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[1.] Analyse:Mma/Fragment 005 05 - Diskussion
Bearbeitet: 23. January 2013, 10:19 Graf Isolan
Erstellt: 23. January 2013, 10:19 (Graf Isolan)
Fragment, Gewies 2003, KomplettPlagiat, Mma, SMWFragment, Schutzlevel, ZuSichten

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1. Introduction

1. Apoptosis

1.1. The development of the term apoptosis

[...] Apoptosis is of Greek origin, having the meaning "falling off or dropping off", in analogy to leaves falling off trees or petals dropping off flowers. This analogy emphasizes that the death of living matter is an integral and necessary part in the life cycle of organisms.

Since the mid-nineteenth century, many observations have indicated that cell death plays a considerable role during physiological processes of multicellular organisms, particularly during embryogenesis and metamorphosis (Lockshin et al, 2001). The term programmed cell death was introduced in 1964, proposing that cell death during development is not of accidential nature but follows a sequence of controlled steps leading to locally and temporally defined self-destruction (Lockshin et al, 2001).

Eventually, the term apoptosis had been coined in order to describe the morphological processes leading to controlled cellular self-destruction and was first introduced in a publication by Kerr, Wyllie and Currie (Kerr et al, 1972). The apoptotic mode of cell death is an active and defined process which plays an important role in the development of multicellular organisms and in the regulation and maintenance of the cell populations in tissues upon physiological and pathological conditions. It should be stressed that apoptosis is a well-defined and possibly the most frequent form of programmed cell death, but that other, non-apoptotic types of cell death, e.g. necrosis also are of biological significance (Leist et al, 2001).

1.2. The significance of apoptosis

The development and maintenance of multicellular biological systems depends on a sophisticated interplay between the cells forming the organism. It sometimes even seems to involve an altruistic behavior of individual cells in favor of the organism as a whole. During development many cells are produced in excess, which eventually undergo [programmed cell death and thereby contribute to sculpturing many organs and tissues (Meier et al, 2000).]

Introduction to Apoptosis

1. The development of the term apoptosis

Already since the mid-nineteenth century, many observations have indicated that cell death plays a considerable role during physiological processes of multicellular organisms, particularly during embryogenesis and metamorphosis [Gluecksmann, 1951; Lockshin, 2001]. The term programmed cell death was introduced in 1964, proposing that cell death during development is not of accidential nature but follows a sequence of controlled steps leading to locally and temporally defined self-destruction [Lockshin, 1964].

Eventually, the term apoptosis had been coined in order to describe the morphological processes leading to controlled cellular self-destruction and was first introduced in a publication by Kerr, Wyllie and Currie [Kerr, 1972]. Apoptosis is of greek origin, having the meaning "falling off or dropping off", in analogy to leaves falling off trees or petals dropping off flowers. This analogy emphasizes that the death of living matter is an integral and necessary part of the life cycle of organisms. The apoptotic mode of cell death is an active and defined process which plays an important role in the development of multicellular organisms and in the regulation and maintenance of the cell populations in tissues upon physiological and pathological conditions. It should be stressed that apoptosis is a well-defined and possibly the most frequent form of programmed cell death, but that other, non-apoptotic types of cell death also might be of biological significance [Leist, 2001].

2. The significance of apoptosis

The development and maintenance of multicellular biological systems depends on a sophisticated interplay between the cells forming the organism, it sometimes even seems to involve an altruistic behaviour of individual cells in favour of the organism as a whole. During development many cells are produced in excess which eventually undergo programmed cell death and thereby contribute to sculpturing many organs and tissues [Meier, 2000].

Anmerkungen

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[2.] Analyse:Mma/Fragment 006 01 - Diskussion
Bearbeitet: 23. January 2013, 12:11 Graf Isolan
Erstellt: 23. January 2013, 12:10 (Graf Isolan)
Fragment, Gewies 2003, KomplettPlagiat, Mma, SMWFragment, Schutzlevel, ZuSichten

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[During development many cells are produced in excess, which eventually undergo] programmed cell death and thereby contribute to sculpturing many organs and tissues (Meier et al, 2000).

