Deletion of Galectin‐3 attenuates acute pancreatitis in mice by affecting activation of innate inflammatory cells

Stojanović, Bojan; Jovanović, Ivan; Stojanović, Bojana; Stojanovic, Milica Dimitrijevic; Gajovic, Nevena; Radosavljević, Gordana; Pantic, Jelena; Arsenijević, Nebojša; Lukić, Miodrag L.

doi:10.1002/eji.201847890

Cited by 11 publications

(15 citation statements)

References 16 publications

(21 reference statements)

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“…In particular, expression of these pro-inflammatory cytokines were enhanced in the Saline group while in the tFNAs treatment group, fluorescence intensity of IL-1β and IL-6 were significantly weaker (Figure S2b,c,f,g). Thus, myeloperoxidase (MPO), an enzyme that is positively correlated with neutrophil activity, was used to evaluate the degree of neutrophil infiltration in pancreatic tissue of each mouse . As shown in Figure S2d,h, the accumulation of MPO in the saline group was more apparent when compared to the SO group, while tFNAs reduced the fluorescence intensity of MPO markedly in the treatment group.…”

Section: Synthesis and Characterization Of Tfnasmentioning

confidence: 99%

Tetrahedral Framework Nucleic Acids Can Alleviate Taurocholate-Induced Severe Acute Pancreatitis and Its Subsequent Multiorgan Injury in Mice

Wang

Gao

et al. 2022

Nano Lett.

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Severe acute pancreatitis (SAP) is an inflammatory disease of the pancreas accompanied by tissue injury and necrosis. It not only affects the pancreas but also triggers a systemic inflammatory response that leads to multiorgan failure or even death. Moreover, there is no effective treatment currently that can reverse the disease progression. In this study, tetrahedral framework nucleic acids (tFNAs) were utilized to treat SAP in mice for the first time and proved to be effective in suppressing inflammation and preventing pathological cell death. Serum levels of pancreatitis-related biomarkers witnessed significant changes after tFNAs treatment. Reduction in the expression of certain cytokines involved in local and systemic inflammatory response were observed, together with alteration in proteins related to cell death and apoptosis. Collectively, our results demonstrate that tFNAs could both alleviate SAP and its subsequent multiorgan injury in mice, thus offering a novel and effective option to deal with SAP in the future.

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Section: Synthesis and Characterization Of Tfnasmentioning

confidence: 99%

Tetrahedral Framework Nucleic Acids Can Alleviate Taurocholate-Induced Severe Acute Pancreatitis and Its Subsequent Multiorgan Injury in Mice

Wang

Gao

et al. 2022

Nano Lett.

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“…In our study (80) we have discovered that severe form of experimental acute pancreatitis induced by ligation of bilepancreatic duct increased expression of Gal-3 in the infiltrating leukocytes indicating the role of Gal-3 in the development of acute pancreatitis. Also, we revealed that Galectin-3 and TLR-4 are co-localized on the surface of the same infiltrating leukocytes.…”

Section: Galectin-3/tlr4 Binding and Acute Pancreatitismentioning

confidence: 57%

“…Similarly, the deletion of Gal-3 reduced the production of pro-inflammatory TNF-α and IL-1β from neutrophils, macrophages, and dendritic cells (DCs). Hence, lack of galectin-3 binding to TLR-4 results in diminishing severity of AP by attenuating the early influx of neutrophils and inflammatory mononuclear cells of innate immunity (80). The interaction between Gal-3 and TLR-4 in acute pancreatitis is depicted in Figure 1.…”

Section: Galectin-3/tlr4 Binding and Acute Pancreatitismentioning

confidence: 99%

The Role of TLR-4 and Galectin-3 Interaction in Acute Pancreatitis

Stojanovic

Stojanović

Arsenijević

et al. 2020

Serbian Journal of Experimental and Clinical Research

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Toll-like receptor-4 (TLR-4) is a member of evolutionarily conserved type I transmembrane proteins that can initiate sterile inflammatory cascade in the pancreas. Expression of TLR-4 is up-regulated in pancreatic tissue, as well as, on peripheral blood innate immune cells in human and experimental models of acute pancreatitis. TLR-4 plays important pro-inflammatory roles during development of acute pancreatitis: it recognize alarmins released from injured acinar cells and promotes activation and infiltration of innate immune cells after the premature and intraacinar activation of tripsinogen. Galectin-3 is β-galactoside-binding lectin that plays pro-inflammatory roles in a variety autoimmune diseases, acute bacterial infections and during tumorigenesis. It is reported that Galectin-3 is alarmin in experimental models of neuroinflammation and binds to TLR-4 promoting the pro-inflammatory phenotype of microglia. Also, in experimental model of acute pancreatitis Galectin-3 is colocalized with TLR-4 on innate inflammatory cells resulted in enhanced production of inflammatory cytokines, TNF-α and IL-1β, increased infiltration of pro-inflammatory N1 neutrophils, macrophages and dendritic cells and increased damage of pancreatic tissue. This review paper discusses the role of TLR-4/Gal-3 axis in the pathogenesis of acute pancreatitis.

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“…Expression of TLR4 and Galectin-3 were also increased in burn-induced peripheral neuroinflammation [103]. TLR4 appears to be universal receptor for Galectin-3 in inflammation in different tissues [104]. Galectin-3 seems to be an important mediator in injuryinduced innate immune response/TLR2 signaling [72].…”

Section: Galectin-3 In the Cns Injurymentioning

confidence: 99%

Galectin-3: Roles in Neurodevelopment, Neuroinflammation, and Behavior

et al. 2020

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There is a plethora of evidence to suggest that Galectin-3 plays an important role in normal functions of mammalian cells, as well as in different pathogenic conditions. This review highlights recent data published by researchers, including our own team, on roles of Galectin-3 in the nervous system. Here, we discuss the roles of Galectin-3 in brain development, its roles in glial cells, as well as the interactions of glial cells with other neural and invading cells in pathological conditions. Galectin-3 plays an important role in the pathogenesis of neuroinflammatory and neurodegenerative disorders, such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. On the other hand, there is also evidence of the protective role of Galectin-3 due to its anti-apoptotic effect in target cells. Interestingly, genetic deletion of Galectin-3 affects behavioral patterns in maturing and adult mice. The results reviewed in this paper and recent development of highly specific inhibitors suggests that Galectin-3 may be an important therapeutic target in pathological conditions including the disorders of the central nervous system.

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Deletion of Galectin‐3 attenuates acute pancreatitis in mice by affecting activation of innate inflammatory cells

Cited by 11 publications

References 16 publications

Tetrahedral Framework Nucleic Acids Can Alleviate Taurocholate-Induced Severe Acute Pancreatitis and Its Subsequent Multiorgan Injury in Mice

Tetrahedral Framework Nucleic Acids Can Alleviate Taurocholate-Induced Severe Acute Pancreatitis and Its Subsequent Multiorgan Injury in Mice

The Role of TLR-4 and Galectin-3 Interaction in Acute Pancreatitis

Galectin-3: Roles in Neurodevelopment, Neuroinflammation, and Behavior

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