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TÜRKÇE
Poster - 166
Molecular Profiling of Liver Fibrosis: LECT2, α-SMA, and COL1A1 Expression in Post-Kasai Biliary Atresia Patients
Nabilah Anisa Novebri, muhammad Zain, Henggar Allest Pratama, diaz pradana, Fiqih Vidiantoro Halim, Pramana Adhityo, sahal Muttaqin, nunik Agustriani, Andi Dwihantoro, Akhmad Makhmudi, Gunadi .
1Pediatric Surgery Division, Department of Surgery/Genetics Working Group/Translational Research Unit, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada/Dr. Sardjito Hospital, Yogyakarta, Indonesia
Abstract
Background: Biliary atresia (BA) is the most common cause of neonatal cholestasis and often results in progressive liver fibrosis and cirrhosis, even after successful Kasai portoenterostomy. LECT2, a hepatokine, is believed to influence fibrogenic pathways by regulating TGF-β signalling and its downstream targets such as α-SMA and COL1A1. However, the specific role of LECT2 in BA-associated fibrogenesis remains unclear.
Objective: This study aimed to evaluate the hepatic expression of LECT2, α-SMA, and COL1A1 in patients with BA who had undergone the Kasai procedure and to explore their association with liver fibrosis.
Methods: Liver tissue samples from BA patients were compared with those from non-BA controls using quantitative real-time PCR to assess gene expression levels of LECT2, α-SMA, and COL1A1. Patients with BA were further classified based on histopathological evidence of liver fibrosis. Correlations between LECT2 and fibrotic markers were analyzed using linear regression and Spearman correlation tests.
Results: BA liver samples showed significantly lower expression of LECT2 (ΔCT 11.7 ± 5.59 vs. 7.0 ± 4.55; p = 0.022), α-SMA (ΔCT 10.93 ± 3.16 vs. 5.37 ± 5.81; p = 0.006), and COL1A1 (ΔCT 5.34 ± 6.16 vs. 0.11 ± 1.33; p = 0.031) compared to controls. However, within the BA group, those with liver fibrosis had higher levels of LECT2 (ΔCT 10.3 ± 8.17 vs. 7.08 ± 5.53; p = 0.012), α-SMA (5.76 ± 5.36 vs. 12.1 ± 6.57; p = 0.035), and a trend toward increased COL1A1 (−5.81 ± 7.7 vs. 2.11 ± 9.7; p = 0.052). LECT2 expression was significantly linked with α-SMA (R² = 0.253, p = 0.01) and COL1A1 (R² = 0.223, p = 0.017). Spearman analysis also found a moderate correlation between LECT2 and COL1A1 (r = 0.48, p = 0.014).
Conclusion: Our findings indicate that patients with BA show abnormal expression of pro-fibrotic cytokines, specifically LECT2, α-SMA, and COL1A1. This suggests that these genes could be associated with the development of liver fibrosis in BA and may serve as potential predictors for liver fibrosis in BA patients following the Kasai procedure.