Secretory Phospholipase A2 Tipe Ii (Spla Ii) pada Penyakit Kardiovaskuler
Abstract
Reaksi inflamasi berperan dalam beberapa pathogenesis kondisi kardiovaskuler seperti atherosklerosis dan kerusakan iskemikpada infark miokard akut (IMA). Di antara mediator-mediator yang terlibat dalam inflamasi tersebut adalah enzim secretory
phospholipase A2 tipe II (sPLA2-II). Meskipun beberapa sel memang memproduksi sPLA2-II, namun sintesis oleh sel-sel tertentu
seperti hepatosit, adalah khas sebagai reaktan fase akut. Literatur terbaru menyatakan banyaknya peran dari sPLA2-II dalam
penyakit kardiovaskuler. Dalam tulisan berikut, akan mendiskusikan peran sPLA2-II dalam berbagai model atherosklerosis
atau IMA, baik in vitro maupun in vivo, termasuk perspektif terapeutik dari sPLA2-II inhibitor. Disimpulkan bahwa sPLA2-II
merupakan mediator inflamasi yang penting dalam penyakit kardiovaskuler.
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References
Lagrand WK, Visser CA, Hermens WT et al. C-reactive protein
as a cardiovascular risk factor? Circulation 1999;100;96-102
Wiklund O, Mattsson-Hulten L, Hurt-Camejo E et al. Effects
Gambar 2. Overview peran sPLA2-II pada atherosclerosis
dan kerusakan cardiomyocyte post IMA. Pada pembuluh
darah, sPLA2-II menginduksi atherosclerosis. sPLA2-II
ditemukan pada plak atherosclerotic di mana sPLA2-II
menginduksi peningkatan (small dense) LDL, penurunan
HDL, dan memicu makrofag untuk mengekspresikan
enzim tertentu dan membentuk foam cell. Atherosclerosis
dapat memicu IMA. sPLA2-II menginduksi kerusakan
cardiomyocyte selama reaksi inflamasi akibat iskemia
miokard. sPLA2-II dapat berikatan dengan membran
flip flop [PE dan PS] sehingga menyebabkan kematian
sel melalui aktivasi caspase 3, yang menyebabkan nekrosis
sekunder. sPLA2-II juga menginduksi ikatan CRP yang akan
menginduksi aktivasi komplemen sehingga menimbulkan
nekrosis sekunder. (Niessen. HWM. Caerdiovascular R.
2003)
Sargowo D: Spla Ii pada Penyakit Kardiovaskular
Jurnal Kardiologi Indonesia • Vol. 34, No. 4 • Oktober - Desember 2013 279
of simvastatin and atorvastatin on inflammation markers in
plasma. J Intern Med 2002; 251;338-347.
Ross R. Atherosclerosis: An inflamatory disease. N Engl J Med
1999; 340; 115 – 126
Morre SA, Stooker W, Lagrand WK et al. Microorganisms in the
aetiology of atherosclerosis, J Clin Pathol 2000;53:647-654
Libby P, Maroko PR, Bloor CM et al. Reduction of experimental
myocardial infarct size by corticosteroid administration. J Clin
invest 1973;52;599-607.
Maroko PR, Carpenter CB, Chiarillo M et al. Reduction by
cobra venom factor of myocardial necrosis after coronary artery
occlusion. J Clin Invest 1978;61:661-670.
De Zwaan C, Kleine AH, Diris JH et al. Continuous 48-h Cl
inhibitor treatment, following reperfusion theraphy, in patients
with accute myocardial infarction. Eur Heart J 2002;23:1670-
1677
Snitko Y, Yoon ET, Cho . High specificity of human secretory
class II phospholipase A2 for phosphatidic acid. Biochem J
1997;321:737-754
Baker SF, Othman R, Wilton DE, Tryptophan-caontaining
mutant of human (group Iia) secreted phospholipase A2 has a
dramatically increased ability to hydrolize phosphatidilcholine
vesicle and cell membranes. Biochemistry 1998;161:5008-
5015.
