MicroRNA-122 as a Novel Non-Invasive Marker of Liver Fibrosis in Hepatitis C Virus Patients

Omran, Ahmed Abdel Samie; Osman, Khalid Saied; Kamel, Hanan; Abdel-Naem, Emad A; Hasan, Dalia E El-Deen

doi:10.7754/clin.lab.2015.151141

Cited by 8 publications

(13 citation statements)

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“… 41 The relationship between miR-122 and liver fibrosis is also confirmed in patients with hepatitis C virus, endowing it a potential to be a bio-marker for the severity of disease. 42 Similar to the findings of miR-122 in liver, miR-24 was noticed to be able to inhibit cardiac fibrosis subsequent to infarction in a rat model by downregulating the expression of furin, a subtilisin-like proprotein convertase that can facilitate the activation of TGF-β. 43 However, the role of miR-24 and miR-122 in skeletal muscle after injury is unclear.…”

Section: Discussionsupporting

confidence: 56%

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

Sun

Wang

et al. 2018

Molecular Therapy - Nucleic Acids

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Fibrosis is common after skeletal muscle injury, undermining tissue regeneration and function. The mechanism underlying skeletal muscle fibrosis remains unveiled. Transforming growth factor-β/Smad signaling pathway is supposed to play a pivotal role. However, how microRNAs interact with transforming growth factor-β/Smad-related muscle fibrosis remains unclear. We showed that microRNA (miR)-24-3p and miR-122-5p declined in skeletal muscle fibrosis, which was a consequence of transforming growth factor-β. Upregulating Smad4 suppressed two microRNAs, whereas inhibiting Smad4 elevated microRNAs. Luciferase reporter assay and chromatin immunoprecipitation confirmed that Smad4 directly inhibited two microRNAs. On the other hand, overexpression of these two miRs retarded fibrotic process. We further identified that Smad2 was a direct target of miR-24-3p, whereas miR-122-5p targeted transforming growth factor-β receptor-II. Both targets were important participants in transforming growth factor-β/Smad signaling. Taken together, a positive feedback loop in transforming growth factor-β/Smad4 signaling pathway in skeletal muscle fibrosis was identified. Transforming growth factor-β/Smad axis could be downregulated by microRNAs. This effect, however, was suppressed by Smad4, the downstream of transforming growth factor-β.

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Section: Discussionsupporting

confidence: 56%

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

Sun

Wang

et al. 2018

Molecular Therapy - Nucleic Acids

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“…Thus, the upregulation in miRNA-122 expression may result in the inhibition of EMT of HSCs. This result was in line with reports from Omran et al and Nakamura et al (14,15), wherein the morphology and functional study demonstrated that the overexpression of miRNA-122 may effectively promote the differentiation and maturation of liver cells. The expression of miRNA-122 at appropriate concentrations may adjust the balance between liver cell proliferation and differentiation, as well as that between EMT and mesenchymal epithelial transition.…”

Section: Discussionsupporting

confidence: 92%

“…In addition, miRNA-122 expression is significantly lower in chronic inflammation than in normal conditions and early inflammation (32). Previous findings have indicated that miRNA-122 is considered a marker of liver fibrosis (14). An miRNA-122 lentiviral vector was constructed and successfully transfected into HSCs in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…miRNA-122 accounts for 70% of all identified miRNAs in the liver and serves a pivotal role in liver physiology (12). miRNA-122 is associated with various pathological changes in the liver, including chronic inflammation of the liver (13), liver fibrosis (14,15), cirrhosis (16) and liver cancer, and is considered a non-invasive diagnostic predictor of liver fibrosis (14). In addition, miRNA-122 can act as a tumor suppressor miRNA and regulate metastasis of liver cancer (17,18).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑122 inhibits epithelial‑mesenchymal transition of hepatic stellate cells induced by the TGF‑β1/Smad signaling pathway

