Search

Your search keyword '"He, Mindi"' showing total 166 results
Start Over Author "He, Mindi"
166 results on '"He, Mindi"'

2. Long-term cadmium exposure induces epithelial-mesenchymal transition in breast cancer cells by activating CYP1B1-mediated glutamine metabolic reprogramming in BT474 cells and MMTV-Erbb2 mice

Author

Li, Jingdian, Gao, Peng, Qin, Mingke, Wang, Junhua, Luo, Yan, Deng, Ping, Hao, Rongrong, Zhang, Lei, He, Mindi, Chen, Chunhai, Lu, Yonghui, Ma, Qinlong, Li, Min, Tan, Miduo, Wang, Liting, Yue, Yang, Wang, Hui, Tian, Li, Xie, Jia, Chen, Mengyan, Yu, Zhengping, Zhou, Zhou, and Pi, Huifeng

Published
2024
Full Text
View/download PDF

5. SIRT5‐Mediated Desuccinylation of RAB7A Protects Against Cadmium‐Induced Alzheimer's Disease‐Like Pathology by Restoring Autophagic Flux

Author

Deng, Ping, primary, Fan, Tengfei, additional, Gao, Peng, additional, Peng, Yongchun, additional, Li, Min, additional, Li, Jingdian, additional, Qin, Mingke, additional, Hao, Rongrong, additional, Wang, Liting, additional, Zhang, Lei, additional, Chen, Chunhai, additional, He, Mindi, additional, Lu, Yonghui, additional, Ma, Qinlong, additional, Luo, Yan, additional, Tian, Li, additional, Xie, Jia, additional, Chen, Mengyan, additional, Xu, Shangcheng, additional, Zhou, Zhou, additional, Yu, Zhengping, additional, and Pi, Huifeng, additional

Published
2024
Full Text
View/download PDF

11. Terahertz radiation exposure results in altered gene expression profile in mouse retina

Author

LU Yonghui, CHEN Chunhai, GAO Peng, MA Qinlong, HE Mindi, ZHANG Lei, and YU Zhengping

Subjects
terahertz, retina, waunds and injuries, rna-seq analysis, gene expression, Medicine (General), R5-920
Abstract

Objective To explore the global changes of gene expression profile in the retina after terahertz (THz) radiation exposure in order to reveal the signal pathways and key genes involved in the process of visual system damage. Methods Mouse eyes were exposed to THz radiation at an average power density of 80 mW for 2 min. Then the retinal tissues were harvested to extract total RNA for RNA-seq analysis. The differential expression genes (DEGs) and their functions were identified with a certain condition for Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Real-time PCR was used to further explore the time-dependent effects of THz exposure on the expression of the key genes related to retinal injury from DEGs. Results There were 625 up-regulated genes and 9 down-regulated genes screened out through the condition of P < 0.05 and |logFC|≥1. The GO analysis revealed that the DEGs were mainly composed of extracellular components as the complementary biological concept of cellular component (CC), mainly related to protein binding as the concept of molecular function (MF), and were associated with response to external stimulus and cell proliferation as the concept of biological process (BP). The KEGG analysis indicated that most DEGs were enriched in the PPAR, PI3K-Akt, and tumor- and calcium-related signaling pathways. Real-time PCR displayed that the expression levels of Krt12, Cfd, Wnt3a and Adipoq were up-regulated, while those of Krt12, Cfd, Wnt3a and Adipoq were up-regulated, while those of Foxe3, Serpine3, Lix1, Rpe65, Rgr and Arsi were down-regulated in the injured retinal tissues after THz irradiation exposure for 5 min and 24 h, and the changes were more significant after 5 minutes' than 24 hours' exposure. Conclusion THz radiation exposure causes abnormal expression of a large number of genes in retinal tissue, indicating the exposure may induce retinal injury.

