miRNA-221 and miRNA-222 are promising biomarkers for progression of liver fibrosis in HCV Egyptian patients

Abdel-Al, Amanda; El‐Ahwany, Eman; Zoheiry, Mona; Hassan, Marwa; Ouf, Amged; Abu-Taleb, Hoda; Rahim, Ali Abdel; El-Talkawy, Mohamed Darwish; Zada, Suher

doi:10.1016/j.virusres.2018.06.007

Cited by 33 publications

(13 citation statements)

References 26 publications

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“…Many studies have confirmed that miRNAs play an important role in liver fibrosis. MiR-221 and miR-222 are enhanced in early and late liver fibrosis and have potential use as PLOS NEGLECTED TROPICAL DISEASES biomarkers of liver fibrosis [41]. MiR-31 targets FIH1 and activates HSCs during liver fibrosis [42].…”

Section: Plos Neglected Tropical Diseasesmentioning

confidence: 99%

The role of let-7b in the inhibition of hepatic stellate cell activation by rSjP40

et al. 2021

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Background Hepatic stellate cells (HSCs) are one of the main cell types involved in liver fibrosis induced by many factors, including schistosomes. Previous studies in our lab have shown that recombinant P40 protein from Schistosoma japonicum (rSjP40) can inhibit HSC activation in vitro. Let-7b is a member of the let-7 microRNA family and plays an inhibitory role in a variety of diseases and inflammatory conditions. In this study, we investigated the role of let-7b in the inhibition of HSC activation by rSjP40. Methods Expression of let-7b was detected by quantitative real-time PCR. A dual luciferase assay was used to confirm direct interaction between let-7b and collagen I. We also used western blot to assess protein levels of TGFβRI and collagen type I α1 (COL1A1). Results We found that rSjP40 up-regulates expression of let-7b in HSCs. Let-7b inhibits collagen I expression by directly targeting the 3’UTR region of the collagen I gene. Furthermore, we discovered that let-7b inhibitor partially restores the loss of collagen I expression caused by rSjP40. Conclusion Our research clarifies the role of let-7b in the inhibition of HSC activation by rSjP40 and will provide new insights and ideas for the inhibition of HSC activation and treatment of liver fibrosis.

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Section: Plos Neglected Tropical Diseasesmentioning

confidence: 99%

The role of let-7b in the inhibition of hepatic stellate cell activation by rSjP40

et al. 2021

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“…Validation. Eighty-three patients with chronic HBV were divided into S0 (10), S1 (15), S2 (13), S3 (10), S4 (10), compensated cirrhosis (13), and decompensated cirrhosis groups (12) according to the Scheuer and Child-Pugh scoring system. Table 1 shows the demographic and clinical characteristics of all subjects included in the study.…”

Section: Clinical Characteristics Of the Subjects For Hub Mirnamentioning

confidence: 99%

“…miRNAs are a class of small noncoding RNAs with~22 nucleotides that regulate 20~80% of the host genes [9,10]. A lot of studies have proven that different miRNA expressions are associated with liver fibrosis [11][12][13]. Wang et al [14] found that miR-122, miR-194/192, miR-223, miR-21, miR155, and miR-29 were specifically expressed or enriched in several types of hepatic cells or in circulation, playing important roles in the pathogenesis of liver diseases.…”

Section: Introductionmentioning

confidence: 99%

The Diagnosis Value of a Novel Model with 5 Circulating miRNAs for Liver Fibrosis in Patients with Chronic Hepatitis B