A particularly instructive example for the implication of programmed cell death in animal development is the formation of free and independent digits by massive cell death in the interdigital mesenchymal tissue (Zuzarte-Luis et al, 2002). Other examples are the development of the brain, during which half of the neurons that are initially created will die in later stages when the adult brain is formed (Hutchins et al, 1998), as well as the development of the reproductive organs (Meier et al, 2000). Also cells of an adult organism constantly undergo physiological cell death, which must be balanced with proliferation in order to maintain homeostasis in terms of constant cell numbers. The majority of the developing lymphocytes die either during genetic rearrangement events during the formation of the antigen receptor, during negative selection or in the periphery, thereby tightly controlling the pool of highly efficient and functional but not self-reactive immune cells, and at the same time keeping lymphocyte numbers relatively constant (Rathmell et al, 2002). Taken together, apoptotic processes are of widespread biological significance; being involved in e.g. development, differentiation, proliferation/homoeostasis, regulation and function of the immune system and in the removal of defect and therefore harmful cells. Thus, dysfunction or dysregulation of the apoptotic program is implicated in a variety of pathological conditions. Defects in apoptosis can result in cancer, autoimmune diseases and spreading of viral infections, neurodegenerative disorders and AIDS (Fadeel et al, 1999).

Due to its importance in such various biological processes, programmed cell death is a widespread phenomenon, occurring in all kinds of metazoans (Tittel et al, 2000) such as in mammals, insects (Richardson et al, 2002), nematodes (Liu et al, 1999), and cnidaria (Cikala et al, 1999). Moreover, programmed cell death also might play a role in plant biology (Solomon et al, 1999), and apoptosis-like cell death mechanisms even have been observed and used as a model system in yeast (Fröhlich et al, 2000; Skulachev et al, 2002). Fascinating insights into the origin and evolution of programmed cell death might possibly be given by the fact, that programmed cell death is also an integral part of the life cycle of other unicellular eukaryotes (such as the kinetoplastid parasite Trypanosoma brucei, the ciliate Tetrahymena thermophila, and the slime mold Dictyostelium [discoideum), and that even prokaryotes (such as Bacillus subtilis, Streptomyces and Myxobacteria) sometimes undergo regulated cell death (Ameisen et al, 2002).]

[page 2]

During development many cells are produced in excess which eventually undergo programmed cell death and thereby contribute to sculpturing many organs and tissues [Meier, 2000].

[page 3]

A particularly instructive example for the implication of programmed cell death in animal development is the formation of free and independent digits by massive cell death in the interdigital mesenchymal tissue [Zuzarte-Luis, 2002]. Other examples are the development of the brain, during which half of the neurons that are initially created will die in later stages when the adult brain is formed [Hutchins, 1998] and the development of the reproductive organs [Meier, 2000]. Also cells of an adult organism constantly undergo physiological cell death which must be balanced with proliferation in order to maintain homeostasis in terms of constant cell numbers. The majority of the developing lymphocytes die either during genetic rearrangement events in the formation of the antigen receptor, during negative selection or in the periphery, thereby tightly controlling the pool of highly efficient and functional but not self-reactive immune cells and at the same time keeping lymphocyte numbers relatively constant [Rathmell, 2002].

Taken together, apoptotic processes are of widespread biological significance, being involved in e.g. development, differentiation, proliferation/homoeostasis, regulation and function of the immune system and in the removal of defect and therefore harmful cells. Thus, dysfunction or dysregulation of the apoptotic program is implicated in a variety of pathological conditions. Defects in apoptosis can result in cancer, autoimmune diseases and spreading of viral infections, while neurodegenerative disorders, AIDS and ischaemic diseases are caused or enhanced by excessive apoptosis [Fadeel, 1999a].

[page 4]

Due to its importance in such various biological processes, programmed cell death is a widespread phenomenon, occuring in all kinds of metazoans [Tittel, 2000] such as in mammals, insects [Richardson, 2002], nematodes [Liu, 1999], and cnidaria [Cikala, 1999]. Moreover, programmed cell death also might play a role in plant biology [Solomon, 1999], and apoptosis-like cell death mechanisms even have been observed and used as a model system in yeast [Frohlich, 2000; Skulachev, 2002]. Fascinating insights into the origin and evolution of programmed cell death might possibly be given by the fact, that programmed cell death is also an integral part of the life cycle of other unicellular eukaryotes (such as the kinetoplastid parasite Trypanosoma brucei brucei, the ciliate Tetrahymena thermophila, and the slime mold Dictyostelium discoideum) and that even prokaryotes (such as Bacillus subtilis, Streptomyces and Myxobacteria) sometimes undergo regulated cell death [Ameisen, 2002].