Published
2020
Full Text
View/download PDF

12. NLRP3 inflammasome activation mediates terahertz exposure-induced skin aseptic inflammation in mice

Author

GAO Peng, LU Yonghui, MA Qinlong, LI Min, CHEN Chunhai, HE Mindi, and YU Zhengping

Subjects
terahertz, skin, inflammation, nlrp3 inflammasome, oxidative stress, Medicine (General), R5-920
Abstract

Objective To investigate the biological effects of terahertz (THz) exposure on the skin injury of mice, and explore the mechanism of the induced skin aseptic inflammation. Methods The hair-removed skin in the back of C57BL/6J mice were exposed to 0.22 THz irradiation, at a peak power density of 25, 80 and 160 mW/cm2, respectively and a duty factor of 1: 5, for 5 or 10 min. The release of inflammatory factors, oxidative stress and activation of NLR P3 inflammasome were detected after the exposure. Caspase-1 specific inhibitor Z-YVAD was employed to determine the role of the activation in the inflammation. Results Exposure to 160 mW/cm2 THz irradiation for 10 min induced oxidative stress, and the releases of PGE2, IL-1β and IL-6 in the skin (P < 0.05). And the 80 mW/cm2 and 160 mW/cm2 THz exposure activated the NLRP3 inflammasome in the skin, and the Caspase-1 inhibitor reduced the inflammatory factors induced by the THz irradiation (P < 0.05). Conclusion THz exposure induces oxidative stress and aseptic inflammation. Activation of NLRP3 inflammasome mediates the skin aseptic inflammation induced by THz irradiation, which might be associated with oxidative stress.

Published
2020
Full Text
View/download PDF

15. Chronic Cadmium Exposure Triggered Ferroptosis by Perturbing Steap3-Mediated Glutathione Redox Balance is Linked to the Altered Metabolomic Signatures in Humans

Author

Deng, Ping, primary, Li, Jingdian, additional, Lu, Yonghui, additional, Hao, Rongrong, additional, He, Mindi, additional, Li, Min, additional, Tan, Miduo, additional, Gao, Peng, additional, Wang, Liting, additional, Hong, Huihui, additional, Tao, Jiawen, additional, Lu, Muxue, additional, Chen, Chunhai, additional, Ma, Qinlong, additional, Yue, Yang, additional, Wang, Hui, additional, Tian, Li, additional, Xie, Jia, additional, Chen, Mengyan, additional, Luo, Yan, additional, Yu, Zhengping, additional, Zhou, Zhou, additional, and Pi, Huifeng, additional

Published
2023
Full Text
View/download PDF

21. 1,800 MHz Radiofrequency Electromagnetic Irradiation Impairs Neurite Outgrowth With a Decrease in Rap1-GTP in Primary Mouse Hippocampal Neurons and Neuro2a Cells

Author

Li, Yanqi, primary, Deng, Ping, additional, Chen, Chunhai, additional, Ma, Qinlong, additional, Pi, Huifeng, additional, He, Mindi, additional, Lu, Yonghui, additional, Gao, Peng, additional, Zhou, Chao, additional, He, Zhixin, additional, Zhang, Yanwen, additional, Yu, Zhengping, additional, and Zhang, Lei, additional

Published
2021
Full Text
View/download PDF

22. NAC antagonizes arsenic-induced neurotoxicity through TMEM179 by inhibiting oxidative stress in Oli-neu cells

Author

He, Zhixin, primary, Zhang, Yajing, additional, Zhang, Huijie, additional, Zhou, Chao, additional, Ma, Qinlong, additional, Deng, Ping, additional, Lu, Muxue, additional, Mou, Zhenlin, additional, Lin, Min, additional, Yang, Lingling, additional, Li, Yanqi, additional, Yue, Yang, additional, Pi, Huifeng, additional, Lu, Yonghui, additional, He, Mindi, additional, Zhang, Lei, additional, Chen, Chunhai, additional, Zhou, Zhou, additional, and Yu, Zhengping, additional

Published
2021
Full Text
View/download PDF

25. Long-term bisphenol A exposure exacerbates diet-induced prediabetes via TLR4-dependent hypothalamic inflammation

Author

Ma, Qinlong, primary, Deng, Ping, additional, Lin, Min, additional, Yang, Lingling, additional, Li, Le, additional, Guo, Lu, additional, Zhang, Lei, additional, He, Mindi, additional, Lu, Yonghui, additional, Pi, Huifeng, additional, Zhang, Yanwen, additional, Yu, Zhengping, additional, Chen, Chunhai, additional, and Zhou, Zhou, additional

Published
2021
Full Text
View/download PDF

27. KIF5A-dependent axonal transport deficiency disrupts autophagic flux in trimethyltin chloride-induced neurotoxicity

Author

Liu, Mengyu, primary, Pi, Huifeng, additional, Xi, Yu, additional, Wang, Liting, additional, Tian, Li, additional, Chen, Mengyan, additional, Xie, Jia, additional, Deng, Ping, additional, Zhang, Tao, additional, Zhou, Chao, additional, Liang, Yidan, additional, Zhang, Lei, additional, He, Mindi, additional, Lu, Yonghui, additional, Chen, Chunhai, additional, Yu, Zhengping, additional, and Zhou, Zhou, additional

