Review
Year 2016,
Volume: 6 Issue: 4, 166 - 172, 15.12.2016
Abstract
Programlanmış hücre ölümü olan apoptoz birçok fizyolojik süreçte aktif rol oynamaktadır. Apoptozun, büyüme faktörlerinin eksikliği, DNA hasarı ve birden fazla faktörü içeren çeşitli hücresel stresle aktive olan ‘hücre içi’ ve ölüm reseptörlerine ligandın bağlanmasıyla kaspazların aktive olduğu ‘hücre dışı’ olmak üzere iki yolağı vardır. Apoptotik hücre sayısı ile organizmanın sağlıklı olup olmadığı belirlenir. Apoptoz oranının azalması hücre sayısını arttırırken, apoptoz oranının artması hücre sayısını azaltarak dokularda tahribata neden olmaktadır. Apoptotik sinyallemede düzensizlik çeşitli hastalıklarda/bozukluklarda primer ya da sekonder rol oynamaktadır. Son yıllarda apoptozun nörodejeneratif hastalıklarla ilgili çalışmaları ön plana çıkmaya başlamıştır. Apoptotik sinyal yolaklarının daha iyi tanımlanması, pro- ve anti-apoptotik genlerin belirlenmesiyle, çalışmalar hız kazanmıştır. Travma Sonrası Stres Bozukluğu gibi nörodejeneratif bozukluklarda beyindeki yapısal ve fonksiyonel değişiklikler mitokondriyal stres ile ilişkilidir. Fizyolojik koşullarda hayati öneme sahip olan apoptoz, patolojik koşullarda mekanizmanın tetiklenmesine ve kontrolsüz hücre çoğalmasına yol açmaktadır. Hücre ölümünü engelleyen terapötik ilaçların geliştirilmesiyle apoptoz aracılı nörodejenaratif bozuklukların tedavisine yeni umutlar oluşacaktır.
References
- 1. McIlwain DR, Berger T, Mak TW. Caspase functions in cell death and disease. Cold Spring Harb Perspect Biol 2013; 5: a008656. [CrossRef] 2. Saikumar P, Dong Z, Mikhailov V, Denton M, Weinberg JM, Venkatachalam MA. Apoptosis definition, mechanism and relevance to disease. Am J Med 1999; 107: 489-506. [CrossRef] 3. Reed JC. Apoptosis-based therapies. Nat Rev Drug Discov 2002; 1: 111- 21. [CrossRef] 4. Carson DA, Ribeiro JM. Apoptosis and disease. Lancet 1993; 341: 1251-4. [CrossRef] 5. Duman RS, Monteggia LM. A Neutrophic model for stress-related mood disorders. J Biopsych 2006; 59: 1116-27. 6. McEwen B, Sapolsky RM. Stress and hippocampus plasticity. Curr Opin Neurobiol 1999; 5: 205-16. [CrossRef] 7. Duman RS, Malberg J, Thome J. Neural Plasticity to stress and ntidepressant treatment. Biol Physchiatry 1999; 46: 1181-91. [CrossRef] 8. Lockshin RA, Williams CM. Programmed cell death. II. Endocrine potentiation of the breakdown of the intersegmental muscles of silk moths. J Insect Physiol 1964; 10: 643-9. [CrossRef] 9. Searle J, Kerr JF, Bishop CJ. Necrosis and apoptosis distinct modes death with fundamentally different significance. Pathol Annu 1982; 17: 229-59. 10. Meier P, Finch A, Evan G. Apoptosis in development. Nat 2000; 407: 796- 801. [CrossRef] 11. Hutchins JB, Barger SW. Why neurons die: cell death in the nervous system. Anat Rec 1998; 253: 79-90. [CrossRef] 12. Billig H, Furuta I, Hsueh AJW. Estrogens inhibit and androgens enhance ovarian granulosa cell apoptosis. Endocrinol 1993; 133: 2204-12. [CrossRef] 13. Billig H, Furuta I, Hsueh AJW. Gonadotropin-releasing hormone directly induces apoptotic cell death in the rat ovary: biochemical and in situ detection of deoxyribonucleic acid fragmentation in granulosa cells. J Endocrinol 1994; 134: 245-52. [CrossRef] 14. Hengartner MO. The biochemistry of apoptosis. Nature 2000; 407: 770-6. [CrossRef] 15. Denault JB, Salvesen GS. Caspases: keys in the ignition of cell death. Chem Rev 2002; 102: 4489-500. [CrossRef] 16. Weil M, Jacobson MD, Coles HS, Davies TJ, Gardner RL, Raff KD, et al. Constitutive expression of the machinery for programmed cell death. J Cell Biol 1996; 133: 1053-9. [CrossRef] 17. