DISTRIBUSI MITOKONDRIA DAN EKSPRESI BAX PADA HUVEC’s YANG MENGALAMI APOPTOSIS AKIBAT INDUKSI OX-LDL
DOI:
https://doi.org/10.21776/ub.jkb.2006.022.02.4Abstract
ABSTRACT It had been revealed that endothelial dysfunction which is caused by oxydized LDL is related to TNF Receptor Apoptosis Including Ligand (TRAIL) mechanism. However, there is study to see the involvement of mitochondrial mecanism in Ox-LDL endothelial cells dysfunction. This study was done to see the effect of Ox-LDL treatment on apoptosis of HUVEC’s culture  whether  associated  with  the  distribution  of  mitochondria  or  BAX  expression,  the  main  protein  mitochondria apoptosis mechanism. HUVEC’s culture was divided into two groups: control group and treatment group ( 50 mg/ml Ox-LDL for 24 hours). Doublestaining for DNA fragmented (TUNEL) and BAX expression were done respectively, as well as immunochemistry  using  monoclonal  Ab  of  mitochondria.  In  the  control  group  mitochondria  was  distributed  firmly  on cytoplasma of endothelial cells. In contrast, mitochondria were only found near nuclear membrane cells on treatment group  (this  future  usually  found  on  divided  cells) there  was  also  an  increasing  of  BAX  expression  and  a  mount  of apoptotic cells on treatment group compared with control group. It can be concluded that mitochondria is involved in apoptosis of Ox-LDL endothelial cells in order to serve the abundant energy. Keywords: Mitochondria distribution, Bax expresson, Apoptotic, Ox-LDLDownloads
References
DAFTAR KEPUSTAKAAN
Riawan W. Wibowati S. Pengaruh pemberian ox-LDL terhadap Aktivasi NF-KB dan PPAR serta apoptosis pada kultur HJVEC's journal Kedokteran Brawijaya 2006;23-29.
Kita T. LOX-1. A possible Clue to The Missing Link Between Hypertension and Atherogenesis Circ res 999;84;1113-1115.
Metha J. The role of LOX-1, A Novel Lectin Like Receptor for Oxidized LDL, in Atherosclerosis. Can J Cardiol 2004;20;32B-36B.
Dimmeler S. Upregulation of Superoxide Dismutase and Nitric Oxide Synthase Mediates The Apoptosis-Suppressive Effect of Shear Stress on E. cells. University of Wizbury. Germany;1999.
Stefanec T. Endothelial Apoptosis Chest 2000;117;841-854.
Husada J.J. The Role of Appoptosis in Brain Injury. Simposium Neuro Intensif Quality-Hotel, Solo. 9-10 Oktober 2004.
Daniel, P. Regulation of cell death by pro-apoptotic Bcl-2 family members. Clinical and Molecular Oncology Program USA;2004.
Green DG and JD Reed. Mitochondrial and Apoptosis. Science 1998;281:1309-12.
Freshney I. Culture of animal cell: a manual of basic technique. 2eds. New York: Alan R Liss Inc;1987
Krinjen PAJ, R Nijimeijer, CLJM Meijer, CA Veisser, CE Hack, HWM Niessen. Apoptosis in myocardial ischemia and infraction. Journal of Clinical Pathology 2002;55:801-811
Gauthier, Eric. Cell Death: The Basic Mechanism. Apo Review Journal 2004;82(3).
Carafoli E. Chiesi M. Gazzotti P. The Membrane carriers related to intracellular calcium regulation, Hypertension Pathophysiotogy, Diagnosis and Mannagement 1990;62:978.
Crompton M. The mitochondrial permeability transition pore and its role in cell death, Biochem 1999;(J.341):233-249.
Downloads
Published
Issue
Section
License
Authors who publish with this journal agree to the following terms:- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).