurons also appeared to be very sensitive to cell death after flavonoid treatment in concentration dependent manner. Over 50% of cells died after incubation with 15 ?g/ml of flavonoid while 1 ?g/ ml of quercetin induced cell death only in 5%. Staining with Hoechst 33342 and propidium ioidide revealed the two types of cell death: apoptosis and necrosis. The number of apoptotic cells was comparable with necrotic ones. These results suggest toxic effect of quercetin on neurons what should be taken into consideration in further studies on using quercetin as therapeutic agent.
12

BH3-only proteins: the lords of death

80%
Fleischer A., Rebollo A., Ayllon V.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 1
9-17
EN
Although the mechanisms by which Bcl-2 family proteins control the apoptotic machinery of the cell are not fully understood, it becomes clear that the role of BH3-only proteins consists in serving as sensors or sentinels of cellular damage, transducing the apoptotic stimuli to the mitochondria. For this reason, mammalian cells have developed several strategies for their strict regulation throughout evolution. This review aims to highlight the different ways by which BH3-only proteins are controlled, including transcriptional regulation, post-translational modifications and subcellular localization.
13

Dimerization, ROS formation, and biological activity of o-methoxyphenols

80%
Fujisawa S., Atsumi T., Murakami Y., Kadoma Y.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
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vol. 53
|
issue 1
28-38
EN
o-Methoxyphenols are antioxidants widely used in the cosmetic and food industries. Dimers from 1, 2, or 3 were synthesized and their radical-scavenging and biological activities were compared with those of the original or other phenols. Radical-scavenging was evaluated from a kinetic induction period method (IPM). To simulate biomimetic thiolcooxidation with antioxidants, the behavior of mixtures of 1, 2, 4, or catechin with mercaptomethylimidazole (MMI), a thiol was investigated using IPM. Polyphenols 4 and catechin was accompanied by extensive oxygen uptake, suggesting the formation of thiyl radicals from MMI and their reaction with molecular oxygen. In contrast, 1 markedly enhanced radical-scavenging without oxygen uptake, probably because of the formation of EUGQM/MMI-conjugates. 2 showed relatively small oxygen uptake, probably resulting from the predominant formation of benzyl radicals. Intracellular reactive oxygen species (ROS) in cancer cells by 4, but not by compounds 1, 2, 6, 7, 8, 9, and 10 was found, suggesting a possible link between physicochemical oxygen-uptake and intracellular ROS. The induction of apoptosis by 4 in HL-60 cells was accompanied by intracellular ROS. Dimers 6 and 7 inhibited nuclear factor (NF)-kappaB activation stimulated by lipopolysaccharide (LPS) in RAW 264.7 cells. Also, 6, 7, and 9 inhibited LPS-induced cyclooxygenase-2 expression in RAW 264.7 cells in a dose-dependent manner, whereas 1, 2 and 3 did not. Dimerization of o-methoxyphenols may be a useful tool for the design of drugs to act as potent chemopreventive and anticancer agents.
14
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Erythropoietin preconditioning suppresses neuronal death following status epilepticus in rats

80%
Yang J., Huang Y., Yu X., Sun H., Li Y., Deng Y.
|
EN
Status epilepticus (SE) is a grave condition in which the brain undergoes lasting seizures which can lead to neuronal loss. Our previous study suggested that preconditioning with erythropoietin (Epo) suppressed neuronal apoptosis in hippocampus of rats following SE in vivo by inhibiting caspase-3. In this study, we investigated the mechanisms by which Epo preconditioning may exert its anti-apoptotic effects using a lithium-pilocarpine induced SE model in rats. The effects of Epo on neuronal cell death were evaluated using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and the role of the Bcl-2 protein family, which have been shown to be anti- (Bcl-2, Bcl-w) or pro- (Bid, Bim) apoptotic, was examined with immunofluorescence. We found Epo preconditioning decreased the total number of TUNEL, Bim and Bid positive cells, but increased the total number of Bcl-w and Bcl-2 positive cells. These results suggest that systemic Epo pretreatment protects neurons in an acute phase of SE and may result in further suppression of neuronal apoptosis in hippocampus by regulating the balance between pro- and anti-apoptotic Bcl-2 family proteins.
15

Toll-like receptors types 2 and 6 and the apoptotic process in human neutrophils

80%
Jablonska E., Marcinczyk M., Jablonski J.
|
EN
Introduction: Neutrophils (PMN) apoptosis plays an important role in limiting the last phase of inflammatory processes. It is unknown whether Toll-like receptor (TLR)2 acts independently or together with TLR6 in this process. Materials and Methods: The aim of this study was to estimate the relationship between the expressions of TLR2 and TLR6 and the apoptosis of human neutrophils in physiological conditions. We investigated the influence of recombinant human interleukin (IL)-18 and N-formyl-metionyl-leucyl-phenylalanine (fMLP) on the relationships between these receptors and neutrophil apoptosis. Results: Our results showed that after 4-h incubation, the percentage of apoptotic PMNs significantly increased compared with PMN counts before incubation. The stronger expression of TLR2 on the neutrophils suggests that this receptor contributes more significantly to the induction of PMN apoptosis than does TLR6. We also demonstrated an influence of recombinant human IL-18 (rhIL-18) on the expression of TLR6, whereas this effect was not observed in the expression of TLR2. We observed that both rhIL-18 and fMLP inhibited the apoptosis of PMNs and that rhIL-18 had a stronger effect than fMLP. Conclusions: The obtained results suggest that not only TLR2, but also TLR6 plays an important role in the regulation of the apoptosis of PMNs. Changes in the expression of TLR6 and inhibition of apoptosis of PMNs by rhIL-18 seem to confirm the vital role this receptor and of rhIL-18 in regulating the survival of these cells. These data can be useful in developing methods to regulate PMN apoptosis in conditions associated with their excessive and unfavorable activation.
16

