Volume 18, Issue 6 (June 2020)                   IJRM 2020, 18(6): 439-448 | Back to browse issues page

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Negara K S, Suwiyoga K, Sudewi R, Astawa N M, Kamasan Arijana G N, Tunas K et al . The role of caspase-dependent and caspase-independent pathways of apoptosis in the premature rupture of the membranes: A case-control study. IJRM 2020; 18 (6) :439-448
URL: http://ijrm.ir/article-1-1122-en.html
The role of caspase-dependent and caspase-independent pathways of apoptosis in the premature rupture of the membranes: A case-control study
Ketut Surya Negara * 1, Ketut Suwiyoga2 , Raka Sudewi3 , Nyoman Mantik Astawa4 , Gusti Nyoman Kamasan Arijana5 , Ketut Tunas6 , Tjokorda Gede Astawa Pemayun2
1- Department of Obstetrics and Gynecology, Medical Faculty of Udayana University, Sanglah Hospital, Bali, Indonesia. , tutsuryanegara@gmail.com
2- Department of Obstetrics and Gynecology, Medical Faculty of Udayana University, Sanglah Hospital, Bali, Indonesia.
3- Department of Neurology, Medical Faculty of Udayana University, Sanglah Hospital Bali, Indonesia.
4- Laboratory of Veterinary Medicine, Udayana University Bali, Indonesia.
5- Biomedic Laboratory of Medical Faculty Udayana University, Bali, Indonesia.
6- Department of Public Health, Dhyana Pura University Bali, Indonesia.
Abstract:   (2241 Views)
Background: Premature rupture of membrane (PROM) remains a problem in obstetrics, the mechanisms of PROM have not been clearly defined. Apoptosis is thought to play a key role in the mechanism, via caspase-dependent and caspase-independent pathways. Caspase-3, Apoptosis-inducing factor (AIF), and anti-apoptosis B-cell lymphoma 2 (Bcl-2) are hypothesized to be involved in PROM.
Objective: To determine the role of caspase-dependent and caspase-independent pathways in the mechanism of PROM.
Materials and Methods: This was a case-control study involving 42 pregnant women with gestational age between 20-42 wk. Participants were divided into the case group (with PROM) and control group (without PROM). Amniotic membranes were collected immediately after the delivery, and samples were taken from the site of membrane rupture. Immunohistochemical examination was done to determine the expression of Caspase-3, AIF, and Bcl-2.
Results: The expressions of Caspase-3 (OR = 9.75; 95% CI = 2.16-43.95; p = 0.001) and AIF (OR = 6.60; 95% CI = 1.48-29.36; p = 0.009) were significantly increased, whereas, Bcl-2 expressions (OR = 8.00; 95% CI = 1.79-35.74; p = 0.004) were significantly decreased in the case group.
Conclusion: High Caspase-3, AIF, and low Bcl-2 expression were the risk factors for PROM. Thus, it is evident that caspase-dependent and caspase-independent pathways are involved in the mechanism of PROM.
Keywords: Premature, Membrane, Apoptosis, Caspase, Pregnancy.
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Type of Study: Original Article | Subject: Pregnancy Health
References
1. Adeniji AO, Atanda OA. Interventions and neonatal outcomes in patients with premature rupture of fetal membranes at and beyond 34 weeks gestational age at a tertiary health facility in Nigeria. Br J Med Med Res 2013; 3: 1388-1397. [DOI:10.9734/BJMMR/2013/3428]
2. Endale T, Fentahun N, Gemada D, Hussen MA. Maternal and fetal outcomes in term premature rupture of membrane. World J Emerg Med 2016; 7: 147-152. [DOI:10.5847/wjem.j.1920-8642.2016.02.011] [PMID] [PMCID]
3. Budijaya M, Surya Negara IK. Labor profile with premature rupture of membranes (PROM) in Sanglah Hospital, Denpasar, Bali, Period January 1-31 December 2015. Int J Sci Res 2017; 6: 348-353.
