CD24 Gene Expression as a Risk Factor for Non-Alcoholic Fatty Liver Disease

Amin, Maha M; Ragab, Halla M.; Maksoud, Nabila Abd El; Elaziz, Wafaa Abd

doi:10.3390/diagnostics13050984

Diagnostics

2023

DOI: 10.3390/diagnostics13050984

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CD24 Gene Expression as a Risk Factor for Non-Alcoholic Fatty Liver Disease

Maha M Amin

Halla M. Ragab

Nabila Abd El Maksoud

et al.

Abstract: In light of increasing NAFLD prevalence, early detection and diagnosis are needed for decision-making in clinical practice and could be helpful in the management of patients with NAFLD. The goal of this study was to evaluate the diagnostic accuracy of CD24 gene expression as a non-invasive tool to detect hepatic steatosis for diagnosis of NAFLD at early stage. These findings will aid in the creation of a viable diagnostic approach. Methods: This study enrolled eighty individuals divided into two groups; a stud… Show more

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Cited by 3 publications

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Bilirubin, a hepatoprotective agent that activates SIRT1, PGC-1α, and PPAR-α, while inhibiting NF-κB in rats with metabolic-associated fatty liver disease

Taghizadeh,

Maleki,

Vakili

et al. 2024

Sci Rep

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Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disorder characterized by fatty liver disease alongside overweight or obesity and/or type 2 diabetes mellitus (T2DM). Timely intervention is crucial for a potential cure. This study aimed to investigate the effects of bilirubin, an endogenous antioxidant, on lipid metabolism and inflammation in MAFLD. Specifically, it examined bilirubin’s impact on SIRT1, PPAR-α, and NF-κB in the livers of rats with MAFLD induced by a high-fat diet (HFD) and streptozotocin (STZ) administration. Forty eight-week adult male Sprague Dawley rats were divided into five groups (n = 8): Control, HFD-STZ, HFD-S-BR6, HFD-S-BR14, and C-BR14. In the last three groups, bilirubin administration was performed intraperitoneally for 6 and 14 weeks (10 mg/kg/day). We selected the key genes associated with MAFLD and subsequently performed GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) analyses to explore the enriched biological processes and signaling pathways. Hence, the gene expression of SIRT1, PGC-1α, PPAR-α, and inflammatory genes (NF-κB, TNF-α, IL-6, and IL-1β) was measured using Real-time quantitative PCR. Stereological and histopathological alterations of liver structure as well as lipid profile, biochemical indices, and liver indices, were also assessed among different groups. The enrichment analysis identified that several signaling pathways and biological processes might be related to MAFLD. Bilirubin-treated rats contained higher PPAR-α, PGC-1α, and SIRT1 expression levels by approximately 5.7-, 2.1-, and 2.2-fold, respectively, compared to the HFD-receiving rats (p < 0.0001, p < 0.05, and p < 0.05). Whereas, the genes involved in the inflammatory cascades, including NF-κB, TNF-α, and IL-6, were downregulated by 0.6-fold (p < 0.05) following 14-week treatment of bilirubin, while only significantly decreased expression of NF-κB and IL-6 (approximately 0.6-fold, p < 0.05) were observed after 6-week treatment of bilirubin. Remarkably, bilirubin administration favorably reversed the effects of HFD on the liver’s volume and cell numbers and ameliorated the related structural changes. It also improved lipid profile, biochemical parameters, and liver indices of HFD-STZ rats. This study indicated that bilirubin acts as a protective/ameliorative compound against MAFLD, particularly through regulating the key genes involved in lipid metabolism and inflammation in HFD-STZ rats.

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Bilirubin, a hepatoprotective agent that activates SIRT1, PGC-1α, and PPAR-α, while inhibiting NF-κB in rats with metabolic-associated fatty liver disease

Taghizadeh,

Maleki,

Vakili

et al. 2024

Sci Rep

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Plasma CD24 level as a promising prognostic biomarker of hepatocellular carcinoma

