Cytokine-Induced JAK2-STAT3 Activates Tissue Regeneration under Systemic or Local Inflammation

Kim, Young Kyu; Lee, Ju Young

doi:10.3390/ijms23042262

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…The JAK2/STAT3 signaling pathway is implicated in various physiological and pathological processes, including cancer, inflammation, and tissue injury. In inflammation, JAK2/STAT3 activation produces proinflammatory cytokines and mediates immune responses [23]. In this study, we observed variations in the mRNA levels of Tnf, Il-1, and Il-10 and the phosphorylation levels of JAK2 and STAT3 proteins, with significant increases noted in the T-2 treatment group.…”

Section: Discussionmentioning

confidence: 55%

Tert-Butylhydroquinone Mitigates T-2-Toxin-Induced Testicular Dysfunction by Targeting Oxidative Stress, Inflammation, and Apoptosis in Rats

Chen,

Zhang,

Lan

et al. 2024

Toxics

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Tert-butylhydroquinone (tBHQ) has emerged as a promising candidate for mitigating the adverse effects of T-2-induced reproductive toxicity. The protective effects of tBHQ on rat sperm quality, testicular injury, apoptosis, and inflammation induced by T-2 toxin exposure were investigated. Histopathological examination of testicular tissues revealed severe damage in the T-2-treated group, characterized by disorganized germ cell arrangement, thinning of the convoluted seminiferous tubule walls, and significant cellular necrosis. However, tBHQ administration, either as a preventive or therapeutic measure, mitigated this structural damage. Image analysis confirmed an increase in the cross-sectional area and height of the convoluted seminiferous tubules in the tBHQ-treated groups compared to the T-2-treated group (p < 0.05), indicating tBHQ’s efficacy in alleviating testicular damage. Additionally, tBHQ treatment significantly inhibited T-2-induced apoptosis of testicular tissue cells, as evidenced by the results showing reduced apoptotic cell counts and downregulation of the BAX/BCL2 ratio and caspase-3 expression (p < 0.05). tBHQ significantly increased the concentrations of the antioxidant factors SOD, CAT, TAC, and GSH-PX. Furthermore, tBHQ attenuated the inflammatory response induced by T-2 exposure, as indicated by the decreased mRNA expression of the proinflammatory cytokines Tnf, Il1, and Il10 in testicular tissue (p < 0.05). Additionally, tBHQ treatment alleviated the decline in serum testosterone induced by the T-2 and promoted testosterone synthesis gene expression, including for the genes 17β-HSD and Cyp11a1, in rat testes (p < 0.05). These findings underscore tBHQ’s role as a therapeutic agent combatting T-2-induced reproductive toxicity, highlighting its antioxidative, anti-apoptotic, and anti-inflammatory properties. Further elucidation of tBHQ’s mechanisms of action may offer novel strategies for preventing and treating reproductive disorders induced by environmental toxins.

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Section: Discussionmentioning

confidence: 55%

Tert-Butylhydroquinone Mitigates T-2-Toxin-Induced Testicular Dysfunction by Targeting Oxidative Stress, Inflammation, and Apoptosis in Rats

Chen,

Zhang,

Lan

et al. 2024

Toxics

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“…Janus kinase 2 (JAK2)/signal transducer and the activator of transcription 3 (STAT3) pathway are widely engaged in inflammation, immune regulation, cell differentiation, apoptosis and proliferation [72][73][74]. After acute or chronic systemic inflammation, the JAK2/STAT3 pathway is closely associated with regeneration of the heart, lung, liver, and kidney tissues in lipopolysaccharide (LPS)-induced mice [75]. In addition, the JAK2/STAT3 pathway plays a role in the onset and progression of sepsis [76].…”

Section: Discussionmentioning

confidence: 99%

Xuebijing injection protects sepsis induced myocardial injury by mediating TLR4/NF-κB/IKKα and JAK2/STAT3 signaling pathways