4. Mercer BM. Preterm premature rupture of the membranes. Obstet Gynecol 2003; 101: 178-193. https://doi.org/10.1097/00006250-200301000-00033 [DOI:10.1016/S0029-7844(02)02366-9] [PMID]
5. Rodrigo MRR, Kannamani A. Perinatal and maternal outcome in premature rupture of membranes. J Evol Med Dent Sci 2016; 5: 3245-3247. [DOI:10.14260/jemds/2016/753]
6. Thombre MK. A review of the etiology epidemiology prediction and interventions of preterm premature rupture of membranes. [MSc thesis]. US, Michigan State University; 2014.
7. Benirschke, K. Anatomy and Pathology of the Placental Membranes. In: Benirschke K, Burton GJ, Baergen RN. Pathology of Human placenta. 3rd Ed. Springer, USA; 2012: 249-307. [DOI:10.1007/978-3-642-23941-0_11]
8. Vishwakarma K, Patel SK, Yadav K, Pandey A. Impact of premature rupture of membranes on maternal & neonatal health in Central India. J Evidence Based Med Healthcare 2015; 2: 8505-8508. [DOI:10.18410/jebmh/2015/1165]
9. Tency I, Verstraelen H, Kroes I, Holtappels G, Verhasselt B, Vaneechoutte M, et al. Imbalances between matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) in maternal serum during preterm labor. PLoS One 2012; 7: e49042. [DOI:10.1371/journal.pone.0049042] [PMID] [PMCID]
10. Garite TJ. Premature rupture of the membrane. In: Creasy RK, Resnik R. Maternal Fetal Medicine, Principle and Practice. 5th Ed. Netherland, Elsevier; 2004; 723-739.
11. Rangaswamy N, Kumar D, Moore RM, Mercer BM, Mansour JM, Redline R, et al. Weakening and rupture of human fetal membranes-biochemistry and biomechanics. Available at: https://www.intechopen.com/books/preterm-birth-mother-and-child/weakening-and-rupture-of-human-fetal-membranes-biochemistry-and-biomechanics.
12. Sukhikh GT, Kan NE, Tyutyunnik VL, Sannikova MV, Dubova EA, Pavlov KA, et al. The role of extracellular inducer of matrix metalloproteinases in premature rupture of membranes. J Matern Fetal Neonatal Med 2016; 29: 656-659. [DOI:10.3109/14767058.2015.1015416] [PMID]
13. Xu J, Wang HL. Role of caspase and MMPs in amniochorionic during PROM. J Reprod Contracept 2005; 16: 219-224.
14. Elmore S. Apoptosis: a review of programmed cell death. Toxicol Pathol 2007; 35: 495-516. [DOI:10.1080/01926230701320337] [PMID] [PMCID]
15. Hongmei Z. Extrinsic and intrinsic apoptosis signal pathway review. Available at: https://www.intechopen.com/books/apoptosis-and-medicine/extrinsic-and-intrinsic-apoptosis-signal-pathway-review.
