Pemendekan Telomer Dan Apoptosis

Endang Purwaningsih

Abstract


Sel normal akan mengalami kematian sel yang terprogram atau apoptosis.Apoptosis ini merupakan proses penting dalam pengaturan homeostasis normal sel, yang menghasilkan keseimbangan dalam jumlah sel jaringan tertentu melalui eliminasi sel yang rusak dan proliferasi sel. Terjadinya deregulasi apoptosis dapat menimbulkan keadaan patologis, termasuk proliferasi yang tidak terkontrol seperti dijumpai pada sel kanker atau keadaan yang berhubungan proses penuaan dan kematian sel.

Penuaan atau kematian sel berhubungan dengan struktur nukleotida di ujung kromosom di dalam inti sel eukariot yang disebut telomer. Pada sel somatik normal terjadi pemendekan telomer seiring meningkatnya usia, termasuk stem cell yang dimaksudkan untuk pembaharuan sel. Sel somatik mempunyai program proses penuaan (aging). Telomer dipelihara dan dipertahankan oleh enzim telomerase.

Stabilitas dan viabilitas kromosom memerlukan fungsi telomer yang baik dan stabil. Gangguan fungsi telomer dapat disebabkan oleh pemendekan telomer atau adanya mutasi protein telomer yang dapat mengakibatkan peningkatan apoptosis. Sebaliknya, apoptosis yang diakibatkan oleh adanya kerusakan DNA, dapat memicu terjadinya pemendekan telomer. 

Keywords


Apoptosis; pemendekan telomer; penuaan; kerusakan DNA

Full Text:

PDF

References


Alenzi FQB 2004. Links between apoptosis, proliferation, the cell cycle. British J Biomed Sci 61 (2); 1- 4

Artandi SE, and DePinho RA 2010. Telomeres and telomerase in cancer. Carcinogenesis 3 (1): 9-18

AubertG and Lansdorp P 2007. Telomeres and Aging. Physiol Rev 88: 557-570 Blackburn E 2005. Telomerase and Cancer. Mol Cancer Res 3 (9) as DOI: 110.1158/1541-7786-MCR-05-0147

Granato T, Muscoli, Sgura A et al., 2009. Apoptosis and telomere shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line. BMC Neuroscience 10: 51 doi:10.1186/471:-2202-10-51

Gregory CD and Devitt A 2004. The Macrophage and the apoptotic cell: an innate immune interaction viewed simplistically?. Immunology 113: 1 – 14

Greider CW and Blackburn EH 1996. Telomeres, Telomerase and Cancer. Scientific American, p: 92. http://www.genethik.de/telomerase.htm

Jones CJ, Kipling D, Morris M et al, 2000. Evidence for a telomere-independent “clock” limiting RAS oncogenic driven proliferation of human tyroid epithelial cells Mol cell Biol 20: 5690-5699

King RJB 2000 Cancer Biology, Second Ed, Pearson Ecucation Limited, London, Lubis SL and Delyuzar H, 2010. Proses Penuaan. Departemen Patologi Anatomi, FK USU. Medan. http://proses penuaan. com Diakses pada tanggal 27 Oktober 2010.

Ludlow AT and Roth SM 2011. Review Article. Physical activity and Tlomere Biology: Exploring the Link with Aging-Releted Disease Prevention. J of Aging Res. As doi:10.4061/2011/790378.

Lumongga F 2008. Apoptosis. USU Repository, Medan.

Ramirez R, Carracedo J, Jimenez et al., 2003. Massive Telomere Loss Is an Early Event of DNA Damage-induced Apoptosis. J Bio Chem 272 (2): 836-842

Ratnawati H 2002. Enzim Telomerase dan Karsinogenesis. JKM 2 (1): 39-50

Rochmah W and Aswin S 2001. Tua dan Proses menua. Berkala ilmu Kedokteran 33 (4): 221-227

Shammas MA, Koley H, Beer DG, Li C, Goyal AK, and Munshi 2004. Growth Arrest, Apoptosis, and Telomere Shorttening of Barrett’s Associated Adenocarcinoma Cells by a Telomerase Inhibitor. Gastroenterology 126: 1337-1346

Shay JW, Zou Y, Hiyama E, and Wright WE 2001. Telomerase and Cancer. Hum Mol Gen 10 (7): 677-685.

Shlush LI, Skorecki KL, Yehezkel S et al ., 2011. Telomere elongation followed by telomere length reduction, in Leukocytes from divers exposed to intense oxidative stress-Implications for tissue and Organismal aging. Mech Ageing Dev 132: 123-130.

Syeed SA, Vohra H, Gupta A, Ganguly NK 2001. Apoptosis: Molecular Machinary, Current Sci 80(3): 349 – 360.

Underwood JCE, 2009. General and Systematic Pathology. Fifth Ed. Churchill Livingstone, New York-London : p 117- 119.

Volkmann N, Marassiz FM, Newmeyers DD, and Hanein D 2014. The Rheostat in the Membrane : Bcl-2 family Proteins and apoptosis. Cell Death and Deff 21: 206 – 2015.

Wong IM Collins K 2003. Telomere maintenance and disease. Lancet 362: 983-988.

Wright WE and Shay JW 2001. Cellular Senescence as a Tumor protection mechanism: the essential role of counting. Current Opinion in Genetics & Development 11: 98-103.

Wyllie A, Donahue V, Fischer B, Hill D, Keesey J, and Manzow S 2000. Cell Death Apoptosis and Necrosis, Rosche Diagnostic Corporation.




DOI: https://doi.org/10.33476/jky.v22i2.309

Refbacks

  • There are currently no refbacks.


Copyright (c) 2017 YARSI Medical Journal

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

__________________________________________________________________________________________

Copyright of YARSI Medical Journal.

Powered by OJS.

Creative Commons License

This work is licensed under a Creative Commons Attribution- NonCommercial 4.0 International License.