Hernandez M, Burillo SL, Crespo SL, Crespo MS et al. Secretory
phospholipase A2 activates the cascade of mitogen-activated
protein kinase and cytosolic phospolipase A2 in the human astrocytoma
cell line 1321N1. J Biol Chem 1998;273:606-612.
Kutawa H, Yamamoto S, Miyazaki Y et al. Studies on a
mechanism by which cytosolic phohpolipase A2. J Immunol
2000;165:4024-4031.
Marshall J, Krump E, Lindsay T et al. Involvement of cytosolic
phospholipase A2 and secretory phospholipase A2 in
arachidomic acid release from human neutrophils. J Immunol
2000;164:2084-2091.
Thommesen L, Sjursen W. Gasvik K et al. Selective inhibitors
of cytosolic or secretory phospholipase A2 block TNF-induced
activeation of transcription factor kappa-B and expression of
ICAM-1. J Immunol 1998;161:3421-3430.
Milella M, Gismondi A, Roncaioli P et al. CD 16 cross-linking
induces both secretory and extracelullar signal-regulated kinase
(ERK)-dependent cytosolic phospholipase A2 (PLA2) acrivity
in human natural killer cells: involvement of ERK, but
not PLA2, in CD16-triggered granule exocytosis. J Immunol
1997;158:3148-3154.
Eckey R, Menschikowsaki M, Yamamoto S et al, Minimal
oxidation and storage of low density lipoproteins result in an
increased susceptibility to phospolipase A2. Atherosclerosis
1997;19:165-176.
Kugiyama K, Ota Y, Sugiyama S et al. Prognosis value of plasma
levels of secretory type II phospholipase A2 in patients with
unstable angina pectoris. Am J Cardiol 2000;86:718-722
Menschikowski M, Kasper M, Lattke P et al. Analysis of secretory
group II phospholipase A2 in human aortic plaques.
Atherosclerosis 1995;118:173-181.
Schiering A, Menschikowski M, Mueller E et al. Analysis of
secretory group II phospholipase A2 in human aortic tissue is
dependence on the degree of etherosclerosis. Atherosclerosis
1999;144:73-78.
Elinder LS, Demitrescu A. Larsson P et al, Expression of phoepholipase
A2 isoform in human normal and arterosclerosis arterial
wall. Arterioscler Throm Vasc Biol 1997;17: 2257-2263.
as a cardiovascular risk factor? Circulation 1999;100;96-102
Wiklund O, Mattsson-Hulten L, Hurt-Camejo E et al. Effects
Gambar 2. Overview peran sPLA2-II pada atherosclerosis
dan kerusakan cardiomyocyte post IMA. Pada pembuluh
darah, sPLA2-II menginduksi atherosclerosis. sPLA2-II
ditemukan pada plak atherosclerotic di mana sPLA2-II
menginduksi peningkatan (small dense) LDL, penurunan
HDL, dan memicu makrofag untuk mengekspresikan
enzim tertentu dan membentuk foam cell. Atherosclerosis
dapat memicu IMA. sPLA2-II menginduksi kerusakan
cardiomyocyte selama reaksi inflamasi akibat iskemia
miokard. sPLA2-II dapat berikatan dengan membran
flip flop [PE dan PS] sehingga menyebabkan kematian
sel melalui aktivasi caspase 3, yang menyebabkan nekrosis
sekunder. sPLA2-II juga menginduksi ikatan CRP yang akan
menginduksi aktivasi komplemen sehingga menimbulkan
nekrosis sekunder. (Niessen. HWM. Caerdiovascular R.
2003)
Sargowo D: Spla Ii pada Penyakit Kardiovaskular
Jurnal Kardiologi Indonesia • Vol. 34, No. 4 • Oktober - Desember 2013 279
of simvastatin and atorvastatin on inflammation markers in
plasma. J Intern Med 2002; 251;338-347.