et al. 2018

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Transforming growth factor (TGF)-β1 may stimulate the activation of hepatic stellate cells (HSCs), resulting in the development of liver fibrosis. As micro RNA (miRNA)-122 is known to be associated with liver inflammation, its effects on the epithelial-mesenchymal transition (EMT) of HSCs through the inhibition of the TGF-β1/drosophila mothers against decapentaplegic protein 4 (Smad4) signaling pathway were investigated. The MTT assay was performed to explore the optimum TGF-β1 concentration suitable for HSC stimulation. Fluorescence microscopy was used to observe the transfection efficiency and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to observe gene and protein expression levels of α-smooth muscle actin (α-SMA), E-cadherin, N-cadherin and Smad4, respectively, in HSCs treated with TGF-β1 or TGF-β1 and miRNA-122. MTT assay results indicated that the concentration of 10 µg/l TGF-β1 was suitable for maximum growth and survival of HSCs. Notably, the mRNA expression levels of N-cadherin and α-SMA were significantly increased (each, P<0.05), but the expression levels of E-cadherin were decreased following 10 µg/l TGF-β1 treatment. Similar results were observed regarding the protein expression levels of N-cadherin, α-SMA and E-cadherin. Furthermore, the expression of F-actin was increased in the 10 µg/l TGF-β1 treated group compared with the 0 µg/l TGF-β1 treaded group and stretching of the muscle fiber filament was observed. miRNA-122 lentiviral vector transfection significantly decreased the mRNA expression of N-cadherin and increased the mRNA expression of E-cadherin in HSCs stimulated with TGF-β1, as evident from RT-qPCR results. Similar results were also observed regarding the protein expression levels of N-cadherin and E-cadherin. The expression levels of Smad4, the primary component of the TGF-β1 signaling pathway, were significantly lower in cells treated with TGF-β1 and miRNA-122 (P<0.01) compared those treated with TGF-β1. Thus, miRNA-122 may inhibit the activation and EMT of HSCs stimulated by TGF-β1.

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“…In adults, several noninvasive methods are recognized for the diagnosis of liver fibrosis, including the simple cohortderived markers such as APRI, 13 microRNA 122, and Forns, 14 and algorithms including extracellular matrix turnover factors, such as fibrometer, 5 fibrotest, 15 and hepa-score. 16 Serum markers often cannot differentiate sufficiently between the degrees of fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic Performance of Noninvasive Methods for Liver Biopsy by Fibroscan in Pediatric

Heidari

Motamed

Heirati

et al. 2021

Journal of Child Science

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Liver biopsy is the gold standard for the diagnosis and management of various liver diseases; however, noninvasive diagnostic modalities may help prevent adverse effects of anesthesia, prolonged hospitalization, sampling error, and other serious complications, particularly in pediatric patients. The aim of this study is to compare the results of liver biopsy and fibroscan in children with chronic liver diseases. All patients presenting chronic liver disease admitted in the ward or clinic of Tehran's Children Medical Center were enrolled in the study. Required laboratory tests were performed to diagnose the disease, followed by elastography using fibroscan 402 (M-probe) Echosens machine and liver biopsy using Menghini technique. Samples were scored by using METAVIR scoring system. Thirty-two patients were reported (68.8%, female) with autoimmune hepatitis (18.8%), Wilson disease (12.5%), and glycogen storage disease (12.5%). The most common pathologic stage and fibroscan result was stage III and F0 (46.9%), respectively. Association between pathology and fibroscan results was not significant. Nonetheless, age and diagnosis, age and Fibroscan score, and pathology and liver function test were significantly associated with each other. Fibroscan cannot be used as an alternative to liver biopsy; however, it can be a useful accessory tool.

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MicroRNA-122 as a Novel Non-Invasive Marker of Liver Fibrosis in Hepatitis C Virus Patients

Abstract: The study concluded that there was increased expression of mcroiRNA-122 in Egyptian chronic hepatitis C virus (CHCV) infected patients. MicroRNA 122 has a strong potential to serve as one of the novel noninvasive markers of early liver fibrosis.

Cited by 8 publications

References 0 publications

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis

MicroRNA‑122 inhibits epithelial‑mesenchymal transition of hepatic stellate cells induced by the TGF‑β1/Smad signaling pathway

Diagnostic Performance of Noninvasive Methods for Liver Biopsy by Fibroscan in Pediatric

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