8,170 research outputs found
sj-pdf-1-iji-10.1177_20587384221076472 – Supplemental Material for ETS variant transcription factor 6 enhances oxidized low-density lipoprotein-induced inflammatory response in atherosclerotic macrophages via activating NF-κB signaling
No full textSupplemental Material, sj-pdf-1-iji-10.1177_20587384221076472 for ETS variant transcription factor 6 enhances oxidized low-density lipoprotein-induced inflammatory response in atherosclerotic macrophages via activating NF-κB signaling by Xiaofang Xiong, Zheng Yan, Wei Jiang and Xuejun Jiang in International Journal of Immunopathology and Pharmacology</p
sj-docx-1-jom-10.1177_01492063231195590 - Supplemental material for Government Corruption and Corporate Social Responsibility: An Instrumental Perspective
No full textSupplemental material, sj-docx-1-jom-10.1177_01492063231195590 for Government Corruption and Corporate Social Responsibility: An Instrumental Perspective by Cuili Qian, David H. Weng, Louise Yi Lu, and Xuejun Jiang in Journal of Management</p
Vrsanskysajda Jiang, Xing & Li, 2023, nom. nov.
No full textGenus Vrsanskysajda nom. nov. Sajda Vršanský, 2021: 27 (Blattaria: Corydiidae: Holocompsinae). Preoccupied by Sajda Dworakowska, 1981: 244 (Homoptera: Cicadellidae: Typhlocybinae). Type species: Vrsanskysajda equatorialis (Vršanský in Vršanský et al. 2021) comb. nov. Etymology. The replacement name for the genus is derived from the name of Peter Vršanský, the author of the genus Sajda. Gender: feminine. Distribution. Brezina, Algeria.Published as part of Jiang, Lina, Xing, Jichun & Li, Yujian, 2023, New replacement name for the genus Sajda Vršanský, 2021 (Blattaria: Corydiidae: Holocompsinae), pp. 343-344 in Zootaxa 5270 (2) on page 343, DOI: 10.11646/zootaxa.5270.2.10, http://zenodo.org/record/784970
Inventing A Wolfish China - On Jiang Rong'S Wolf Totem
No full textThe Wolf Totem by Jiang Rong has won great success both in and out of China. Jiang Rong criticizes Han Chinese and embraces the culture of the northern ethnic minority group, the Mongols, because of its stronger sense of competition and domination. In the epilogue of this novel, Jiang argues that the wolf totem was the most ancient totem for all Chinese people and retells Chinese history using this framework. This paper explores the background of the novel and its author, as well as supporting materials the author uses in his proposal concerning the wolf totem, and suggests that the wolf totem is a purely ideological invention of Jiang Rong. This invention reflects Jiang's own philosophy and caters to the cultural needs of modern Chinese people. In inventing the wolf totem, the author uses historical documents, archeological findings, as well as a far-fetched bodily metaphor. However, none of this evidence is validated by scholarly research
Antiferroptotic approach for the treatment of diabetes-induced liver pathology: the effects of ethyl pyruvate
No full textWe showed recently that ferroptosis contributes to liver pathological changes in diabetes. So, targeting of ferroptosis-related pathways could be novel approach for treatment of diabetes- related liver diseases. Ethyl pyruvate (EP) showed antidiabetic action due to anti-oxidative, - inflammatory and -apoptotic properties. We aimed to examine its potential antiferroptotic action in diabetes-related liver pathology.
Male Wistar rats were divided into four groups: control; diabetic (STZ, 65 mg/kg); diabetic pre- treated with EP (80 mg/kg/day, starting one week before STZ and continuing following 4 weeks) and diabetic treated with EP, starting with STZ and lasted 4 weeks.
Both modes of EP treatment induced attenuation of ferroptotic events in the liver of diabetic rats: accumulation of lipid peroxides (4-HNE), disturbances in iron metabolism (decreased FTH and increased TFR expression), decrease in expression level/activity of ferroptosis- related antioxidative-defense molecules (GPX4, GCL, GSS, Nrf2, HO-1), and activation of ferroptosis-related pro-inflammatory events (HMGB1 nucleus-to-cytosol and NF-kB cytosol-to- nucleus translocation). Those changes reflected on the improvement of diabetes-related morphological alterations such as liver fibrosis and binucleation.