Published
2020
Full Text
View/download PDF

28. Inhibition of SERPINA3N‐dependent neuroinflammation is essential for melatonin to ameliorate trimethyltin chloride–induced neurotoxicity

Author

Xi, Yu, primary, Liu, Mengyu, additional, Xu, Shuzhen, additional, Hong, Huihui, additional, Chen, Mengyan, additional, Tian, Li, additional, Xie, Jia, additional, Deng, Ping, additional, Zhou, Chao, additional, Zhang, Lei, additional, He, Mindi, additional, Chen, Chunhai, additional, Lu, Yonghui, additional, Reiter, Russel J., additional, Yu, Zhengping, additional, Pi, Huifeng, additional, and Zhou, Zhou, additional

Published
2019
Full Text
View/download PDF

29. KIF5A-dependent axonal transport deficiency disrupts autophagic flux in trimethyltin chloride-induced neurotoxicity.

Author

Liu, Mengyu, Pi, Huifeng, Xi, Yu, Wang, Liting, Tian, Li, Chen, Mengyan, Xie, Jia, Deng, Ping, Zhang, Tao, Zhou, Chao, Liang, Yidan, Zhang, Lei, He, Mindi, Lu, Yonghui, Chen, Chunhai, Yu, Zhengping, and Zhou, Zhou

Subjects
AUTOPHAGY, TRIMETHYLTIN, NEUROTOXICOLOGY, FUNGICIDES, BIOINFORMATICS, LYSOSOMES
Abstract

Trimethyltin chloride (TMT) is widely used as a constituent of fungicides and plastic stabilizers in the industrial and agricultural fields, and is generally acknowledged to have potent neurotoxicity, especially in the hippocampus; however, the mechanism of induction of neurotoxicity by TMT remains elusive. Herein, we exposed Neuro-2a cells to different concentrations of TMT (2, 4, and 8 μM) for 24 h. Proteomic analysis, coupled with bioinformatics analysis, revealed the important role of macroautophagy/autophagy-lysosome machinery in TMT-induced neurotoxicity. Further analysis indicated significant impairment of autophagic flux by TMT via suppressed lysosomal function, such as by inhibiting lysosomal proteolysis and changing the lysosomal pH, thereby contributing to defects in autophagic clearance and subsequently leading to nerve cell death. Mechanistically, molecular interaction networks of Ingenuity Pathway Analysis identified a downregulated molecule, KIF5A (kinesin family member 5A), as a key target in TMT-impaired autophagic flux. TMT decreased KIF5A protein expression, disrupted the interaction between KIF5A and lysosome, and impaired lysosomal axonal transport. Moreover, Kif5a overexpression restored axonal transport, increased lysosomal dysfunction, and antagonized TMT-induced neurotoxicity in vitro. Importantly, in TMT-administered mice with seizure symptoms and histomorphological injury in the hippocampus, TMT inhibited KIF5A expression in the hippocampus. Gene transfer of Kif5a enhanced autophagic clearance in the hippocampus and alleviated TMT-induced neurotoxicity in vivo. Our results are the first to demonstrate KIF5A-dependent axonal transport deficiency to cause autophagic flux impairment via disturbance of lysosomal function in TMT-induced neurotoxicity; manipulation of KIF5A may be a therapeutic approach for antagonizing TMT-induced neurotoxicity. Abbreviations: 3-MA: 3-methyladenine; AAV: adeno-associated virus; ACTB: actin beta; AGC: automatic gain control; ATG: autophagy-related; ATP6V0D1: ATPase H+ transporting lysosomal V0 subunit D1; ATP6V1E1: ATPase H+ transporting lysosomal V1 subunit E1; CA: cornu ammonis; CQ: chloroquine; CTSB: cathepsin B; CTSD: cathepsin D; DCTN1: dynactin subunit 1; DG: dentate gyrus; DYNLL1: dynein light chain LC8-type 1; FBS: fetal bovine serum; GABARAP: GABA type A receptor-associated protein; GABARAPL1: GABA type A receptor associated protein like 1; GABARAPL2: GABA type A receptor associated protein like 2; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IPA: Ingenuity Pathway Analysis; KEGG: Kyoto Encyclopedia of Genes and Genomes; KIF5A: kinesin family member 5A; LAMP: lysosomal-associated membrane protein; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; NBR1: NBR1 autophagy cargo receptor; OPTN: optineurin; PBS: phosphate-buffered saline; PFA: paraformaldehyde; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PRM: parallel reaction monitoring; siRNA: small interfering RNA; SQSTM1/p62: sequestosome 1; SYP: synaptophysin; TAX1BP1: Tax1 binding protein 1; TMT: trimethyltin chloride; TUB: tubulin. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