Ross R. Atherosclerosis: An inflamatory disease. N Engl J Med
1999; 340; 115 – 126
Morre SA, Stooker W, Lagrand WK et al. Microorganisms in the
aetiology of atherosclerosis, J Clin Pathol 2000;53:647-654
Libby P, Maroko PR, Bloor CM et al. Reduction of experimental
myocardial infarct size by corticosteroid administration. J Clin
invest 1973;52;599-607.
Maroko PR, Carpenter CB, Chiarillo M et al. Reduction by
cobra venom factor of myocardial necrosis after coronary artery
occlusion. J Clin Invest 1978;61:661-670.
De Zwaan C, Kleine AH, Diris JH et al. Continuous 48-h Cl
inhibitor treatment, following reperfusion theraphy, in patients
with accute myocardial infarction. Eur Heart J 2002;23:1670-
1677
Snitko Y, Yoon ET, Cho . High specificity of human secretory
class II phospholipase A2 for phosphatidic acid. Biochem J
1997;321:737-754
Baker SF, Othman R, Wilton DE, Tryptophan-caontaining
mutant of human (group Iia) secreted phospholipase A2 has a
dramatically increased ability to hydrolize phosphatidilcholine
vesicle and cell membranes. Biochemistry 1998;161:5008-
5015.
Hernandez M, Burillo SL, Crespo SL, Crespo MS et al. Secretory
phospholipase A2 activates the cascade of mitogen-activated
protein kinase and cytosolic phospolipase A2 in the human astrocytoma
cell line 1321N1. J Biol Chem 1998;273:606-612.
Kutawa H, Yamamoto S, Miyazaki Y et al. Studies on a
mechanism by which cytosolic phohpolipase A2. J Immunol
2000;165:4024-4031.
Marshall J, Krump E, Lindsay T et al. Involvement of cytosolic
phospholipase A2 and secretory phospholipase A2 in
arachidomic acid release from human neutrophils. J Immunol
2000;164:2084-2091.
Thommesen L, Sjursen W. Gasvik K et al. Selective inhibitors
of cytosolic or secretory phospholipase A2 block TNF-induced
activeation of transcription factor kappa-B and expression of
ICAM-1. J Immunol 1998;161:3421-3430.
Milella M, Gismondi A, Roncaioli P et al. CD 16 cross-linking
induces both secretory and extracelullar signal-regulated kinase
(ERK)-dependent cytosolic phospholipase A2 (PLA2) acrivity
in human natural killer cells: involvement of ERK, but
not PLA2, in CD16-triggered granule exocytosis. J Immunol
1997;158:3148-3154.
Eckey R, Menschikowsaki M, Yamamoto S et al, Minimal
oxidation and storage of low density lipoproteins result in an
increased susceptibility to phospolipase A2. Atherosclerosis
1997;19:165-176.
Kugiyama K, Ota Y, Sugiyama S et al. Prognosis value of plasma
levels of secretory type II phospholipase A2 in patients with
unstable angina pectoris. Am J Cardiol 2000;86:718-722
Menschikowski M, Kasper M, Lattke P et al. Analysis of secretory
group II phospholipase A2 in human aortic plaques.
Atherosclerosis 1995;118:173-181.
Schiering A, Menschikowski M, Mueller E et al. Analysis of
secretory group II phospholipase A2 in human aortic tissue is
dependence on the degree of etherosclerosis. Atherosclerosis
1999;144:73-78.
Elinder LS, Demitrescu A. Larsson P et al, Expression of phoepholipase
A2 isoform in human normal and arterosclerosis arterial
wall. Arterioscler Throm Vasc Biol 1997;17: 2257-2263.
Published
2015-04-01
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How to Cite
Sargowo, D. (2015). Secretory Phospholipase A2 Tipe Ii (Spla Ii) pada Penyakit Kardiovaskuler. Indonesian Journal of Cardiology, 34(4), 271-9. https://doi.org/10.30701/ijc.v34i4.386
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