Overall, EP interferes with ferroptosis signaling pathways and exerts antiferroptotic activity in the liver in diabetic state. This highlighting the significance of ferroptosis targeting in diabetes- related liver diseases and novel mechanisms/targets of EP beneficial actions.Conrad M, Jiang X, Fedorova M, Friedmann Angeli JP, editors. EMBO Workshop: Ferroptosis: When metabolism meets cell death; 2023 Apr 23-27; Seeon, Germany. EMBO; 2023. p. 40
Sulforaphane prevents diabetes-induced liver ferroptosis through activation of Nrf2 signaling axis
No full textRecently, we characterized the ferroptotic phenotype of the liver of diabetic mice and revealed the inactivation of Nrf2 as an integral part of diabetes-induced liver ferroptosis. We aim here to examine does sulforaphane, an Nrf2 activator and antioxidant, prevent diabetes-induced liver ferroptosis and the mechanisms involved.
For that purpose, male C57BL/6 mice were divided into three groups: control, diabetic (streptozotocin-treated, 40 mg/kg/5 consecutive days), diabetic+sulforaphane treated (2.5 mg/kg, from day 1-42).
Results showed that diabetes-induced inactivation of Nrf2 and decreased expression of its downstream antiferroptotic parameters crucial for antioxidative defense (HO-1, catalase, SOD), iron metabolism (ferroportin, ferritin), glutathione synthesis (xCT, GCLC, CTH, CBS) and recycling (GR) were reversed/increased by sulforaphane treatment. Antiferroptotic effect of sulforaphane in the diabetic liver was further evidenced through the increased level of glutathione, decreased accumulation of liable iron and lipid peroxides (4-HNE) and decreased tissue damage (fibrosis and infiltration). Finally, diabetes-induced increase in serum glucose, ALT, AST and triglyceride level was significantly reduced by sulforaphane.
These findings revealed for the first time that sulforaphane prevents in vivo diabetes-induced liver ferroptosis through activation of Nrf2 signaling axis. This suggests sulforaphane as a promising therapeutic tool for preventing ferroptosis at least in diabetes and diabetes-related pathologies.Conrad M, Jiang X, Fedorova M, Friedmann Angeli JP, editors. EMBO Workshop: Ferroptosis: When metabolism meets cell death; 2023 Apr 23-27; Seeon, Germany. EMBO; 2023. p. 39
Interviews with Yang Jiang
No full textYang Jiang was born, under her real name of Yang Jikang, in 1911. She is the author of a novel, several plays, and a large number of sanwen. Her first writing dates back to 1933, and her latest work, Women sa (We Three), in which she recalls family memories, appeared in July 2003, and has been highly successful, with 180,000 copies sold within two months. However, for thirty years, from 1949 to 1981, for obvious reasons, Yang Jiang preferred to devote herself entirely to teaching, research—she is also an expert on Chinese and foreign literature—, and translation: she is the translator, most notably, of the Chinese version of Don Quixote. She is now devoting herself to the publication of the work of her husband, the scholar Qian Zhongshu (1910-1998). In France she is best known for her narratives of the Cultural Revolution, published by Christian Bourgois.The two interviews that follow were carried out in 2005. Yang Jiang gave written answers to the questions I had sent her, which explains the slightly abrupt nature of our exchanges, given that it was not possible for me, by the nature of the interviews, to respond spontaneously to her words. If we seem to jump from one subject to another, it is because I had asked her to clarify certain details that I planned to use in my research into her work (« La Figure de l’intellectuel chez Yang Jiang » [“The Intellectual in The Work of Yang Jiang”], which became my doctoral thesis in Chinese Studies, under the direction of Isabelle Rabut, Inalco, Paris, December 2005, 404 pp.). Yet, to me, these words of Yang Jiang are of interest just as they are, since she uses words so sparingly and generally refuses to do interviews. In any case, and I am grateful to her for this, she only allowed these words to be published precisely because she had written them herself
CD31 Expression Determines Redox Status and Chemoresistance in Human Angiosarcomas
No full textAbstract
Purpose: Angiosarcomas are soft tissue sarcomas with endothelial differentiation and vasoformative capacity. Most angiosarcomas show strong constitutive expression of the endothelial adhesion receptor CD31/PECAM-1 pointing to an important role of this molecule. However, the biological function of CD31 in angiosarcomas is unknown.
Experimental Design: The expression levels of CD31 in angiosarcoma cells and its effects on cell viability, colony formation, and chemoresistance were evaluated in human angiosarcoma clinical samples and in cell lines through isolation of CD31high and CD31low cell subsets. The redox-regulatory CD31 function linked to YAP signaling was determined using a CD31-blocking antibody and siRNA approach and was further validated in CD31-knockout endothelial cells.