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol 2007; 35: 495-516. [CrossRef] 18. Galluzzi L, Blomgren K, Kroemer G. Mitochondrial membrane permeabilization in neuronal injury. Nature Rev Neurosci 2009; 10: 481-94. [CrossRef] 19. Shi YA. Structural view of mitochondria mediated apoptosis. Nos Struct Biol 2001; 8: 394-401. [CrossRef] 20. Ow YLP, Green RD, Hao Z, Mak TW. Cytochrome c: functions beyond respiration. Nat Rev Mol Cell Biol 2008; 9: 532-42. [CrossRef] 21. Antonsson B, Martinou JC. The Bcl-2 protein family. Exp Cell Res 2000; 256: 50-7. [CrossRef] 22. Borner C. The Bcl-2 protein family: sensors and checkpoints for life-or-death decisions. Mol Immunol 2003; 39: 615-47. [CrossRef] 23. Tsujimoto Y. Role of Bcl-2 family of proteins in apoptosis, apoptosomes or mitochondria? Genes Cell 1998; 3: 697-707. [CrossRef] 24. Taneja N, Tjalkens R, Philbert MA, Rehemtulla A. Irradiation of mitochondria initiates apoptosis in a cell free system. Oncogene 2001; 20: 167-77. [CrossRef] 25. Yehuda R, Giller EL, Southwick SM, Lowy MT, Mason JW. Hypothalamicpituitary-adrenal dysfunction in posttraumatic stress disorder. Biol Psychiatry 1991; 30: 1031-48. [CrossRef] Bremner JD. Functional neuroimaging in post-traumatic stress disorder. Expert Rev Neurother 2007; 7: 393-405. [CrossRef] 27. Carrion VG, Weems CF, Watson C, Eliez S, Menon V, Reiss AL. Converging evidence for abnormalities of the prefrontal cortex and evaluation of midsagittal structures in pediatric posttraumatic stress disorder: an MRI study. Psychiatry Res 2009; 172: 226-34. [CrossRef] 28. Blanchard RJ, McKittrick CR, Blanchard DC. Animal model of social stress: effects on behavior and brain neuro- chemical systems. Physiol Behav 2001;73: 261-71. [CrossRef] 29. Aykaç A, Aydın B, Cabadak H, Gören MZ. The change in muscarinic receptor subtypes in different brain regions of rats treated with fluoxetine or propranolol in a model of posttraumatic stress disorder. Behav Brain Res 2012; 232: 124-9. [CrossRef] 30. Aykac A, Suer K, Taskiran C. Models of rat behavior used for studies of anxiety. Marmara Medical J 2015; 28: 1-7. 31. Bremner JD, Innis RB, Southwick SM, Staib L, Zonghbi S, Charney DS. Decreased benzodiazepine re-ceptor binding in prefrontal cortex in combat-related posttraumatic stress disorder. Am J Psychiatry 2000; 157: 1120-6. [CrossRef] 32. Lee T, Jarome T, Li SJ, Kim JJ, Helmstetter FJ. Chronic stress selectively reduces hippocampal vol-ume in rats: a longitudinal magnetic resonance imaging study. Neuroreport 2009; 20: 1554-8. [CrossRef] 33. Gao J, Wang H, Liu Y, Li YY, Chen C, Liu LM, et al. Glutamate and GABA imbalance promotes neuronal apoptosis in hippocampus after stress. Med Sci Monit 2014; 20: 499-512. [CrossRef] 34. Han F, Yan S, Shi Y. Single-prolonged stress induces endoplasmic reticulum-dependent apoptosis in the hippocampus in a rat model of post-traumatic stress disorder. PLoS One 2013; 8: e69340. [CrossRef] 35. Morin LP, Meyer-Bernstein EL. The ascending serotonergic system in the hamster: comparison with projections of the dorsal and median raphe nuclei. Neurosci 1999; 91: 81-105. [CrossRef] 36. Iwamoto Y, Morinobu S, Takahashi T, Yamawaki