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Article ; Online: Gasdermin E promotes translocation of p65 and c-jun into nucleus in keratinocytes for progression of psoriatic skin inflammation.

Long, Fangyuan / Wei, Xuecui / Chen, Yujie / Li, Min / Lian, Ni / Yu, Shanshan / Chen, Sihan / Yang, Yong / Gu, Heng / Chen, Xu

Cell death & disease

2024 Volume 15, Issue 3, Page(s) 180

Abstract: Gasdermin E (GSDME) has recently been identified as a critical executioner to mediate pyroptosis. While epidermal keratinocytes can initiate GSDME-mediated pyroptosis, the role of keratinocyte GSDME in psoriatic dermatitis remains poorly characterized. ... ...

Abstract	Gasdermin E (GSDME) has recently been identified as a critical executioner to mediate pyroptosis. While epidermal keratinocytes can initiate GSDME-mediated pyroptosis, the role of keratinocyte GSDME in psoriatic dermatitis remains poorly characterized. Through analysis of GEO datasets, we found elevated GSDME levels in psoriatic lesional skin. Additionally, GSDME levels correlated with both psoriasis severity and response to biologics treatments. Single-cell RNA sequencing (scRNA-seq) from a GEO dataset revealed GSDME upregulation in keratinocytes of psoriasis patients. In the imiquimod (IMQ)-induced psoriasis-like dermatitis mouse model, both full-length and cleaved forms of caspase-3 and GSDME were elevated in the epidermis. Abnormal proliferation and differentiation of keratinocytes and dermatitis were attenuated in Gsdme
MeSH term(s)	Animals ; Humans ; Mice ; Dermatitis/metabolism ; Dermatitis/pathology ; Gasdermins/metabolism ; Imiquimod/adverse effects ; Inflammation/pathology ; Keratinocytes/pathology ; Psoriasis/metabolism ; Psoriasis/pathology ; Transcription Factor RelA/metabolism ; Proto-Oncogene Proteins c-jun/metabolism
Chemical Substances	Gasdermins ; Imiquimod (P1QW714R7M) ; GSDME protein, human ; Gsdme protein, mouse ; Transcription Factor RelA ; Proto-Oncogene Proteins c-jun
Language	English
Publishing date	2024-03-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-024-06545-5
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Article ; Online: https://elsevier.proofcentral.com/en-us/landing-page.html?token=baf280639f2773e07701834b1c13daInhibition of spermatogenesis by hypoxia is mediated by V-ATPase via the JNK/c-Jun pathway in mice.

Yin, Jun / He, Wenjuan / Zhang, Mengjie / He, Wei / Zhang, Gang / Ni, Bing

Reproductive biology

2023 Volume 23, Issue 2, Page(s) 100761

Abstract: Spermatocyte apoptosis is the primary cause of a poor outcome after hypoxia-triggered spermatogenesis reduction (HSR). Vacuolar ... ...

Abstract	Spermatocyte apoptosis is the primary cause of a poor outcome after hypoxia-triggered spermatogenesis reduction (HSR). Vacuolar H
MeSH term(s)	Male ; Mice ; Animals ; Signal Transduction ; Adenosine Triphosphatases/pharmacology ; Spermatogenesis ; MAP Kinase Signaling System ; Apoptosis ; Hypoxia
Chemical Substances	Adenosine Triphosphatases (EC 3.6.1.-)
Language	English
Publishing date	2023-04-04
Publishing country	Poland
Document type	Journal Article
ZDB-ID	2189316-0
ISSN	2300-732X ; 1642-431X
ISSN (online)	2300-732X
ISSN	1642-431X
DOI	10.1016/j.repbio.2023.100761
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Zs.A 6095: Show issues

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Article ; Online: JNK/c-Jun pathway activation is essential for HBx-induced IL-35 elevation to promote persistent HBV infection.

