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All Journal The Indonesian Biomedical Journal Indonesian Journal of Perinatology
Sutandi, Chatrine
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Biochemistry, Genetics & Molecular Biology Health Professions Medicine & Pharmacology Nursing Public Health

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The effect of maternal diabetes on the formation of fetal surfactant Sanjaya, I Nyoman Hariyasa; Sutandi, Chatrine
Indonesian Journal of Perinatology Vol. 5 No. 1 (2024): Available online: 1 June 2024
Publisher : The Indonesian Society of Perinatology, South Jakarta, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.51559/inajperinatol.v5i1.42

Abstract

Elevated maternal blood glucose levels in pregnancy correlate with increased risk of pregnancy complications, labor, and pregnancy outcomes. Type II alveolus cells produce a combination of fat and protein called pulmonary surfactant. To assist in preserving lung stability, pulmonary surfactant plays a crucial function in lowering the propensity of the alveolus to recoil and preventing alveolus collapse. The hallmark of maternal diabetes is the malfunctioning of pancreatic β-cells, which results in insufficient insulin production to sustain proper blood glucose levels. Respiratory distress syndrome (RDS) in newborns is caused by surfactant lack of sufficiency, which is caused by fetal hyperglycemia and hyperinsulinism brought on by maternal diabetes. Appropriate treatments are required to improve glycemic management since maternal diabetes raises the risk of RDS in term newborns. These therapies include a deeper comprehension of the molecular mechanisms behind gestational diabetes mellitus that impact the surfactant system. Phosphatidylglycerol levels are either nonexistent or extremely low in infants with RDS. Phosphatidylglycerol synthesis during pregnancy in diabetics is known to be delayed in comparison to the non-diabetic control group. For this reason, proper care is essential to enhancing long-term health and neonatal outcomes. These findings underscore the need for early detection and management of maternal diabetes to mitigate the risk of RDS and improve neonatal health.
The Role of Cytokines, Hormones, and Cellular Regulation in Improving Maternal and Fetal Well-Being Hariyasa Sanjaya, I Nyoman; Sutandi, Chatrine; Syauta, Fetrisya
Indonesian Journal of Perinatology Vol. 5 No. 1 (2024): Available online: 1 June 2024
Publisher : The Indonesian Society of Perinatology, South Jakarta, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.51559/inajperinatol.v5i1.51

Abstract

Maternal and fetal well-being is a complex interplay of various factors. A key factor is that women receiving early and adequate pregnancy care are more likely to achieve positive pregnancy outcomes. Several studies have identified internal maternal factors as significant contributors to the well-being of both mother and fetus. However, scientific research and discussions on the role of cytokines, hormones, and cellular regulation in maternal and fetal well-being outcomes still need to be completed. Progesterone, a vital hormone for pregnancy and humans, influences immune function directly and through mediators by promoting the synthesis of T helper cell-type cytokines. The favorable benefits of dydrogesterone on repeated spontaneous miscarriages and impending miscarriages may be attributed to the regulating effects of these cytokines and the hormone's capacities. T helper cell-produced cytokines are linked to allograft rejection. Lastly, our finding of cellular regulatory mechanisms, including apoptosis, autophagy, and cellular senescence, highlights the multifaceted nature of maintaining maternal and fetal health during pregnancy. This review aims to delve deeper into the role of cytokines, hormones, and cellular regulation in enhancing maternal and fetal well-being.
Promoter Methylation and Low Placental Expression of Metalloproteinase (MMP)-9, Human Leukocyte Antigen (HLA)-G, Vascular Endothelial Growth Factor (VEGF), and Highly Soluble Endoglin (sEng) as Risk Factors for Preeclampsia Kusuma, Anak Agung Ngurah Jaya; Darmayasa, I Made; Mulyantari, Ni Kadek; Mayasari, Ni Nyoman Wistya Tri; Sutandi, Chatrine; Bay, Godefridus Paulo; Nugraha, Cokorda Gde Angga Ary
The Indonesian Biomedical Journal Vol 18, No 1 (2026)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v18i1.3921

Abstract

BACKGROUND: Dysregulated expressions of metalloproteinase (MMP)-9, human leucocyte antigen (HLA)-G, vascular endothelial growth factor (VEGF), and soluble endoglin (sEng) reflect impaired angiogenesis, immune tolerance, endothelial function, and trophoblast invasion that characterize abnormal placental development in preeclamptic (PE) pregnancies. However, the role of promoter methylation of these markers in linking the pathways to altered protein expression remains unclear. Hence, this study compared promoter methylation and placental expression of MMP-9, HLA-G, VEGF, and sEng between women with PE and normotensive pregnancies, and evaluate their diagnostic performance as potential biomarkers.METHODS: This case–control study included 30 women with PE and 30 controls. Placental tissue samples were collected within 15 minutes postpartum. Placental promoter methylation was assessed using methylation-specific polymerase chain reaction (PCR), and protein expression was measured using enzyme-linked immunosorbent assay (ELISA). Group differences were analyzed, diagnostic accuracy was evaluated using receiver operating characteristic (ROC) curves, and associations were expressed as adjusted odds ratios (AOR).RESULTS: Compared with controls, placentas from women with PE significantly showed higher methylation of HLA-G (58.9% vs. 37.3%) and sEng (6.7% vs. 4.1%), and lower methylation of VEGF (30.4% vs. 48.1%) and MMP-9 (36.1% vs. 44.9%). Expression of MMP-9, HLA-G, and VEGF was significantly reduced, while sEng expression was increased in PE. Multivariate analysis identified HLA-G hypermethylation (AOR 5.36), VEGF hypomethylation (AOR 8.55), sEng methylation (AOR 4.57), low expression of MMP-9, HLA-G, and VEGF, and high sEng expression (AOR 4.77) as independent predictors of PE. sEng expression demonstrated the best discrimination (AUC 0.835), followed by sEng methylation (AUC 0.785) and HLA-G methylation (AUC 0.774).CONCLUSION: PE is associated with distinct placental methylation–expression alterations, with sEng- and HLA-G–related markers showing the strongest diagnostic value.KEYWORDS: preeclampsia, DNA methylation, angiogenesis, MMP-9, HLA-G, sEng, placenta, epigenetics
Co-Authors Bay, Godefridus Paulo I Made Darmayasa I Nyoman Hariyasa Sanjaya Kusuma, Anak Agung Ngurah Jaya Mayasari, Ni Nyoman Wistya Tri Ni Kadek Mulyantari Nugraha, Cokorda Gde Angga Ary Syauta, Fetrisya