Expression of microRNA‐155 correlates positively with the expression of Toll‐like receptor 7 and modulates hepatitis B virus via C/EBP‐<i>β</i> in hepatocytes

Sarkar, Neelakshi; Panigrahi, Rajesh; Pal, Ananya; Biswas, Avik; Singh, Shivram Prasad; Kar, Sanjib; Bandopadhyay, Manikankana; Das, Dipanwita; Saha, Debraj; Kanda, Tatsuo; Sugiyama, Masaya; Chakrabarti, Shibdas; Banerjee, Arup; Chakravarty, Runu

doi:10.1111/jvh.12390

Cited by 43 publications

(41 citation statements)

References 45 publications

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“…Previous reports have shown that TLR4 expression remains down regulated in HepG2.2.15 cells compared to HepG2 cells[14]. This was re-affirmed in our study (Figure 1A).…”

Section: Resultssupporting

confidence: 92%

“…In an attempt to identify the pathway that is responsible for viral elimination, different chemical inhibitors (PDTC for NF-κB, LY294002 for PI3K, SP600125 for JNK and SB203580 for p38) were used, after which LPS was used to stimulate the TLR4 signaling pathway. These chemical blockers block MAPKs and NF-κB activation specifically, and have been used in several studies previously for pathway analysis[14,17]. Interestingly, on blocking NF-κB with its inhibitor eliminated the anti-viral role of TLR4.…”

Section: Resultsmentioning

confidence: 99%

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Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

Das

Sarkar

Sengupta

et al. 2016

WJG

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AIMToll like receptors plays a significant anti-viral role in different infections. The aim of this study was to look into the role of toll like receptor 4 (TLR4) in hepatitis B virus (HBV) infection.METHODSReal time PCR was used to analyze the transcription of TLR4 signaling molecules, cell cycle regulators and HBV DNA viral load after triggering the HepG2.2.15 cells with TLR4 specific ligand. Nuclear factor (NF)-κB translocation on TLR4 activation was analyzed using microscopic techniques. Protein and cell cycle analysis was done using Western Blot and FACS respectively.RESULTSThe present study shows that TLR4 activation represses HBV infection. As a result of HBV suppression, there are several changes in host factors which include partial release in G1/S cell cycle arrest and changes in host epigenetic marks. Finally, it was observed that anti-viral action of TLR4 takes place through the NF-κB pathway.CONCLUSIONThe study shows that TLR4 activation in HBV infection brings about changes in hepatocyte microenvironment and can be used for developing a promising therapeutic target in future.

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“…Previous reports have shown that TLR4 expression remains down regulated in HepG2.2.15 cells compared to HepG2 cells[14]. This was re-affirmed in our study (Figure 1A).…”

Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

Das

Sarkar

Sengupta

et al. 2016

WJG

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“…Our previous studies have showed that TLR7 mRNA expression is highly compromised in HBV replicating HepG2.2.15 cells when compared to the HepG2 cells [9]. It is believed that HBV represses the innate immune response during a natural infection.…”

Section: Resultsmentioning

confidence: 99%

“…The maintenance and plating of hepatoblastoma cell lines HepG2 and HepG2.2.15 was done as described previously [9]. …”

Section: Methodsmentioning

confidence: 99%

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Anti-hepatitis B virus (HBV) response of imiquimod based toll like receptor 7 ligand in hbv-positive human hepatocelluar carcinoma cell line

et al. 2017

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BackgroundToll like receptors (TLRs) play an important role in innate immunity and various studies suggest that TLRs play a crucial role in pathogenesis of hepatitis B virus (HBV) infection. The present study aims in looking into the status of crucial host and viral gene expression on inciting TLR7.MethodsThe transcription of TLR7 pathway signaling molecules and HBV DNA viral load were quantified by Real Time-PCR after stimulation of TLR7 with its imiquimod based ligand, R837. Cell cycle analysis was performed using flow-cytometry. Expression of TLR7 and chief cell cycle regulator governing G1/S transition, p53 was also seen in liver biopsysss samples of CHB patients. HBV induced alteration in histone modifications in HepG2 cells and its restoration on TLR7 activation was determined using western blot.ResultsThe TLR7 expression remains downregulated in HepG2.2.15 cells and in liver biopsy samples from CHB patients. Interestingly HBV DNA viral load showed an inverse relationship with the TLR7 expression in the biopsy samples. We also evaluated the anti-viral activity of R837, an agonist of TLR7. It was observed that there was a suppression of HBV replication and viral protein production upon TLR7 stimulation. R837 triggers the anti-viral action probably through the Jun N-terminal Kinase (JNK) pathway. We also observed a downregulation of histone H3K9Me3 repression mark upon R837 treatment in HBV replicating HepG2.2.15 cells, mimicking that of un-infected HepG2 cells. Additionally, the G1/S cell cycle arrest introduced by HBV in HepG2.2.15 cells was released upon ligand treatment.ConclusionThe study thus holds a close insight into the changes in hepatocyte micro-environment on TLR7 stimulation in HBV infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-017-2189-z) contains supplementary material, which is available to authorized users.

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The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

Chen

Ming

et al. 2020

Cell Biochemistry & Function

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As small conserved RNAs without a coding function, microRNAs are expressed in multicellular organisms and contribute to the modulation of multiple cellular reactions, such as viral replication, as well as autophagy. microRNAs can regulate host gene expression and inhibit or reinforce hepatitis B virus (HBV) replication. Hepatic cells express miR-155 noticeably. Consequently, our study explored miR-155 modulation of HBV replication and investigated the potential mechanism involved. miR-155 was inhibited on HBV infection. miR-155 transfection remarkably reinforced HBV replication, antigen expression, and progeny secretion in HepG2215 cells. Moreover, miR-155 impaired the inhibition of the cytokine signalling 1 (SOCS1)/Akt/ mTOR axis and reinforced HepG2215 autophagy. Additionally, the autophagy inhibitor (3-MA) eliminated HBsAg secretion triggered by miR-155. Taken together, miR-155 reinforced HBV replication by reinforcing SOCS1-triggered autophagy.Significance of the study: The research studied the potential mechanism involved in HBV replication and miR-155 that miR-155 reinforces HBV replication by reinforcing the SOCS1/Akt/mTOR axis-stimulated autophagy, and therefore, it can provide medical practitioners with the inspiration that chronic HBV might be cured or improved by regulating the activation of miR-155 in cells. In the study, the experiments show that autophagy inhibitors (3-MA) counteracted miR-155 contribution to HBV replication, and it might be a practicable way to improve HBV through some therapies that can repress the autophagy in related cells. K E Y W O R D S autophagy, HBV replication, infection, miR-155, SOCS1

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Expression of microRNA‐155 correlates positively with the expression of Toll‐like receptor 7 and modulates hepatitis B virus via C/EBP‐β in hepatocytes

Cited by 43 publications

References 45 publications

Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

Anti-viral role of toll like receptor 4 in hepatitis B virus infection: An in vitro study

Anti-hepatitis B virus (HBV) response of imiquimod based toll like receptor 7 ligand in hbv-positive human hepatocelluar carcinoma cell line

The microRNA‐155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling–induced autophagy

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