Li, Xuefen / Zhu, Qiaoyun / Ye, Bo / Zhu, Chunxia / Dong, Yuejiao / Ni, Qin

Journal of clinical laboratory analysis

2023 Volume 37, Issue 5, Page(s) e24860

Abstract: ... Jun pathway was analyzed and chromatin immunoprecipitation followed by sequencing and luciferase ... reporter assays were performed to determine whether c-Jun could regulate IL-35 transcription.: Results ... The relevant pathway mechanism showed that the expression of JNK and c-Jun genes was significantly higher ...

Abstract	Background: Immunoregulation plays pivotal roles during chronic hepatitis B virus (HBV) infection. Studies have shown that Interleukin (IL)-35 is an important molecule associated with inadequate immune response against HBV. However, the mechanisms involved in the up-regulation of IL-35 expression during persistent HBV infection remain unknown. Methods: In this study, we constructed a plasmid expressing the HBV X protein (pCMV-HBx) to evaluate the relationship between HBx and IL-35. Activation of the JNK/c-Jun pathway was analyzed and chromatin immunoprecipitation followed by sequencing and luciferase reporter assays were performed to determine whether c-Jun could regulate IL-35 transcription. Results: HBx can significantly activate IL-35 promoter in both LO2 and HepG2 cells compared to the control plasmid (pCMV-Tag2) using the dual-luciferase assay. Whereas other viral proteins, such as S, preS1, the core protein, had no significant effect on IL-35 expression. Similarly, WB and qRT-PCR also showed that HBx can significantly promote IL-35 expression at protein and mRNA levels in the aforementioned cells. The relevant pathway mechanism showed that the expression of JNK and c-Jun genes was significantly higher in transfected cells carrying pCMV-HBx than in the pCMV-Tag2-transfected and -untransfected cells. WB analysis revealed that phosphorylated JNK and c-Jun were overexpressed after HBx action. Conversely, the addition of the JNK/c-Jun signaling pathway inhibitor could significantly suppress HBx-induced IL-35 expression in a dose-dependent manner. Conclusions: A novel molecular mechanism of HBV-induced IL-35 expression was revealed, which involves JNK/c-Jun signaling in up-regulating IL-35 expression via HBx, resulting in transactivation of the IL-35 subunit EBI3 and p35 promoter.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/genetics ; Hepatitis B/genetics ; Hepatitis B virus/physiology ; Hepatitis B, Chronic ; Interleukins/genetics ; Liver Neoplasms/genetics ; Luciferases
Chemical Substances	Interleukins ; Luciferases (EC 1.13.12.-) ; interleukin-35, human
Language	English
Publishing date	2023-03-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	645095-7
ISSN	1098-2825 ; 0887-8013
ISSN (online)	1098-2825
ISSN	0887-8013
DOI	10.1002/jcla.24860
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Zs.A 2471: Show issues

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Article ; Online: Jun-mediated lncRNA-IMS promotes the meiosis of chicken spermatogonial stem cells via gga-miR-31-5p/stra8.

Wang, Yingjie / Zhang, Lei / Kong, Ruihong / Hu, Cai / Zhao, Zongyi / Wu, Yuhui / Zuo, Qisheng / Li, Bichun / Zhang, Ya-Ni

Molecular reproduction and development

2023 Volume 90, Issue 5, Page(s) 275–286

Abstract: ... of transcription factors, deletion/overexpression of binding sites, knockdown/overexpression of Jun, and dual-luciferase ... reporter analysis confirmed that Jun positively activated transcription of lncRNA-IMS. Our findings further ...