Rasmy,

Awad,

Mohamed

et al. 2024

Egypt Liver Journal

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Background Hepatocellular carcinoma constitutes the most common primary hepatic cancer and remains a major medical burden in both developing and developed world. It ranks fifth in terms of global cases and second in terms of deaths for males.CD24 is known as a heavily glycosylated cell surface molecule that is highly expressed in a wide variety of human malignancies. It plays an important role in self-renewal, proliferation, migration, invasion, and drug resistance. The aim of this work was to evaluate the potential role of serum CD24 in the diagnosis and prediction of response to interventional therapy among hepatocellular carcinomas. Methods This study included 40 adult Egyptian patients who had liver cirrhosis and hepatocellular carcinoma (HCC group). Another group of 20 patients with liver cirrhosis only served as controls (Cirrhosis group). All patients underwent standard laboratory tests and abdominal ultrasound. For HCC patients, a triphasic CT scan, alpha-fetoprotein was done. CD24 levels were measured in all patients, and in HCC patients at baseline and one month after intervention. Results Baseline CD24 was significantly higher among HCC group in comparison to cirrhosis group (19.463 ± 8.573 vs. 0.725 ± 0.125 mg/L) with an overall p value < 0.001. Serum CD24 levels significantly declined after locoregional treatment from 19.463 ± 8.573 mg/L to 3.569 ± 1.248 mg/L (p < 0.001). Baseline CD24 was a useful marker in eligibility for HCC intervention with 80% sensitivity and 74.29% specificity at a cutoff of ≤ 23 mg/L, and it also had 62.96% sensitivity and 100% specificity in prediction of cure after locoregional treatment at a cutoff of ≤ 19.5 mg/L. Conclusion CD24 could be a helpful diagnostic and prognostic marker for HCC, as its baseline level is useful in predicting both eligibility for intervention and cure after locoregional treatment.

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Carnitine palmitoyltransferase-II inactivity promotes malignant progression of metabolic dysfunction-associated fatty liver disease via liver cancer stem cell activation

Wang,

Lu,

Wang

et al. 2024

World J Gastroenterol

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BACKGROUND Metabolic dysfunction-associated fatty liver disease (MAFLD) is one of the main chronic liver diseases. However, the roles of mitochondrial carnitine palmitoyl transferase-II (CPT-II) downregulation and liver cancer stem cell (LCSC) activation remain to be identified. AIM To investigate the dynamic alterations in CPT-II inactivity and LCSC activation during the malignant progression of MAFLD. METHODS Dynamic models of mouse MAFLD were generated via the consumption of a high-fat diet or the addition of 2-fluorenylacetamide for hepatocarcinogenesis. The mice were divided into groups on the basis of hematoxylin and eosin staining. Biochemistries, CPT-II, intrahepatic T cells, and LCSCs were determined and confirmed in clinical samples. The mitochondrial membrane potential (MMP) was analyzed. Differentially expressed genes were screened via RNA sequencing and enriched in KEGG pathways or GO functions. RESULTS Dynamic models of MAFLD malignant transformation were successfully generated on the basis of pathological examination. Hepatic lipid accumulation was associated with the loss of mitochondrial CPT-II activity and alterations in the MMP, with decreases in liver CD3+ or CD4+ T cells and increased AFP levels. In the lipid accumulation microenvironment, mitochondrial CPT-II was inactivated, followed by aberrant activation of CD44+ or CD24+ LCSCs, as validated in MAFLD or hepatocellular carcinoma patient samples. In terms of mechanism, the biological process category focused mainly on the metabolic regulation of cells in response to external stimuli. The enriched molecular functions included protein binding, cell apoptosis, and cell proliferation. CONCLUSION CPT-II inactivity promotes the malignant progression of MAFLD via the loss of innate immune function and abnormal LCSC activation.

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CD24 Gene Expression as a Risk Factor for Non-Alcoholic Fatty Liver Disease

Cited by 3 publications

References 36 publications

Bilirubin, a hepatoprotective agent that activates SIRT1, PGC-1α, and PPAR-α, while inhibiting NF-κB in rats with metabolic-associated fatty liver disease

Bilirubin, a hepatoprotective agent that activates SIRT1, PGC-1α, and PPAR-α, while inhibiting NF-κB in rats with metabolic-associated fatty liver disease

Plasma CD24 level as a promising prognostic biomarker of hepatocellular carcinoma

Carnitine palmitoyltransferase-II inactivity promotes malignant progression of metabolic dysfunction-associated fatty liver disease via liver cancer stem cell activation

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