Zhang

et al. 2021

Mediators of Inflammation

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Background and Aim. miRNAs play an important role in the development of human fibrosis. However, miRNA expression profiles during different stages of chronic hepatitis B (CHB) are not well defined. In this study, we aimed to further validate the features of 5 miRNA candidates from our previous study during different fibrotic stages and the value of diagnosis for liver fibrosis. Methods. Differential expression of five selected miRNAs (hsa-mir-1225-3p, hsa-mir-1238, hsa-miR-3162-3P, hsa-miR-4721, and hsa-miR-H7) was verified by qRT-PCR in the plasma of 83 patients and 20 healthy controls. The relative expression of these miRNAs was analyzed in different groups to screen target miRNA. A logistic regression analysis was performed to assess factors associated with fibrosis progression. The receiver operating characteristic (ROC) curve and discriminant analyses validated the ability of these predicted variables to discriminate the nonsignificant liver fibrosis group from the significant liver fibrosis group. Furthermore, the established models were compared with other prediction models to evaluate the diagnostic efficiency. Results. These five tested miRNAs all had signature correlations with hepatic fibrotic level ( p < 0.05 ), and the upregulation trends were consistent with miRNA microarray analysis previously. The multivariate logistic regression analysis identified that a model of five miRNAs (miR-5) had a high diagnostic accuracy in discrimination of different stages of liver fibrosis. The ROC showed that the miR-5 has excellent value in diagnosis of fibrosis, even better than the Forns score, FIB-4, S index, and APRI. GO functions of different miRNAs mainly involved in various biological processes were markedly involved in HBV and revealed signaling pathways dysregulated in liver fibrosis of CHB patients. Conclusions. It was validated that the combination of these five miRNAs was a new set of promising molecular diagnostic markers for liver fibrosis. The diagnosis model (miR-5) can distinguish significant and nonsignificant liver fibrosis with high sensitivity and specificity.

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“…Differentially expressed serum miRs are considered important non-invasive biomarkers for different stages of HCV-associated liver fibrosis progression in patients [41]. A study using an Egyptian patient cohort indicated that miR-16, miR-146a, miR-221 and miR-222 can be used as effective biomarkers for HCV-induced fibrosis, since these miRs are upregulated in early and late fibrosis, and miR-222 and miR-221 are important for their high sensitivity and specificity in late-stage fibrosis [42]. miR-122, the most abundant microRNA in the liver, was found to be negatively associated with fibrosis in HCV-infected patients [43,44].…”

Section: Mechanisms Of Hcv-associated Liver Fibrosismentioning

confidence: 99%

Mechanisms Underlying Hepatitis C Virus-Associated Hepatic Fibrosis

Khatun

Ray

2019

Cells

134

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Hepatitis C virus (HCV) infection often causes liver diseases, including fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Liver fibrosis is the outcome of the wound healing response to tissue damage caused by chronic HCV infection. This process is characterized by the excessive accumulation of extracellular matrix (ECM) proteins, such as collagen fibers secreted by activated hepatic stellate cells (HSCs). Activation of HSCs from the quiescent stage is mediated by different mechanisms, including pro-inflammatory cytokines and chemokines released from HCV-infected hepatocytes and liver macrophages. HCV infection modulates the expression of different microRNAs that can be transported and delivered to the HSCs via exosomes released from infected cells, also leading to the development of advanced disease pathogenesis. Although recent advancements in direct-acting antiviral (DAA) treatment can efficiently control viremia, there are very few treatment strategies available that can be effective at preventing pathogenesis in advanced liver fibrosis or cirrhosis in patients. Assessment of fibrosis is considered to be the major part of proper patient care and decision making in clinical practice. In this review, we highlighted the current knowledge of molecular mechanisms responsible for the progression of liver fibrosis in chronically HCV-infected patients, and currently available methods for evaluation of fibrosis in patients. A detailed understanding of these aspects at the molecular level may contribute to the development of new therapies targeting HCV-related liver fibrosis.

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miRNA-221 and miRNA-222 are promising biomarkers for progression of liver fibrosis in HCV Egyptian patients

Cited by 33 publications

References 26 publications

The role of let-7b in the inhibition of hepatic stellate cell activation by rSjP40

The role of let-7b in the inhibition of hepatic stellate cell activation by rSjP40

The Diagnosis Value of a Novel Model with 5 Circulating miRNAs for Liver Fibrosis in Patients with Chronic Hepatitis B

Mechanisms Underlying Hepatitis C Virus-Associated Hepatic Fibrosis

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