Abstract	Meiosis, a key step in spermatogenesis, is affected by many factors. Current studies have shown that long noncoding RNAs (lncRNAs) are potential factors regulating meiosis, and their regulatory mechanisms have received much attention. However, little research has been done on its regulatory mechanism in the spermatogenesis of roosters. Here, we found that lncRNA involved in meiosis and spermatogenesis (lncRNA-IMS) was involved in the regulation of Stra8 by gga-miR-31-5p and hindered the inhibition of Stra8 by gga-miR-31-5p. The acquisition and loss of function experiments demonstrated that lncRNA-IMS was involved in meiosis and spermatogenesis. In addition, we predicted and determined the core promoter region of lncRNA-IMS. Prediction of transcription factors, deletion/overexpression of binding sites, knockdown/overexpression of Jun, and dual-luciferase reporter analysis confirmed that Jun positively activated transcription of lncRNA-IMS. Our findings further enrich the TF-lncRNA-miRNA-mRNA regulatory network during male meiosis and provide new ideas for studying the molecular mechanism of meiosis and spermatogenesis in chicken spermatogonial stem cells.
MeSH term(s)	Animals ; Male ; Adult Germline Stem Cells/metabolism ; Chickens/genetics ; Chickens/metabolism ; Meiosis ; MicroRNAs/genetics ; MicroRNAs/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Avian Proteins/metabolism
Chemical Substances	MicroRNAs ; RNA, Long Noncoding ; Avian Proteins
Language	English
Publishing date	2023-03-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	20321-x
ISSN	1098-2795 ; 1040-452X
ISSN (online)	1098-2795
ISSN	1040-452X
DOI	10.1002/mrd.23682
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Zs.A 2759: Show issues

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Article ; Online: Etanercept Reduces Neuron Injury and Neuroinflammation via Inactivating c-Jun N-terminal Kinase and Nuclear Factor-κB Pathways in Alzheimer's Disease: An In Vitro and In Vivo Investigation.

Li, Yuanlong / Fan, Hua / Ni, Ming / Zhang, Wei / Fang, Fengqin / Sun, Jun / Lyu, Pin / Ma, Peizhi

Neuroscience

2021 Volume 484, Page(s) 140–150

Abstract: ... Moreover, ETN repressed the activation of c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB ...

Abstract	Inflammation contributes to amyloid beta (Aβ) aggregation and neuron loss in Alzheimer's disease (AD). Meanwhile, tumor necrosis factor-α (TNF-α) inhibitors present strong effect on suppressing inflammation. Thus, this study aimed to investigated the effect and molecular mechanism of etanercept (ETN) (a commonly used TNF-α inhibitor) on neuron injury and neuroinflammation in AD. AD cellular model was constructed by co-culture of primary embryonic neuron cells and microglial cells, followed by Aβ treatment. Subsequently, ETN was used to treat AD cellular model. Besides, APPswe/PS1M146V/tauP301L transgenic (AD) mice were respectively treated with saline or ETN by intravenous injection once per 3 days for 10 times. In vitro data revealed that cell viability and neurite outgrowth were increased, but apoptosis and levels of pro-inflammatory cytokines (including TNF-α, interleukin-1β, Interleukin-6 and C-C motif chemokine ligand 2 (CCL2)) were decreased by ETN treatment in AD cellular model. In vivo experiments found that ETN treatment improved spatial, long-term memory (reflected by Morrison water maze) and working memory (reflected by Y maze) in AD mice. Besides, ETN treatment reduced neuron injury (reflected by Hematoxylin-Eosin (HE) and terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) assays) and levels of pro-inflammatory cytokines (including TNF-α, interleukin-1β, Interleukin-6 and CCL2) in AD mice. Moreover, ETN repressed the activation of c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB) pathways in AD both in vitro and in vivo. In conclusion, ETN exerts neuroprotective function via inactivating JNK and NF-κB pathways in AD, indicating the potential of ETN for improving AD management.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Etanercept/metabolism ; Etanercept/pharmacology ; Etanercept/therapeutic use ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mice ; NF-kappa B/metabolism ; Neuroinflammatory Diseases ; Neurons/metabolism
Chemical Substances	Amyloid beta-Peptides ; NF-kappa B ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Etanercept (OP401G7OJC)
Language	English
Publishing date	2021-12-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	196739-3
ISSN	1873-7544 ; 0306-4522
ISSN (online)	1873-7544
ISSN	0306-4522
DOI	10.1016/j.neuroscience.2021.11.001
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Zs.A 1215: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
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Article: Erratum: lncRNA RP11-147L13.8 suppresses metastasis and chemo-resistance by modulating the phosphorylation of c-Jun protein in GBC.