Reactive oxygen intermediates and serum antioxidative system in patients with chronic C hepatitis treated with IFN-alpha and thymus factor X

80%
Jablonowska E., Tchorzewski H., Lewkowicz P., Kuydowicz J.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 6
529-533
EN
In this study, the chemiluminescence (CL) of peripheral blood polymorphonuclear leukocytes (PMNLs) and the serum total antioxidative system (TAS) were assessed in patients with chronic C hepatitis (CCH) before and after 3 and 6 months of treatment with interferon (IFN)- and thymus factor X (TFX). The study included 26 patients with CCH aged between 25?63 years (mean: 42.67). Combined therapy with IFN-alpha 2a and a TFX preparation was applied. PMNL metabolic activity was assessed applying the whole-blood CL method. We measured CL response of neutrophils unstimulated and stimulated by opsonized zymosan, N-formyl-methionyl-leucyl-phenylalanine (N-fMLP), and phorbol-myristate-acetate (PMA) without and after priming with tumor necrosis factor alpha (10 ng/ml). The assessment of serum TAS was performed directly before the beginning of therapy with IFN-alpha and TFX and after 3 and 6 months of the treatment. A colorimetric method based on the reduction of the cationic radical ABTS+ (cation 2, 2'-azido-bis-[3-ethylobenzothiazolino-6-sulfonate]) in the presence of serum antioxidants was used. As a result of the treatment with IFN-alpha and TFX, the formation of free oxygen radicals by resting (unprimed) neutrophils increased statistically significantly both without stimulation and following stimulation by fMLP and PMA. A statistically significant increase in the serum antioxidant capacity was observed, which suggests the induction of compensatory processes. Increased in vitro reactive oxygen species production by both stimulated and unstimulated peripheral blood neutrophils of patients with CCH was observed. Treatment with IFN-alpha and TFX resulted in a compensatory increase in serum antioxidative capacity.
17

Bcl-2 proteins in ovarian apoptosis

80%
Opiela J., Katska-Ksiazkiewicz L.
Biotechnologia
|
2006
|
issue 1
90-96
EN
Members of the Bcl-2 family are considered principal players in the cascade of events that activate or inhibit apoptosis. Recent evidence strongly supports fundamental role of Bcl-2 and related proteins in regulating ovarian cell death. This article will provide an overview of the current knowledge regarding Bcl-2 proteins in programmed cell death in development of the ovary and the postnatal ovarian cycles.
18

Immunomodulation of macrophages by pathogenic Yersinia species

80%
Ruckdeschel K.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 2
131-138
EN
The interaction between macrophages and bacterial pathogens plays a crucial role in the pathogenesis of infectious diseases. Pathogenic species of the gram-negative bacterium Yersinia deploy complex strategies to disarm macrophages and to disrupt their response to infection. For this purpose, Yersinia spp. engage a type III protein secretion system that mediates polarized translocation of Yersinia virulence factors, the so-called Yops, into the host cell cytoplasm. There, the Yops act on different cellular levels to neutralize a sequence of programmed phagocyte effector functions. Yersiniae initially impair the phagocytic machinery and block the generation of the bactericidal oxidative burst. Furthermore, yersiniae uncouple an array of fine-tuned signals of innate immunity, which leads to suppression of the macrophage TNF- production and to macrophage apoptosis. The impairment of cellular functions results in a scenario, by which Yersinia efficiently resist the attack of the macrophage and finally kills the macrophage by activating its intrinsic cell suicide mechanism. This review highlights the aspects of Yersinia-macrophage interaction that determine the fate of the infected cell.
19

Apoptosis-the programmed cell death

80%
Gora-Tybor J., Robak T.
Postępy Higieny i Medycyny Doświadczalnej
|
1994
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vol. 48
|
issue 3
209-225
EN
Apoptosis is structurally distinct programmed cell death pathway.It takes place during embryogenesis, after withdrawal of the trophic hormones and in the course of normal tissue turnover.Defective regulation of apoptosis may play a very important role in the aetiology of cancer and other diseases.In this paper these and other problems concerning with apoptosis are reviewed.
20

The intestinal trefoil factor (Tff3), also expressed in the inner ear, interacts with peptides contributing to apoptosis

80%
Lubka M., Shah A. A., Blin N., Baus-Loncar M.
Journal of Applied Genetics
|
2009
|
vol. 50
|
issue 2
167-171
EN
The 3 members of the mammalian trefoil factor family (TFF) are expressed and secreted as cytoprotective peptides along the entire length of the normal gastrointestinal tract. More recently, they were shown to display multifunctional properties. Goblet cells of the small and large intestine constitute a major source for the synthesis of the third family member, TFF3 (formerly intestinal trefoil factor, ITF). TFF3, like the other family members, is rapidly up-regulated in response to physical wounding of the digestive tract. In addition, Tff3 was also detected in the posterior pituitary gland. Apart from this Tff3 function as a neuropeptide, also presence of Tff3 in the mouse cochlea was noted and Tff3-deficient animals display hearing impairment and accelerated presbyacusis. To elucidate Tff3's mode of function and its unexpected contribution to the hearing process, we strived to determine Tff3's interacting partners and to establish the functional network. To this end, we used a protein-protein binding assay based on a specific transcriptional regulation in yeast cells (the yeast-two-hybrid assay). We looked for interacting partners of Tff3 in a mouse cochlea cDNA library (from donors aged 3?15 days, P3-P15). Our data show that several binding candidates exist and that they could contribute to the known involvement of the trefoil peptides to apoptosis.
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