Effect of tumour necrosis factor-α on proliferation, activation and protein synthesis of rat hepatic stellate cells
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Activation of Hepatic Stellate Cells Requires Dissociation of E-Cadherin–Containing Adherens Junctions with Hepatocytes
2021, American Journal of PathologyCitation Excerpt :Hematoxylin and eosin staining and immunohistochemical staining for a neutrophil marker, Ly6G, revealed that the infiltration of neutrophils, which secrete exogenous activation factors of HSCs such as reactive oxygen species,25 was present at 12 and 24 hours but not at 6 hours after CCl4 when E-cadherin–mediated adherens junctions disappeared (Figure 4, A and B). As indicated by qPCR, mRNA expression levels in the liver for exogenous stimuli that encode important drivers of HSC activation, including Tgfb1, Pdgf, Tnfa,26 Il1b,27,28 and Il6,29 were still not changed within 6 hours after CCl4 injection (Figure 4C). In addition, the expression of Acta2, which encodes α-smooth muscle actin, a specific marker of HSC activation, tended to increase 3 hours after CCl4 injection.
Modulatory effect of Prosopis juliflora leaves on hepatic fibrogenic and fibrolytic alterations induced in rats by thioacetamide
2019, Biomedicine and PharmacotherapyCitation Excerpt :Several proinflammatory cytokines including TNF-α and IL-6 as well as proteins such as Bcl-2 are involved in stimulating and/or suppressing cell death pathways. TNF-α is a cytokine with proinflammatory and immunoregulatory properties [61]. IL-6, a pleiotropic cytokine, can control both the acute protein synthesis and the acute inflammatory response and is found to be upregulated in several animal models of hepatic injury [62–64].
Emerging role and therapeutic implication of Wnt signaling pathways in liver fibrosis
2018, GeneCitation Excerpt :ECM is deposited by a prominent population of myofibroblasts which are absent from the normal liver and are derived from HSCs in the injured liver (Ramzy et al., 2018). In general, liver fibrosis is an imbalance between ECM synthesis and degradation that can regulate signaling as ligands, repositories and receptors (Knittel et al., 1997; Connolly et al., 2009). In addition, Maggie M. Ramzy et al. demonstrated that remarkable upregulation of α-SMA mRNA indicates the activation of HSCs (Ramzy et al., 2018).
CTRP3 attenuates hepatic stellate cell activation through transforming growth factor-β/Smad signaling pathway
2017, Biomedicine and PharmacotherapyHeavy metal mediated innate immune responses of the Indian green frog, Euphlyctis hexadactylus (Anura: Ranidae): Cellular profiles and associated Th1 skewed cytokine response
2016, Science of the Total EnvironmentCitation Excerpt :Involvement of different cytokines in oxidative stress management in the liver is complicated. For instance, TNFα and IL6 are known for the activation of stellate cells (macrophages) which engage in fundamental steps involved in hepatic inflammation (Knittel et al., 1997). Because the hepatic TNFα and IL6 levels were elevated and were significantly higher in heavy metal exposed frogs than in their reference site counterparts, it may be suggested that these play a role in hepatic inflammatory processes.