Injeksi Serum Mengandung TNF-α Tinggi Menurunkan Konsentrasi VEGF dan Ekspresi Nephrin Glomerulus Mencit Bunting

Authors

  • Syahroni Yudistian Agmar Program Magister Ilmu Biomedik Fakultas Kedokteran Universitas Brawijaya. Malang Indonesia.
  • Siti Candra Windu Batiyani Laboratorium Obstetri dan Ginekologi RSUD dr.Saiful Anwar/Fakultas Kedokteran Universitas Brawijaya, Malang Indonesia.
  • Loeki E Fitri Laboratorium Parasitologi dan Laboratorium Biomedik Fakultas Kedokteran Universitas Brawijaya, Malang Indonesia

DOI:

https://doi.org/10.21776/ub.jkb.2016.029.01.3

Keywords:

nephrin glomerulus, preeklampsia, TNF-α, VEGF

Abstract


Preeklampsia ditandai dengan adanya hipertensi dan proteinuria pada usia kehamilan lebih dari 20 minggu. Preeklampsia diderita oleh 3%-8% wanita hamil dan menjadi penyebab utama kematian pada kehamilan. Tumor Necrosis Factor-α(TNF-α) diduga memiliki peranan penting dalam menimbulkan terjadinya preeklampsia. Tujuan dari penelitian ini adalah untuk mengetahui efek injeksi serum dengan konsentrasi TNF-α tinggi terhadap konsentrasi Vascular Endothelial Growth Factor (VEGF) dan ekspresi protein nephrin glomerulus  pada mencit bunting. Serum dengan konsentrasi TNF-α tinggi diambil dari ibu hamil dan diinjeksikan intraperitoneal pada mencit bunting dengan usia kebuntingan 13 dan 14 hari. Pada usia kebuntingan 18 hari konsentrasi VEGF serum diperiksa menggunakan ELISA dan ekspresi protein nephrin glomerulus dengan imunohistokimia. Penelitian ini menunjukkan injeksi serum TNF-α dapat menurunkan konsentrasi VEGF serum mencit bunting (p=0,021) dan ekspresi protein nephrin glomerulus (p=0,000). Penurunan konsentrasi VEGF dan protein nephrin terjadi pada pasien preeklampsia dan dapat menimbulkan gejala preeklampsia. Dapat disimpulkan bahwa injeksi intraperitoneal serum dengan konsentrasi TNF-α tinggi dapat memberikan gambaran preeklampsia pada mencit bunting.

 

Downloads

Download data is not yet available.

References

Program National High Blood Pressure Education. Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure. American Journal of Obstetrics & Gynecology. 2000; 183(1): S1 - S22.

Duley L. The Global Impact of Pre-Eclampsia and Eclampsia. Seminars in Perinatology. 2009; 33(3): 130 - 137.

Takimoto E, Ishida J, Sugiyama F, Horiguchi H, Murakami K, and Fukamizu. Hypertension Induced in Pregnant Mice by Placental Renin. Science. 1996; 274(5289): 995 - 998.

Zhou CC, Ahmad S, Mi T, et al. Autoantibody from Women with Preeclampsia Induces Soluble Fms-Like Tyrosine Kinase-1 Production via Angiotensin Type 1 Receptor and Calcineurin/Nuclear Factor of Activated T-Cells Signaling. Hypertension. 2008; 51(4): 1010 - 1019.

Maynard SE, Min JY, Merchan J, et al. Excess Placental Soluble Fms-Like Tyrosine Kinase 1 (Sflt1) May Contribute to Endothelial Dysfunction, Hypertension, and Proteinuria in Preeclampsia. The Journal of Clinical Investigation. 2003; 111(5): 649-658.

Zhou CC, Irani RA, Zhang Y, et al. Angiotensin Receptor Agonistic Autoantibody–Mediated Tumor Necrosis Factor-a Induction Contributes to Increased Soluble Endoglin Production in Preeclampsia. Circulation. 2010; 121(3): 436-444.

Sunderland NS, Thomson SE, Heffernan SJ, et al. Tumor Necrosis Factor A Induces A Model Of Preeclampsia In Pregnant Baboons (Papio hamadryas). Cytokine. 2011; 56(2): 192 - 199.

Hyvönen ME, Dumont V, Tienari J, et al. Early-Onset Diabetic E1-DN Mice Develop Albuminuria and Glomerular Injury Typical of Diabetic Nephropathy. BioMed Research International. 2014; 2015: 11.

Rangan GK and Tesch GH. Methods In Renal Research: Quantification Of Renal Pathology By Image Analysis. Nephrology. 2007; 12(6): 553 - 558.

Xu C, Chang A, Hack BK, Eadon MT, Alper SL, and Cunningham PN. TNF-Mediated Damage to Glomerular Endothelium is an Important Determinant of Acute Kidney Injury in Sepsis. Kidney International. 2014; 85(1): 72- 81.

Shibuya M. Vaskular Endothelial Growth Factor Receptor-1 (VEGFR-1/Flt-1): A Dual Regulator for Angiogenesis. Angiogenesis. 2006; 9(4): 225-230.

Maharaj A and D'Amore P. Roles for VEGF in Adult. Microvascular Research. 2007; 74(2-3): 100-113.

Karumanchi SA and Lindheimer MD. Preeclampsia Pathogenesis: “Triple A Ratingâ€-Autoantibodies and Antiangiogenic Factors. Hypertension. 2008; 51(4): 991-992.

Saito Y, Okamura M, Nakajima S, et al. Suppression of Nephrin Expression by TNF-A Via Interfering with the Camp-Retinoic Acid Receptor Pathway. American Journal of Physiology. 2010; 298(6): F1436-F1444.

Okamura M, Takano Y, Saito Y, Yao J, and Kitamura M. Induction of Nephrin Gene Expression by Selective Cooperation of the Retinoic Acid Receptor and the Vitamin D Receptor. Nephrology Dialysis Transplantation. 2009; 24(10): 3006-3012.

Collino F, Bussolati B, Gerbaudo E, et al. Preeclamptic Sera Induce Nephrin Shedding from Podocytes through Endothelin-1 Release by Endothelial Glomerular Cells. American Journal of Physiology. 2008; 294(5): 1185-1194.

Downloads

Published

2016-01-29

Issue

Vol. 29 No. 1 (2016)

Section

Research Article

License

Authors who publish with this journal agree to the following terms:

  1. 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.
  2. 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.
  3. 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).