S. Single prolonged stress increases contextual freezing and the expression of glycine transporter 1 and vesicle-associated membrane protein 2 mRNA in the hippocampus of rats. Prog Neuropsychopharmacol Biol Psychiatry 2007; 31: 642-51. [CrossRef] 37. Takahashi T, Morinobu S, Iwamoto Y, Yamawaki S. Effect of paroxetine on enhanced contextual fear induced by single prolonged stress in rats. Psychopharmacology (Berl) 2006; 189: 165-73. [CrossRef] 38. Imanaka A, Morinobu S, Toki S, Yamawaki S. Importance of early environment in the development of post-traumatic stress disorder-like behaviors. Behav Brain Res 2006; 173: 129-37. [CrossRef] 39. Luo FF, Han F, Shi YX. Change in 5-HT1A receptor in the dorsal raphe nucleus in a rat model of post-traumatic stress disorder. Mol Med Rep 2011; 4: 843-7. [CrossRef] 40. Epel ES, Blackburn EH, Lin J, Dhabhar FS, Adler NE, Morrow JD, et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci 2004; 101: 17312-5. [CrossRef] 41. Garabadu D, Ahmad A, Krishnamurthy S. Risperidone attenuates modified stress-re-stress paradigm-ınduced mitochondrial dysfunction and apoptosis in rats exhibiting post-traumatic stress disorder-like symptoms. J Mol Neurosci 2015; 56: 299-312. [CrossRef] 42. Aykaç A, Aydın B, Cabadak H, Gören MZ. The change in muscarinic receptor subtypes in different brain regions of rats treated with fluoxetine or propranolol in a rat model of post-traumatic stress disorder. Behav Brain Res 2012; 232:124-9. [CrossRef] 43. Zhang L, Zhou R, Li X, Ursano RJ, Li H. Stress-induced change of mitochondria membrane potential regulated by genomic and non-genomic GR signaling: a possible mechanism for hippocampus atrophy in PTSD. Med Hypotheses 2006; 66: 1205-8. [CrossRef] 44. Manoli I, Alesci S, Blackman MR, Su YA, Rennert OM, Chrousos GP. Mitochondria as key components of the stress response. Trends Endocrinol Metab 2007; 18: 190-8. [CrossRef]
Year 2016,
Volume: 6 Issue: 4, 166 - 172, 15.12.2016
Abstract
Apoptosis is programmed cell death, which actively occurs in many physiological processes. It can be triggered in two ways: (i) defects in growth factor, DNA damage, and other many factors that can cause cellular stress, which is an intracellular pathway, and (ii) ligand binding to death receptors and activation of caspases. The apoptotic cell count can be determined by the health of the whole organism. A higher apoptotic ratio can indicate a decrease in the number of cells and tissue damage, while a lower apoptotic ratio can indicate an increase in the number of cells. Irregularity in apoptotic signals can play primary or secondary roles in various diseases/disorders. Research on apoptosis depends on neurodegeneration has been initiated in the past few years. Definition of apoptotic signal pathways and apoptotic regulation and determination of pro- and anti-apoptotic genes are the main topics that have accelerated research on apoptosis. Neurodegenerative disorders such as post-traumatic stress disorder neuronal damage associated with changes in brain structure and function may be related to the mitochondrial stresses. In physiological conditions, apoptosis is crucial for the organism, while in pathological conditions, apoptosis can cause uncontrolled cell division. Development of therapeutic medicine that inhibits the cell death may be the new choice of treatment for neurodegenerative diseases/disorders.
