Interleukin 10 protects primary melanocyte by activation of Stat-3 and PI3K/Akt/NF-κB signaling pathways

Zhou, Jia; Ling, Jingjing; Song, Jing; Wang, Yong; Feng, Bo; Ping, Fengfeng

doi:10.1016/j.cyto.2016.05.013

Cited by 29 publications

(30 citation statements)

References 60 publications

(74 reference statements)

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“…Activation of the PI3K–Akt signalling pathway protects against oxidative stress‐induced cell death . Specifically, geniposide protects cells from H 2 O 2 ‐induced apoptosis by activating the PI3K–Akt signalling pathway .…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, geniposide protects cells from H 2 O 2 ‐induced apoptosis by activating the PI3K–Akt signalling pathway . The Bcl‐2 and caspase families, which are crucial proteins involved in the apoptosis response induced by oxidative stress, are downstream molecules of the PI3K–Akt signalling pathway. Pre‐treatment of H 2 O 2 ‐induced melanocytes with geniposide increased expression of the anti‐apoptotic protein Bcl‐2 and decreased expression of Bax, a pro‐apoptotic protein belonging to the Bcl‐2 family.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Kong

Zhang

et al. 2018

Clin Exp Dermatol

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Kong

Zhang

et al. 2018

Clin Exp Dermatol

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“…6A, 6B), suggesting that the contribution of the JNK pathway to M2 Mφ-enhanced cementoblastic differentiation may be mediated by other signals, such as exosomes [67,68]. There is evidence that the AKT signaling pathway plays a key role in the production of VEGF and IL-10 [69][70][71], and other cytokines, such as IFN-γ and TNF-α, can also regulate this process by activating the AKT or JNK signaling pathway [62][63][64][65][66][67][68][69][70][71][72][73], suggesting that the cytokine-cytokine and cytokine-pathway interactions are bidirectional and very complex. Although further research is necessary before the signals involved in M2-enhanced cementoblastic differentiation can be clarified, the data obtained in the present study suggest that modulation of Mφs in an in vivo milieu to positively influence PDLSCs can be useful for true periodontal regeneration.…”

Section: Stem Cellsmentioning

confidence: 99%

M2 Macrophages Enhance the Cementoblastic Differentiation of Periodontal Ligament Stem Cells via the Akt and JNK Pathways

Kong

et al. 2019

Stem Cells

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Although macrophage (Mφ) polarization has been demonstrated to play crucial roles in cellular osteogenesis across the cascade of events in periodontal regeneration, how polarized Mφ phenotypes influence the cementoblastic differentiation of periodontal ligament stem cells (PDLSCs) remains unknown. In the present study, human monocyte leukemic cells (THP‐1) were induced into M0, M1, and M2 subsets, and the influences of these polarized Mφs on the cementoblastic differentiation of PDLSCs were assessed in both conditioned medium‐based and Transwell‐based coculture systems. Furthermore, the potential pathways and cyto‐/chemokines involved in Mφ‐mediated cementoblastic differentiation were screened and identified. In both systems, M2 subsets increased cementoblastic differentiation‐related gene/protein expression levels in cocultured PDLSCs, induced more PDLSCs to differentiate into polygonal and square cells, and enhanced alkaline phosphatase activity in PDLSCs. Furthermore, Akt and c‐Jun N‐terminal Kinase (JNK) signaling was identified as a potential pathway involved in M2 Mφ‐enhanced PDLSC cementoblastic differentiation, and cyto‐/chemokines (interleukin (IL)‐10 and vascular endothelial growth factor [VEGF]) secreted by M2 Mφs were found to be key players that promoted cell cementoblastic differentiation by activating Akt signaling. Our data indicate for the first time that Mφs are key modulators during PDLSC cementoblastic differentiation and are hence very important for the regeneration of multiple periodontal tissues, including the cementum. Although the Akt and JNK pathways are involved in M2 Mφ‐enhanced cementoblastic differentiation, only the Akt pathway can be activated via a cyto‐/chemokine‐associated mechanism, suggesting that players other than cyto‐/chemokines also participate in the M2‐mediated cementoblastic differentiation of PDLSCs. Stem Cells 2019;37:1567–1580

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“…The glucagon-like peptide-1 (GLP-1) receptor agonist exenatide exhibits neuroprotection through the autocrine release of IL-10 [45]. IL-10 binds to its receptor and regulates downstream signaling, such as JAK1/STAT3 [46,47], PI3K/Akt/NF-κB [48,49], and MAPK [38]. NF-κB plays a very important role, along with IL-10, in diabetic complications, for NF-κB is also associated with AGE-RAGE signaling.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

Bao²,

Men

et al. 2019

Exp Clin Endocrinol Diabetes

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Demyelination resulting from Schwann cell injury is a main pathological feature of diabetic neuropathy, and a key contributor to this process may be inflammation due to advanced glycation end products (AGEs). Therefore, protection by anti-inflammation agents is anticipated. In this study, we showed that interleukin-10 (IL-10), an anti-inflammatory cytokine, inhibits apoptosis of Schwann cells induced by AGEs in vitro. We isolated and cultured Schwann cells from rat sciatic nerves. As detected by flow cytometry, apoptosis of Schwann cells markedly increased following incubation with AGEs for 48 h. However, pretreatment with IL-10 inhibited AGE-induced apoptosis. The effect of IL-10 on NF-κB, which is a very important regulator of inflammation, was also evaluated, and results showed high levels of phospho-NF-κB and nuclear localization of NF-κB in cells incubated with AGEs but low levels of phospho-NF-κB and cytoplasmic localization in the cells incubated with IL-10, indicating the activation of NF-κB by AGEs and inhibition of NF-κB by IL-10. Moreover, incubating Schwann cells with an NF-κB inhibitor (caffeic acid phenethyl ester) for 30 min before adding AGEs mimicked IL-10, lowering the amount of reactive oxygen species and activity of caspase-3 and also decreasing apoptosis in Schwann cells. These results indicate that IL-10 may protect Schwann cells against AGE-induced apoptosis by attenuating oxidative stress via the inhibition of activation of NF-κB.

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Interleukin 10 protects primary melanocyte by activation of Stat-3 and PI3K/Akt/NF-κB signaling pathways

Cited by 29 publications

References 60 publications

Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

M2 Macrophages Enhance the Cementoblastic Differentiation of Periodontal Ligament Stem Cells via the Akt and JNK Pathways

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

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Interleukin 10 protects primary melanocyte by activation of Stat-3 and PI3K/Akt/NF-κB signaling pathways

Cited by 29 publications

References 60 publications

Geniposide prevents H2 O2 -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Geniposide prevents H2 O2 -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

M2 Macrophages Enhance the Cementoblastic Differentiation of Periodontal Ligament Stem Cells via the Akt and JNK Pathways

Interleukin-10 Protects Schwann Cells against Advanced Glycation End Products-Induced Apoptosis via NF-κB Suppression

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Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway

Geniposide prevents H₂ O₂ -induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway