Một Vai Trò Có Thể Có Của Di truyền Nền Trong Các Bệnh Xương Phụ Thuộc Tuổi

Springer Science and Business Media LLC - Tập 8 - Trang 95-99 - 2010
Covadonga Huidobro1, Mario F. Fraga2
1Cancer Epigenetics Laboratory, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), HUCA, Universidad de Oviedo, Oviedo, Spain
2Department of Immunology and Oncology, National Center for Biotechnology, CNB-CSIC, Madrid, Spain

Tóm tắt

Di truyền nền, nghiên cứu về những thay đổi trong biểu hiện gen mà không thay đổi trình tự DNA, đã nổi lên như một lĩnh vực nghiên cứu đầy hứa hẹn trong lĩnh vực các bệnh liên quan đến tuổi tác. Các quá trình di truyền nền, chủ yếu là methyl hóa DNA và acetyl hóa histone, có thể ảnh hưởng đến kiểu gen như một phản ứng với các yếu tố môi trường và ngẫu nhiên. Quá trình lão hóa được coi là sự tích tụ các lỗi phân tử, điều này cũng ảnh hưởng đến các cơ chế di truyền nền và có thể góp phần vào sự xuất hiện của các bệnh liên quan đến tuổi tác. Dựa trên vai trò của di truyền nền trong một số bệnh phụ thuộc vào độ tuổi, trong bài viết này, chúng tôi thảo luận về khả năng ảnh hưởng của nó đến các bệnh xương phụ thuộc tuổi tác như loãng xương và viêm khớp dạng thấp.

Từ khóa

#di truyền nền #bệnh xương tuổi tác #loãng xương #viêm khớp dạng thấp #methyl hóa DNA #acetyl hóa histone