References
- 1. McIlwain DR, Berger T, Mak TW. Caspase functions in cell death and disease. Cold Spring Harb Perspect Biol 2013; 5: a008656. [CrossRef] 2. Saikumar P, Dong Z, Mikhailov V, Denton M, Weinberg JM, Venkatachalam MA. Apoptosis definition, mechanism and relevance to disease. Am J Med 1999; 107: 489-506. [CrossRef] 3. Reed JC. Apoptosis-based therapies. Nat Rev Drug Discov 2002; 1: 111- 21. [CrossRef] 4. Carson DA, Ribeiro JM. Apoptosis and disease. Lancet 1993; 341: 1251-4. [CrossRef] 5. Duman RS, Monteggia LM. A Neutrophic model for stress-related mood disorders. J Biopsych 2006; 59: 1116-27. 6. McEwen B, Sapolsky RM. Stress and hippocampus plasticity. Curr Opin Neurobiol 1999; 5: 205-16. [CrossRef] 7. Duman RS, Malberg J, Thome J. Neural Plasticity to stress and ntidepressant treatment. Biol Physchiatry 1999; 46: 1181-91. [CrossRef] 8. Lockshin RA, Williams CM. Programmed cell death. II. Endocrine potentiation of the breakdown of the intersegmental muscles of silk moths. J Insect Physiol 1964; 10: 643-9. [CrossRef] 9. Searle J, Kerr JF, Bishop CJ. Necrosis and apoptosis distinct modes death with fundamentally different significance. Pathol Annu 1982; 17: 229-59. 10. Meier P, Finch A, Evan G. Apoptosis in development. Nat 2000; 407: 796- 801. [CrossRef] 11. Hutchins JB, Barger SW. Why neurons die: cell death in the nervous system. Anat Rec 1998; 253: 79-90. [CrossRef] 12. Billig H, Furuta I, Hsueh AJW. Estrogens inhibit and androgens enhance ovarian granulosa cell apoptosis. Endocrinol 1993; 133: 2204-12. [CrossRef] 13. Billig H, Furuta I, Hsueh AJW. Gonadotropin-releasing hormone directly induces apoptotic cell death in the rat ovary: biochemical and in situ detection of deoxyribonucleic acid fragmentation in granulosa cells. J Endocrinol 1994; 134: 245-52. [CrossRef] 14. Hengartner MO. The biochemistry of apoptosis. Nature 2000; 407: 770-6. [CrossRef] 15. Denault JB, Salvesen GS. Caspases: keys in the ignition of cell death. Chem Rev 2002; 102: 4489-500. [CrossRef] 16. Weil M, Jacobson MD, Coles HS, Davies TJ, Gardner RL, Raff KD, et al. Constitutive expression of the machinery for programmed cell death. J Cell Biol 1996; 133: 1053-9. [CrossRef] 17. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol 2007; 35: 495-516. [CrossRef] 18. Galluzzi L, Blomgren K, Kroemer G. Mitochondrial membrane permeabilization in neuronal injury. Nature Rev Neurosci 2009; 10: 481-94. [CrossRef] 19. Shi YA. Structural view of mitochondria mediated apoptosis. Nos Struct Biol 2001; 8: 394-401. [CrossRef] 20. Ow YLP, Green RD, Hao Z, Mak TW. Cytochrome c: functions beyond respiration. Nat Rev Mol Cell Biol 2008; 9: 532-42. [CrossRef] 21. Antonsson B, Martinou JC. The Bcl-2 protein family. Exp Cell Res 2000; 256: 50-7. [CrossRef] 22. Borner C. The Bcl-2 protein family: sensors and checkpoints for life-or-death decisions. Mol Immunol 2003; 39: 615-47. [CrossRef] 23. Tsujimoto Y. Role of Bcl-2 family of proteins in apoptosis, apoptosomes or mitochondria? Genes Cell 1998; 3: 697-707. [CrossRef] 24. Taneja N, Tjalkens R, Philbert MA, Rehemtulla A. Irradiation of mitochondria initiates apoptosis in a cell free system. Oncogene 2001; 20: 167-77. [CrossRef] 25. Yehuda R, Giller EL, Southwick SM, Lowy MT, Mason JW. Hypothalamicpituitary-adrenal dysfunction in posttraumatic stress disorder. Biol Psychiatry 1991; 30: 1031-48. [CrossRef] Bremner JD. Functional neuroimaging in post-traumatic stress disorder. Expert Rev Neurother 2007; 7: 393-405. [CrossRef] 27. Carrion VG, Weems CF, Watson C, Eliez S, Menon V, Reiss AL. Converging evidence for abnormalities of the prefrontal cortex and evaluation of midsagittal structures in pediatric posttraumatic stress disorder: an MRI study. Psychiatry Res 2009; 172: 226-34. [CrossRef] 28. Blanchard RJ, McKittrick CR, Blanchard DC. Animal model of social stress: effects on behavior and brain neuro- chemical systems. Physiol Behav 2001;73: 261-71. [CrossRef] 29. Aykaç A, Aydın B, Cabadak H, Gören MZ. The change in muscarinic receptor subtypes in different brain regions of rats treated with fluoxetine or propranolol in a model of posttraumatic stress disorder. Behav Brain Res 2012; 232: 124-9. [CrossRef] 30. Aykac A, Suer K, Taskiran C. Models of rat behavior used for studies of anxiety. Marmara Medical J 2015; 28: 1-7. 