Zheng, Bohao / Wang, Jiwen / Fan, Kun / Sun, Wentao / Wan, Wenze / Gao, Zhihui / Ni, Xiaojian / Zhang, Dexiang / Ni, Xiaoling / Suo, Tao / Liu, Han / Liu, Houbao / Shen, Sheng

Molecular therapy oncolytics

2021 Volume 23, Page(s) 531–533

Abstract: This corrects the article DOI: 10.1016/j.omto.2021.08.016.]. ...

Abstract	[This corrects the article DOI: 10.1016/j.omto.2021.08.016.].
Language	English
Publishing date	2021-11-29
Publishing country	United States
Document type	Published Erratum
ISSN	2372-7705
ISSN	2372-7705
DOI	10.1016/j.omto.2021.11.015
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Article ; Online: Withdrawal: c-Jun regulates shear- and injury-inducible Egr-1 expression, vein graft stenosis after autologous end-to-side transplantation in rabbits, and intimal hyperplasia in human saphenous veins.

Ni, Jun / Waldman, Alla / Khachigian, Levon M

The Journal of biological chemistry

2018 Volume 293, Issue 52, Page(s) 20307

Language	English
Publishing date	2018-12-28
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.W118.007069
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Uc I Zs.108: Show issues

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Article ; Online: Proanthocyanidins attenuate breast cancer-induced bone metastasis by inhibiting Irf-3/c-jun activation.

Guo, Shuangfei / Zhu, Wei / Yin, Ziqing / Xiao, Ding / Zhang, Qiang / Liu, Tang / Ni, Jiangdong / Ouyang, Zhengxiao / Xie, Hongming

Anti-cancer drugs

2019 Volume 30, Issue 10, Page(s) 998–1005

Abstract: We have previously demonstrated the pivotal role of Jnk-mediated Irf-3/c-Jun in regulating nuclear ...

Abstract	We have previously demonstrated the pivotal role of Jnk-mediated Irf-3/c-Jun in regulating nuclear factor kappa-Β ligand (RANKL)-induced osteoclastogenesis. Here, we demonstrated that proanthocyanidins (PACs) target Irf-3 to alleviate breast cancer-induced activation of osteoclasts. We also found that PACs induced apoptosis of osteoclast precursors by upregulating the ratio of bax/bcl-2 and activating caspase-3 activity. Such bone protective effect also could be observed in a bone metastasis model of breast cancer. These findings provided a novel therapeutic intervention targeting abnormal bone metabolism to alleviate bone metastasis of breast cancer.
MeSH term(s)	Animals ; Apoptosis/drug effects ; Bone Neoplasms/drug therapy ; Bone Neoplasms/metabolism ; Bone Neoplasms/secondary ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Culture Media, Conditioned/pharmacology ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Interferon Regulatory Factor-3/genetics ; Interferon Regulatory Factor-3/metabolism ; Male ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Osteoclasts/drug effects ; Osteoclasts/metabolism ; Osteogenesis/drug effects ; Osteogenesis/physiology ; Proanthocyanidins/pharmacology ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism
Chemical Substances	Culture Media, Conditioned ; Interferon Regulatory Factor-3 ; Irf3 protein, mouse ; Proanthocyanidins ; Proto-Oncogene Proteins c-jun
Language	English
Publishing date	2019-10-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1065301-6
ISSN	1473-5741 ; 0959-4973
ISSN (online)	1473-5741
ISSN	0959-4973
DOI	10.1097/CAD.0000000000000852
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Zs.A 3125: Show issues

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Article: Activated STING enhances Tregs infiltration in the HPV-related carcinogenesis of tongue squamous cells via the c-jun/CCL22 signal.

Liang, Ding / Xiao-Feng, Huang / Guan-Jun, Dong / Er-Ling, Hu / Sheng, Chen / Ting-Ting, Wang / Qin-Gang, Hu / Yan-Hong, Ni / Ya-Yi, Hou

Biochimica et biophysica acta

2015 Volume 1852, Issue 11, Page(s) 2494–2503

Abstract: ... U0126) and the silencing of c-jun significantly suppressed CCL22 induction and the recruitment of Tregs ...