Anmerkungen

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[3.] Analyse:Mma/Fragment 007 01 - Diskussion
Bearbeitet: 23. January 2013, 12:18 Graf Isolan
Erstellt: 23. January 2013, 12:17 (Graf Isolan)
Fragment, Gewies 2003, KomplettPlagiat, Mma, SMWFragment, Schutzlevel, ZuSichten

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[Fascinating insights into the origin and evolution of programmed cell death might possibly be given by the fact, that programmed cell death is also an integral part of the life cycle of other unicellular eukaryotes (such as the kinetoplastid parasite Trypanosoma brucei, the ciliate Tetrahymena thermophila, and the slime mold Dictyostelium] discoideum), and that even prokaryotes (such as Bacillus subtilis, Streptomyces and Myxobacteria) sometimes undergo regulated cell death (Ameisen et al, 2002).

1.3. Morphological features of apoptosis

Apoptotic cells can be recognized by stereotypical morphological changes: the cell shrinks, shows deformation and loses contact to its neighbouring cells. Its chromatin condenses and marginates at the nuclear membrane, the plasma membrane is blebbing or budding, and finally the cell is fragmented into compact membrane-enclosed structures, called 'apoptotic bodies' which contain cytosol, the condensed chromatin, and organelles. The apoptotic bodies are engulfed by macrophages and thus are removed from the tissue without causing an inflammatory response. Those morphological changes are a consequence of characteristic molecular and biochemical events occurring in an apoptotic cell, most notably the activation of proteolytic enzymes, which mediate the cleavage of DNA into oligonucleosomal fragments as well as the cleavage of a multitude of specific protein substrates which usually determine the integrity and shape of the cytoplasm or organelles (Saraste et al, 2000). Apoptosis can be distinguesh from necrotic mode of cell-death in which the cells suffer a major insult, resulting in a loss of membrane integrity, swelling and disrupture of the cells. During necrosis, the cellular contents are released uncontrolled into the cells environment which results in damage of surrounding cells and a strong inflammatory response in the corresponding tissue (Leist et al, 2001).

Fascinating insights into the origin and evolution of programmed cell death might possibly be given by the fact, that programmed cell death is also an integral part of the life cycle of other unicellular eukaryotes (such as the kinetoplastid parasite Trypanosoma brucei brucei, the ciliate Tetrahymena thermophila, and the slime mold Dictyostelium discoideum) and that even prokaryotes (such as Bacillus subtilis, Streptomyces and Myxobacteria) sometimes undergo regulated cell death [Ameisen, 2002].

3. Morphological features of apoptosis

Apoptotic cells can be recognized by stereotypical morphological changes: the cell shrinks, shows deformation and looses contact to its neighbouring cells. Its chromatin condenses and marginates at the nuclear membrane, the plasma membrane is blebbing or budding, and finally the cell is fragmented into compact membrane-enclosed structures, called 'apoptotic bodies' which contain cytosol, the condensed chromatin, and organelles (Fig. 2). The apoptotic bodies are engulfed by macrophages and thus are removed from the tissue without causing an inflammatory response. Those morphological changes are a consequence of characteristic molecular and biochemical events occurring in an apoptotic cell, most notably the activation of proteolytic enzymes which eventually mediate the cleavage of DNA into oligonucleosomal fragments as well as the cleavage of a multitude of specific protein substrates which usually determine the integrity and shape of the cytoplasm or organelles [Saraste, 2000]. Apoptosis is in contrast to the necrotic mode of cell-death in which case the cells suffer a major insult, resulting in a loss of membrane integrity, swelling and disrupture of the cells. During necrosis, the cellular contents are released uncontrolled into the cell's environment which results in damage of surrounding cells and a strong inflammatory response in the corresponding tissue [Leist, 2001].

Anmerkungen

A nearly literal copy; nothing has been marked as a citation.