Tài liệu tham khảo

Waddington C. The epigenotype. Endeavour. 1942;1:18–20. Feinberg AP. Epigenetics at the epicenter of modern medicine. Jama. 2008;299:1345–50. Feinberg AP. A genetic approach to cancer epigenetics. Cold Spring Harb Symp Quant Biol. 2005;70:335–41. Graff J, Mansuy IM. Epigenetic dysregulation in cognitive disorders. Eur J Neurosci. 2009;30:1–8. Brooks WH, Le Dantec C, Pers JO, Youinou P, Renaudineau Y. Epigenetics and autoimmunity. J Autoimmunity. 2010;34(3):J207–19. Calvanese V, Lara E, Kahn A, Fraga MF. The role of epigenetics in aging and age-related diseases. Ageing Res Rev. 2009;8:268–76. Luger K, Mader AW, Richmond RK, Sargent DF, Richmond TJ. Crystal structure of the nucleosome core particle at 2.8 A resolution. Nature. 1997;389:251–60. Kouzarides T. Chromatin modifications and their function. Cell. 2007;128:693–705. Berger SL. The complex language of chromatin regulation during transcription. Nature. 2007;447:407–12. Wang Y, Leung FC. An evaluation of new criteria for CpG islands in the human genome as gene markers. Bioinformatics. 2004;20:1170–7. Ehrlich M, Gama-Sosa MA, Huang LH, et al. Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells. Nucleic Acids Res. 1982;10:2709–21. Kim JK, Samaranayake M, Pradhan S. Epigenetic mechanisms in mammals. Cell Mol Life Sci. 2009;66:596–612. Reik W, Dean W, Walter J. Epigenetic reprogramming in mammalian development. Science. 2001;293:1089–93. Klose RJ, Bird AP. Genomic DNA methylation: the mark and its mediators. Trends Biochem Sci. 2006;31:89–97. Jia D, Jurkowska RZ, Zhang X, Jeltsch A, Cheng X. Structure of Dnmt3a bound to Dnmt3L suggests a model for de novo DNA methylation. Nature. 2007;449:248–51. Bird AP, Wolffe AP. Methylation-induced repression—belts, braces, and chromatin. Cell. 1999;99:451–4. Strahl BD, Allis CD. The language of covalent histone modifications. Nature. 2000;403:41–5. Costa FF. Non-coding RNAs, epigenetics and complexity. Gene. 2008;410:9–17. Ambros V, Chen X. The regulation of genes and genomes by small RNAs. Development. 2007;134:1635–41. Ng K, Pullirsch D, Leeb M, Wutz A. Xist and the order of silencing. EMBO Rep. 2007;8:34–9. Weinert BT, Timiras PS. Invited review: theories of aging. J Appl Physiol. 2003;95:1706–16. Fraga MF. Genetic and epigenetic regulation of aging. Curr Opin Immunol. 2009;21:446–53. Bennett-Baker PE, Wilkowski J, Burke DT. Age-associated activation of epigenetically repressed genes in the mouse. Genetics. 2003;165:2055–62. Fraga MF, Ballestar E, Paz MF, et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proc Natl Acad Sci USA. 2005;102:10604–9. Poulsen P, Esteller M, Vaag A, Fraga MF. The epigenetic basis of twin discordance in age-related diseases. Pediatr Res. 2007;61:38R–42R. Bjornsson HT, Sigurdsson MI, Fallin MD, et al. Intra-individual change over time in DNA methylation with familial clustering. Jama. 2008;299:2877–83. Vogt G, Huber M, Thiemann M, van den Boogaart G, Schmitz OJ, Schubart CD. Production of different phenotypes from the same genotype in the same environment by developmental variation. J Exp Biol. 2008;211:510–23. Wong AH, Gottesman II, Petronis A. Phenotypic differences in genetically identical organisms: the epigenetic perspective. Hum Mol Genet. 2005;14(Spec No 1):R11–8. Cropley JE, Suter CM, Beckman KB, Martin DI. Germ-line epigenetic modification of the murine A vy allele by nutritional supplementation. Proc Natl Acad Sci USA. 2006;103:17308–12. Weaver IC, Champagne FA, Brown SE, et al. Reversal of maternal programming of stress responses in adult offspring through methyl supplementation: altering epigenetic marking later in life. J Neurosci. 2005;25:11045–54. Bjornsson HT, Fallin MD, Feinberg AP. An integrated epigenetic and genetic approach to common human disease. Trends Genet. 2004;20:350–8. Waterland RA, Jirtle RL. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol. 2003;23:5293–300. Holliday R. The inheritance of epigenetic defects. Science. 1987;238:163–70. (New York, NY). Poulsen P, Kyvik KO, Vaag A, Beck-Nielsen H. Heritability of type II (non-insulin-dependent) diabetes mellitus and abnormal glucose tolerance—a population-based twin study. Diabetologia. 1999;42:139–45. Williams FM, Spector TD. Recent advances in the genetics of osteoporosis. J Musculoskelet Neuronal Interact. 2006;6:27–35. Chesnut CH III. Theoretical overview: bone development, peak bone mass, bone loss, and fracture risk. Am J Med. 1991;91:2S–4S. Ralston SH. Genetics of osteoporosis. Proc Nutr Soc. 2007;66:158–65. Kannus P, Palvanen M, Kaprio J, Parkkari J, Koskenvuo M. Genetic factors and osteoporotic fractures in elderly people: prospective 25 year follow up of a nationwide cohort of elderly Finnish twins. BMJ. 1999;319:1334–7. (Clinical research ed). Michaelsson K, Melhus H, Ferm H, Ahlbom A, Pedersen NL. Genetic liability to fractures in the elderly. Arch Intern Med. 2005;165:1825–30. Lipsky PE. Why does rheumatoid arthritis involve the joints? N Engl J Med. 2007;356:2419–20. Grabiec AM, Tak PP, Reedquist KA. Targeting histone deacetylase activity in rheumatoid arthritis and asthma as prototypes of inflammatory disease: should we keep our HATs on? Arthritis Res Ther. 2008;10:226. Li E, Bird A. DNA methylation in mammals. In: Allis CD, Jenuwein T, Reinberg D, editors; Marie-Laure Caparros. New York: Cold Spring Harbor Laboratory Press; 2007. p. 341–357. Cashen AF, Schiller GJ, O’Donnell MR, Dipersio JF. Multicenter, phase II study of decitabine for the first-line treatment of older patients with acute myeloid leukemia. J Clin Oncol. 2010;28:556–61. Patel R, Shervington L, Lea R, Shervington A. Epigenetic silencing of telomerase and a non-alkylating agent as a novel therapeutic approach for glioma. Brain Res. 2008;1188:173–81.