Kang,

Lu,

et al. 2023

Aging

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Objective: Compelling evidence has demonstrated that Xuebijing (XBJ) exerted protective effects against SIMI. The aims of this study were to investigate whether TLR4/IKKα-mediated NF-κB and JAK2/STAT3 pathways were involved in XBJ's cardio-protection during sepsis and the mechanisms. Methods: In this study, rats were randomly assigned to three groups: Sham group; CLP group; XBJ group. Rats were treated with XBJ or sanitary saline after CLP. Echocardiography, myocardial enzymes and HE were used to detect cardiac function. IL-1β, IL-6 and TNF-α in serum were measured using ELISA kits. Cardiomyocyte apoptosis were tested by TUNEL staining. The protein levels of Bax, Bcl-2, Bcl-xl, Cleaved-Caspase 3, Cleaved-Caspase 9, Cleaved-PARP, TLR4, p-NF-κB, p-IKKα, p-JAK2 and p-STAT3 in the myocardium were assayed by western blotting. And finally, immunofluorescence was used to assess the level of p-JAK2 and p-STAT3 in heart tissue. Results: The results of echocardiography, myocardial enzyme and HE test showed that XBJ could significantly improve SIMI. The IL-1β, IL-6 and TNF-α levels in the serum were markedly lower in the XBJ group than in the CLP group ( p <0.05). TUNEL staining's results showed that XBJ ameliorated CLP-induced cardiomyocyte apoptosis. Meanwhile, XBJ downregulated the protein levels of Bax, Cleaved-Caspase 3, Cleaved-Caspase 9, Cleaved-PARP, TLR4, p-NF-κB, p-IKKα, p-JAK2 and p-STAT3, as well as upregulated the protein levels of Bcl-2, Bcl-xl ( p <0.05). Conclusions: In here, we observed that XBJ's cardioprotective advantages may be attributable to its ability to suppress inflammation and apoptosis via inhibiting the TLR4/ IKKα-mediated NF-κB and JAK2/STAT3 pathways during sepsis.

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“…Molecular footprints in the bone marrow were probably caused indirectly by increased levels of proinflammatory cytokines in blood because whole bone marrow cells were ZIKV-negative in the sensitive PCR test. In support, systemic inflammation and systemic cytokines can affect JAK2/STAT3 signaling (which was affected in the bone marrow of fetuses and offspring, Figure 4 ) in tissues of mice [ 41 ]. However, like in other virus-negative organs, we cannot exclude earlier direct virus replication followed by virus clearance before sampling.…”

Section: Discussionmentioning

confidence: 99%

Offspring affected with in utero Zika virus infection retain molecular footprints in the bone marrow and blood cells

Udenze

Trus

Lipsit

et al. 2023

Emerging Microbes & Infections

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Congenital virus infections, for example cytomegalovirus and rubella virus infections, commonly affect the central nervous and hematological systems in fetuses and offspring. However, interactions between emerging congenital Zika virus and hematological system—bone marrow and blood—in fetuses and offspring are mainly unknown. Our overall goal was to determine whether silent in utero Zika virus infection can cause functional and molecular footprints in the bone marrow and blood of fetuses and offspring. We specifically focused on silent fetal infection because delayed health complications in initially asymptomatic offspring were previously demonstrated in animal and human studies. Using a well-established porcine model for Zika virus infection and a set of cellular and molecular experimental tools, we showed that silent in utero infection causes multi-organ inflammation in fetuses and local inflammation in the fetal bone marrow. In utero infection also caused footprints in the offspring bone marrow and PBMCs. These findings should be considered in a broader clinical context because of growing concerns about health sequelae in cohorts of children affected with congenital Zika virus infection in the Americas. Understanding virus-induced molecular mechanisms of immune activation and inflammation in fetuses may provide targets for early in utero interventions. Also, identifying early biomarkers of in utero -acquired immunopathology in offspring may help to alleviate long-term sequelae.

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Cytokine-Induced JAK2-STAT3 Activates Tissue Regeneration under Systemic or Local Inflammation

Cited by 4 publications

References 31 publications

Tert-Butylhydroquinone Mitigates T-2-Toxin-Induced Testicular Dysfunction by Targeting Oxidative Stress, Inflammation, and Apoptosis in Rats

Tert-Butylhydroquinone Mitigates T-2-Toxin-Induced Testicular Dysfunction by Targeting Oxidative Stress, Inflammation, and Apoptosis in Rats

Xuebijing injection protects sepsis induced myocardial injury by mediating TLR4/NF-κB/IKKα and JAK2/STAT3 signaling pathways

Offspring affected with in utero Zika virus infection retain molecular footprints in the bone marrow and blood cells

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