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[4.] Analyse:Mma/Fragment 011 03 - Diskussion
Bearbeitet: 13. June 2013, 11:45 Graf Isolan
Erstellt: 13. June 2013, 11:18 (Graf Isolan)
BauernOpfer, Euler-Taimor and Heger 2006, Fragment, Mma, SMWFragment, Schutzlevel, ZuSichten

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At present eight distinct SMAD proteins are known. They can be divided into three different functional classes: (i) the receptor activated R-SMADs (SMAD 1, 2, 3, 5, and 8), (ii) the co-mediator Co-SMAD (SMAD 4) and (iii) the inhibitory I-SMADs (SMAD 6 and 7). In non-activated cells, R-SMADs are predominantly localized in the cytoplasm, Co-SMADs are equally distributed in the cytoplasm and the nucleus and I-SMADs are found mostly in the nucleus. Upon stimulation of receptors of the TGFβ superfamily RSMADs become phosphorylated and activated. They undergo dimerization and form heterotrimers with Co-SMADs. This complex then translocates to the nucleus and influences the transcriptional regulation (Lebrin et al, 2005).

The TGFβ-family members comprise about 30 members in the mammalian system and can be devided [sic] into two groups, the TGFβ/activin family and the BMP group (bone morphogenetic protein). Each group is responsible for activation of different SMAD isoforms.

The recruitment of SMADs to DNA is regulated by cooperation with other transcription factors. These factors facilitate binding of SMADs to DNA. One transcription factor that can interact with SMAD and that is expressed in heart is AP-1. TGFβ is released under several pathophysiologic conditions like ischemia/reperfusion and cardiomyopathy (Poncelet et al., 2001), which simultaneously activate SMAD and AP-1. Both factors, AP-1 and SMAD mediate enhanced expression of TGFβ responsive genes, like collagen (Ross et al, 2004), c-Jun (Lopez-Rovira et al, 2000), endothelin-1 (Sanchez-Elsner et al, 2001). Another functional aspect of AP-1/SMAD signaling is the induction of apoptosis in TGFβ stimulated cells (Kon et al, 1999; Arthur et al, 2000; Euler et al., 2006) and involved in NO induced apoptosis in adult rat cardiomyocytes. Therefore, TGFβ family members may induce apoptosis in this pathway.


Arthur HM, Ure J, Smith AJ, Renforth G, Wilson DI, Torsney E, (2000) Endoglin, an ancillary TGFbeta receptor, is required for extraembryonic angiogenesis and plays a key role in heart development. Dev Biol 217: 42-53.

Euler T G and Heger J (2006) The complex pattern of SMAD signaling in the cardiovascular system. CVR page -----.

Kon A, Vindevoghel L, Kouba DJ, Fujimura Y, Uitto J, Mauviel A (1999) Cooperation between SMAD and NF-kappaB in growth factor regulated type VII collagen gene expression. Oncogene 18: 1837-44.

Lebrin F, Deckers M, Bertolino P, Ten Dijke P (2005) TGF-beta receptor function in the endothelium. Cardiovasc Res 65: 599-608.

Lopez-Rovira T, Chalaux E, Rosa JL, Bartrons R, Ventura F (2000) Interaction and functional cooperation of NF-kappa B with Smads. Transcriptional regulation of the junB promoter. J Biol Chem 275: 28937-28946.

Poncelet AC, Schnaper HW (2001) Sp1 and Smad proteins cooperate to mediate transforming growth factor-beta 1-induced alpha 2 (I) collagen expression in human glomerular mesangial cells. J Biol Chem 276: 6983-6992.

Ross RS (2004) Molecular and mechanical synergy: cross-talk between integrins and growth factor receptors. Cardiovasc Res 63: 381-390.

Sanchez-Elsner T, Botella LM, Velasco B, Corbi A, Attisano L, Bernabeu C (2001) Synergistic cooperation between hypoxia and transforming growth factor-beta pathways on human vascular endothelial growth factor gene expression. J Biol Chem 276: 38527-38535.

[Page 17]

At present eight distinct SMAD proteins are known. They can be divided into three different functional classes: (i) the receptor-activated R-SMADs (SMAD 1, 2, 3, 5, and 8), (ii) the co-mediator Co-SMADs (SMAD 4), and (iii) the inhibitory I-SMADs (SMAD 6 and 7). [...]