31. Bremner JD, Innis RB, Southwick SM, Staib L, Zonghbi S, Charney DS. Decreased benzodiazepine re-ceptor binding in prefrontal cortex in combat-related posttraumatic stress disorder. Am J Psychiatry 2000; 157: 1120-6. [CrossRef] 32. Lee T, Jarome T, Li SJ, Kim JJ, Helmstetter FJ. Chronic stress selectively reduces hippocampal vol-ume in rats: a longitudinal magnetic resonance imaging study. Neuroreport 2009; 20: 1554-8. [CrossRef] 33. Gao J, Wang H, Liu Y, Li YY, Chen C, Liu LM, et al. Glutamate and GABA imbalance promotes neuronal apoptosis in hippocampus after stress. Med Sci Monit 2014; 20: 499-512. [CrossRef] 34. Han F, Yan S, Shi Y. Single-prolonged stress induces endoplasmic reticulum-dependent apoptosis in the hippocampus in a rat model of post-traumatic stress disorder. PLoS One 2013; 8: e69340. [CrossRef] 35. Morin LP, Meyer-Bernstein EL. The ascending serotonergic system in the hamster: comparison with projections of the dorsal and median raphe nuclei. Neurosci 1999; 91: 81-105. [CrossRef] 36. Iwamoto Y, Morinobu S, Takahashi T, Yamawaki S. Single prolonged stress increases contextual freezing and the expression of glycine transporter 1 and vesicle-associated membrane protein 2 mRNA in the hippocampus of rats. Prog Neuropsychopharmacol Biol Psychiatry 2007; 31: 642-51. [CrossRef] 37. Takahashi T, Morinobu S, Iwamoto Y, Yamawaki S. Effect of paroxetine on enhanced contextual fear induced by single prolonged stress in rats. Psychopharmacology (Berl) 2006; 189: 165-73. [CrossRef] 38. Imanaka A, Morinobu S, Toki S, Yamawaki S. Importance of early environment in the development of post-traumatic stress disorder-like behaviors. Behav Brain Res 2006; 173: 129-37. [CrossRef] 39. Luo FF, Han F, Shi YX. Change in 5-HT1A receptor in the dorsal raphe nucleus in a rat model of post-traumatic stress disorder. Mol Med Rep 2011; 4: 843-7. [CrossRef] 40. Epel ES, Blackburn EH, Lin J, Dhabhar FS, Adler NE, Morrow JD, et al. Accelerated telomere shortening in response to life stress. Proc Natl Acad Sci 2004; 101: 17312-5. [CrossRef] 41. Garabadu D, Ahmad A, Krishnamurthy S. Risperidone attenuates modified stress-re-stress paradigm-ınduced mitochondrial dysfunction and apoptosis in rats exhibiting post-traumatic stress disorder-like symptoms. J Mol Neurosci 2015; 56: 299-312. [CrossRef] 42. Aykaç A, Aydın B, Cabadak H, Gören MZ. The change in muscarinic receptor subtypes in different brain regions of rats treated with fluoxetine or propranolol in a rat model of post-traumatic stress disorder. Behav Brain Res 2012; 232:124-9. [CrossRef] 43. Zhang L, Zhou R, Li X, Ursano RJ, Li H. Stress-induced change of mitochondria membrane potential regulated by genomic and non-genomic GR signaling: a possible mechanism for hippocampus atrophy in PTSD. Med Hypotheses 2006; 66: 1205-8. [CrossRef] 44. Manoli I, Alesci S, Blackman MR, Su YA, Rennert OM, Chrousos GP. Mitochondria as key components of the stress response. Trends Endocrinol Metab 2007; 18: 190-8. [CrossRef]
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Details
| Primary Language | Turkish |
|---|---|
| Subjects | Health Care Administration |
| Journal Section | Articles |
| Authors | |
| Publication Date | December 15, 2016 |
| Submission Date | April 18, 2016 |
| Published in Issue | Year 2016 Volume: 6 Issue: 4 |
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