Results: We found that most angiosarcomas contain a small CD31low cell population. CD31low cells had lost part of their endothelial properties and were more tumorigenic and chemoresistant than CD31high cells due to more efficient reactive oxygen species (ROS) detoxification. Active downregulation of CD31 resulted in loss of endothelial tube formation, nuclear accumulation of YAP, and YAP-dependent induction of antioxidative enzymes. Addition of pazopanib, a known enhancer of proteasomal YAP degradation resensitized CD31low cells for doxorubicin resulting in growth suppression and induction of apoptosis.
Conclusions: Human angiosarcomas contain a small aggressive CD31low population that have lost part of their endothelial differentiation programs and are more resistant against oxidative stress and DNA damage due to intensified YAP signaling. Our finding that the addition of YAP inhibitors can resensitize CD31low cells toward doxorubicin may aid in the rational development of novel combination therapies to treat angiosarcomas. Clin Cancer Res; 24(2); 460–73. ©2017 AACR.</jats:p
Functional Interaction Between Pten And Nedd4 In Igf Signaling
No full textPTEN is a master regulator of multiple cellular processes and a potent tumor suppressor. Its biological function is mainly attributed to its lipid phosphatase activity that negatively regulates the PI3K-AKT signaling pathway. A fundamental and highly debated question remains whether PTEN can also function as a protein phosphatase in cells. This study demonstrates that PTEN is a protein tyrosine phosphatase that selectively dephosphorylates insulin receptor substrate-1 (IRS1), a mediator for transduction of insulin and IGF1 signaling. IGF signaling is defective in cells lacking NEDD4, a PTEN ubiquitin ligase, whereas AKT activation triggered by EGF or serum is unimpaired in these cells. Surprisingly, the defect of IGF signaling caused by NEDD4 deletion, including the of phosphorylation of IRS1, upstream of PI3K, can be rescued by PTEN ablation, suggesting PTEN may be a protein phosphatase for IRS1. The nature of PTEN as an IRS1 phosphatase is demonstrated by direct biochemical analysis and confirmed by cellular reconstitution. Further, we find that NEDD4 supports insulin-mediated glucose metabolism, and is required for the proliferation of IGF1 receptor (IGF1R)-dependent but not EGFR-dependent tumor cells. Taken together, PTEN is a protein phosphatase for IRS1, and its antagonism by the ubiquitin ligase NEDD4 promotes IGF/insulin signaling. Finally, we also identified a novel form of PTEN, which is a translational variant, termed UPP, and characterized it using biochemical and cellular studies. UPP is a fast turnover subpopulation of PTEN, and demonstrates a distinctive subcellular localization from PTEN. Co-localization imaging studies indicated that UPP is involved in endocytosis membrane trafficking and adherens junctions. UPP still functions as a lipid phosphatase for PIP3, antagonizing PI3K signaling. Furthermore, UPP was found to be a better binding partner for the PTEN protein substrate, IRS1, in cells
Co-Ordinated Regulation Of Autophagy By Mtorc1 And Protein Phosphatase 2A
No full textAutophagy is a cellular catabolic process critical for cell viability and homeostasis. As a membrane trafficking pathway, it is closely related to endocytosis and shares many points of convergence with endocytosis. In the first part of this dissertation, I find that although the two pathways are closely related, autophagosome fusion with lysosomes is governed by a distinct molecular mechanism from endosomal fusion with lysosomes. In recent years, the discovery of autophagy-essential-genes has accelerated research into the molecular mechanisms governing autophagy. For example, inhibition of mammalian target of rapamycin (mTOR) complex-1 (mTORC1) activates autophagy by relieving its inhibitory effects on autophagy essential gene, ULK1- a mTORC1 substrate whose dephosphorylation is required for autophagy induction. Puzzlingly, I observe that amino acid starvation triggers more rapid autophagy than pharmacological inhibition of mTORC1, although they both block mTORC1 activity with similar kinetics. Here I find that in addition to mTORC1 inactivation, starvation also causes a stimulation in phosphatase activity toward ULK1. In the second part of this dissertation, I identify the starvation-stimulated phosphatase for ULK1 as the PP2A-B55? complex and attempt to elucidate the mechanism of phosphatase stimulation during starvation. I find that treatment of cells with starvation but not mTORC1 inhibitors triggers dissociation of PP2A from its inhibitor Alpha4. Furthermore, pancreatic ductal adenocarcinoma cells (PDACs), whose growth depends on high basal autophagy, possess stronger basal phosphatase activity toward ULK1 and require ULK1 for sustained anchorage-independent growth. Taken together, these results suggest that concurrent mTORC1 inactivation and PP2A-B55? stimulation fuel ULK1-dependent autophagy
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