Abstract	The negative role of the activated stimulator of IFN genes (STING) has been uncovered in autoinflammatory disease and cancer. However, the role of STING in virus-related carcinogenesis is not well known. Herein, HPV(+) tongue squamous cell carcinoma (TSCC) (n=25) and HPV(-) TSCC samples (n=25) were randomly collected and were verified by in situ hybridization (ISH) and p16 immunohistochemistry (IHC) to assess the expression and activated status of STING through IHC. The results showed that the expression of STING was up-regulated during the development of TSCC. Interestingly, although the expression of STING showed no difference between HPV(+/-) TSCC samples, the activated status of STING with dark staining around the nucleus was observed in HPV(+) TSCC samples. The role of activated STING was analyzed in three cell lines by siRNA and indicated that activated STING had no impact on cell viability or apoptosis but promoted the induction of several immunosuppressive cytokines, e.g., IL-10, IDO and CCL22, which facilitated the infiltration of regulatory T cells (Tregs). Moreover, increased infiltration of Foxp3(+) Tregs along with increased expression of CCL22 was confirmed in HPV(+) TSCC samples. An inhibitor of the MAPK/AP-1 pathway (U0126) and the silencing of c-jun significantly suppressed CCL22 induction and the recruitment of Tregs by activated STING. Furthermore, down-regulated miR-27 was verified in independent fresh TSCC samples (n=50) and eight cell lines, which enhanced STING activation and led to increased CCL22 expression for Tregs recruitment in the TSCC microenvironment. Therefore, our findings provided distinct insight into the side effects of activated STING in HPV-related carcinogenesis.
Language	English
Publishing date	2015-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2015.08.011
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Uc I Zs.247: Show issues

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Article: Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation.

Li, Yuan / Ni, Hong-Min / Jaeschke, Hartmut / Ding, Wen-Xing

Liver research

2019 Volume 3, Issue 1, Page(s) 65–74

Abstract: ... decreased APAP-induced c-Jun N-terminal kinase activation without affecting the metabolic activation of APAP ...

Abstract	Background and aim: Overdose of acetaminophen (APAP) leads to liver injury, which is one of the most common causes of liver failure in the United States. We previously demonstrated that pharmacological activation of autophagy protects against APAP-induced liver injury in mice via removal of damaged mitochondria and APAP-adducts (APAP-ADs). Using an image-based high-throughput screening for autophagy modulators, we recently identified that chlorpromazine (CPZ), a dopamine inhibitor used for anti-schizophrenia, is a potent autophagy inducer Methods: Wild type C57BL/6J mice were injected with APAP to induce liver injury. CPZ was administrated either at the same time with APAP (co-treatment) or 2 h later after APAP administration (post-treatment). Hemotoxyline and eosin (H&E) staining of liver histology, terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) staining of necrotic cell death as well as serum levels of alanine aminotransferase (ALT) were used to monitor liver injury. Results: We found that CPZ markedly protected against APAP-induced liver injury as demonstrated by decreased serum levels of ALT, liver necrotic areas as well as TUNEL-positive cells in mice that were either co-treated or post-treated with CPZ. Mechanistically, we observed that CPZ increased the number of autolysosomes and decreased APAP-induced c-Jun N-terminal kinase activation without affecting the metabolic activation of APAP. Pharmacological inhibition of autophagy by chloroquine partially weakened the protective effects of CPZ against APAP-induced liver injury. Conclusions: Our results indicate that CPZ ameliorates APAP-induced liver injury partially via activating hepatic autophagy and inhibiting JNK activation.
Language	English
Publishing date	2019-02-16
Publishing country	China
Document type	Journal Article
ZDB-ID	2899927-7
ISSN	2542-5684 ; 2096-2878
ISSN (online)	2542-5684
ISSN	2096-2878
DOI	10.1016/j.livres.2019.01.004
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