In non-activated cells, R-SMADs are predominantly localized in the cytoplasm, Co-SMADs are equally distributed in the cytoplasm and the nucleus, and I-SMADs are found mostly in the nucleus. Upon stimulation of receptors of the TGFβ superfamily, R-SMADs become phosphorylated and activated, undergoing dimerization and thereafter forming heterotrimers with Co-SMADs. This complex then translocates to the nucleus and influences transcriptional regulation [24].

[Page 18]

The TGFβfamily comprises around 30 members in the mammalian system and can be divided into two groups: the TGFβ/activin family and the BMP group. Each group is responsible for activation of different SMAD isoforms (Fig. 3).

[Page 19]

Consequently, recruitment of SMADs to DNA is regulated by cooperation with other transcription factors. These factors facilitate binding of SMADs to DNA [...]

One of the first transcription factors detected to interact with SMADs is the activator protein AP-1. [...]

TGFβ is a cytokine that is released under several pathophysiologic conditions and that simultaneously activates SMAD and AP-1. Both AP-1 and SMAD mediate enhanced expression of TGFh-responsive genes, such as collagen [42], c-Jun [45], endothelin-1 [46], or peroxisome proliferator activated receptor gamma (PPARg) [47]. [...] Another functional consequence of the concerted action of AP-1/SMAD signaling is the induction of apoptosis in TGFβ-stimulated cells [44,48]: in isolated adult cardiomyocytes, involvement of AP-1/SMAD signaling in apoptosis induction by TGFβ or nitric oxide was demonstrated [4].



[4] Schneiders D, Heger J, Best P, Piper HM, Taimor G. SMAD proteins are involved in apoptosis induction in ventricular cardiomyocytes. Cardiovasc Res 2005;67:87–96.

[24] Liu F, Pouponnot C, Massague J. Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-inducible transcriptional complexes. Genes Dev 1997;11:3157–67.

[42] Zhang Y, Feng XH, Derynck R. Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-beta-induced transcription. Nature 1998; 394:909–13.

[44] Yamamura Y, Hua X, Bergelson S, Lodish HF. Critical role of Smads and AP-1 complex in transforming growth factor-beta-dependent apoptosis. J Biol Chem 2000;275:36295–302.

[45] Wong C, Rougier-Chapman EM, Frederick JP, Datto MB, Liberati N.T, Li JM, et al. Smad3–Smad4 and AP-1 complexes synergize in transcriptional activation of the c-Jun promoter by transforming growth factor beta. Mol Cell Biol 1999;19:1821–30.

[46] Rodriguez-Pascual F, Redondo-Horcajo M, Lamas S. Functional cooperation between Smad proteins and activator protein-1 regulates transforming growth factor-beta-mediated induction of endothelin-1 expression. Circ Res 2003;92:1288–95.

[47] Fu M, Zhang J, Lin Y, Zhu X, Zhao L, Ahmad M, et al. Early stimulation and late inhibition of peroxisome proliferator-activated receptor gamma (PPAR gamma) gene expression by transforming growth factor beta in human aortic smooth muscle cells: role of early growth-response factor-1 (Egr-1), activator protein 1 (AP1) and Smads. Biochem J 2003;370:1019 – 25.

[48] Arsura M, Panta GR, Bilyeu JD, Cavin LG, Sovak MA, Oliver AA, et al. Transient activation of NF-kappaB through a TAK1/IKK kinase pathway by TGF-beta1 inhibits AP-1/SMAD signaling and apoptosis: implications in liver tumor formation. Oncogene 2003;22:412–25.

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Quelle Autor Titel Verlag Jahr Lit.-V. FN
Mma/Euler-Taimor and Heger 2006 Gerhild Euler-Taimor, Jacqueline Heger The complex pattern of SMAD signaling in the cardiovascular system 2005 yes no
Mma/Gewies 2003 Andreas Gewies An Introduction to Apoptosis 2003
Mma/Gewies 2004 Andreas Gewies Investigation of the ubiquitin-specific protease UBP41 and of the lysosomal cysteine proteases cathepsin-L and cathepsin-B as potential mediators of proapoptotic signalling 2004 nein nein


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