16. Estaquier J, Vallette F, Vayssiere JL, Mignotte B. The mitochondrial pathways of apoptosis. Adv Mitochondrial Med 2011;942: 157-183. [DOI:10.1007/978-94-007-2869-1_7] [PMID]
17. Van Loo G, Schotte P, Van Gurp M, Demol H, Hoorelbeke B, Gevaert K, et al. Endonuclease G: a mitochondrial protein released in apoptosis and involved in caspase-independent DNA degradation. Cell Death Differ 2001; 8: 1136-1142. [DOI:10.1038/sj.cdd.4400944] [PMID]
18. Ashkenazi A, Salvesen G. Regulated cell death: signaling and mechanisms. Annu Rev Cell Dev Biol 2014; 30: 337-356. [DOI:10.1146/annurev-cellbio-100913-013226] [PMID]
19. Galluzzi L, Kepp O, Trojel-Hansen C, Kroemer G. Mitochondrial control of cellular life, stress, and death. Circ Res 2012; 111: 1198-1207. [DOI:10.1161/CIRCRESAHA.112.268946] [PMID]
20. Menon R, Fortunato SJ. The role of matrix degrading enzymes and apoptosis in rupture of membranes. J Soc Gynecol Investig 2004; 11: 427-437. [DOI:10.1016/j.jsgi.2004.04.001] [PMID]
21. Perfettini JL, Hospital V, Stahl L, Jungas T, Verbeke P, Ojcius DM. Cell death and inflammation during infection with the obligate intracellular pathogen, Chlamydia. Biochimie 2003; 85: 763-769. [DOI:10.1016/j.biochi.2003.08.006] [PMID]
22. Harirah HM, Borahay MA, Zaman W, Ahmed MS, Hankins GD. Increased apoptosis in chorionic trophoblasts of human fetal membranes with labor at term. Int J Clin Med 2012; 3: 136-142. [DOI:10.4236/ijcm.2012.32027] [PMID] [PMCID]
23. Parsons MJ, Green DR. Mitochondria in cell death. Essays Biochem 2010; 47: 99-114. [DOI:10.1042/bse0470099] [PMID]
24. Vaux DL. Apoptogenic factors released from mitochondria. Biochim Biophys Acta 2011; 1813: 546-550. [DOI:10.1016/j.bbamcr.2010.08.002] [PMID]
25. Saglam A, Ozgur C, Derwig I, Unlu BS, Gode F, Mungan T. The role of apoptosis in preterm premature rupture of the human fetal membranes. Arch Gynecol Obstet 2013: 288: 501-505. [DOI:10.1007/s00404-013-2774-3] [PMID]
26. Kataoka S, Furuta I, Yamada H, Kato EH, Ebina Y, Kishida T, et al. Increased apoptosis of human fetal membranes in rupture of the membranes and chorioamnionitis. Placenta 2002; 23: 224-231. [DOI:10.1053/plac.2001.0776] [PMID]
27. El Khwad M, Stetzer B, Moore RM, Kumar D, Mercer B, Arikat S, et al. Term human fetal membranes have a weak zone overlying the lower uterine pole and cervix before onset of labor. Biol Reprod 2005; 72: 720-726. [DOI:10.1095/biolreprod.104.033647] [PMID]
28. Reti NG, Lappas M, Riley C, Wlodek ME, Permezel M, Walker S, et al. Why do membranes rupture at term? Evidence of increased cellular apoptosis in the supracervical fetal membranes. Am J Obstet Gynecol 2007; 196: 484-e1-e10. [DOI:10.1016/j.ajog.2007.01.021] [PMID]
29. Candé C, Cohen I, Daugas E, Ravagnan L, Larochette N, Zamzami N, et al. Apoptosis-inducing factor (AIF): a novel caspase-independent death effector released from mitochondria. Biochimie 2002; 84: 215-222. [DOI:10.1016/S0300-9084(02)01374-3]
30. Arnoult D, Gaume B, Karbowski M, Sharpe JC, Cecconi F, Youle RJ. Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization. EMBO J 2003; 22: 4385-4399. [DOI:10.1093/emboj/cdg423] [PMID] [PMCID]
31. Akematsu T, Endoh H. Role of apoptosis-inducing factor (AIF) in programmed nuclear death during conjugation in Tetrahymena thermophila. BMC Cell Biol 2010; 11: 1-5. [DOI:10.1186/1471-2121-11-13] [PMID] [PMCID]
32. Negara KS, Suwiyoga K, Arijana K, Tunas K. Role of Caspase-3 as risk factors of premature rupture of membranes. Biomed Pharmacol J 2017; 10: 2091-2098. [DOI:10.13005/bpj/1332]
33. Negara KS, Suwiyoga K, Arijana K, Tunas K. Role of apoptosis inducing factor (AIF) as risk factors of premature rupture of membranes. Biomed Pharmacol J 2018; 11: 719-724. [DOI:10.13005/bpj/1425]
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