30. AKT inhibition-mediated dephosphorylation of TFE3 promotes overactive autophagy independent of MTORC1 in cadmium-exposed bone mesenchymal stem cells

Author

Pi, Huifeng, primary, Li, Min, additional, Zou, Lingyun, additional, Yang, Min, additional, Deng, Ping, additional, Fan, Tengfei, additional, Liu, Menyu, additional, Tian, Li, additional, Tu, Manyu, additional, Xie, Jia, additional, Chen, Mengyan, additional, Li, Huijuan, additional, Xi, Yu, additional, Zhang, Lei, additional, He, Mindi, additional, Lu, Yonghui, additional, Chen, Chunhai, additional, Zhang, Tao, additional, Wang, Zheng, additional, Yu, Zhengping, additional, Gao, Feng, additional, and Zhou, Zhou, additional

Published
2018
Full Text
View/download PDF

32. Melatonin alleviates cadmium-induced liver injury by inhibiting the TXNIP-NLRP3 inflammasome

Author

Cao, Zhengwang, primary, Fang, Yiliang, additional, Lu, Yonghui, additional, Tan, Dunxian, additional, Du, Changhong, additional, Li, Yuming, additional, Ma, Qinlong, additional, Yu, Junmei, additional, Chen, Mengyan, additional, Zhou, Chao, additional, Pei, Liping, additional, Zhang, Lei, additional, Ran, Haiying, additional, He, Mindi, additional, Yu, Zhengping, additional, and Zhou, Zhou, additional

Published
2017
Full Text
View/download PDF

33. Cross regulation between hypoxia-inducible transcription factor-1α (HIF-1α) and transforming growth factor (TGF)-ß1 mediates nickel oxide nanoparticles (NiONPs)-induced pulmonary fibrosis

Author

Qian, Fenghua, He, Mindi, Duan, Weixia, Mao, Lin, Li, Qian, Yu, Zhengping, Zhou, Zhou, and Zhang, Yong

Subjects
Original Article
Abstract

Numerous analyses including in vivo and in vitro experiments have demonstrated that inhalation exposure of NiONPs can result in pulmonary fibrosis. However, the potential mechanisms of this pathological process remain elusive. Here, we investigate the role of HIF-1α and TGF-ß1 in NiONPs-induced pulmonary fibrosis with a focus on the interplay of the above two proteins. In vivo, male Sprague&Dawley rats were exposed to NiONPs and pulmonary fibrosis was demonstrated using H&E staining and immunochemistry of αSMA. In vitro, NiONPs contributed to cell proliferation and increased expressions of collagen-1 and αSMA in human fetal lung fibroblasts. Both HIF-1α and TGF-ß1 were upregulated by NiONPs treatment. Inhibition of HIF-1α reduced TGF-ß1 expression and downregulation of TGF-ß1 reduced HIF-1α protein level. Mechanism investigation revealed that TGF-ß1 affects nuclear translocation activity of HIF-1α. Taken together, these finding provide evidence that HIF-1α and TGF-ß1 act in synergy to foster NiONPs-induced pulmonary fibrosis, and the cross talk between them is a pivotal mechanism of pulmonary fibrosis.

Published
2015

34. AKT inhibition-mediated dephosphorylation of TFE3 promotes overactive autophagy independent of MTORC1 in cadmium-exposed bone mesenchymal stem cells.

Author

Pi, Huifeng, Li, Min, Zou, Lingyun, Yang, Min, Deng, Ping, Fan, Tengfei, Liu, Menyu, Tian, Li, Tu, Manyu, Xie, Jia, Chen, Mengyan, Li, Huijuan, Xi, Yu, Zhang, Lei, He, Mindi, Lu, Yonghui, Chen, Chunhai, Zhang, Tao, Wang, Zheng, and Yu, Zhengping

Abstract

Cadmium (Cd) is a toxic metal that is widely found in numerous environmental matrices and induces serious adverse effects in various organs and tissues. Bone tissue seems to be a crucial target of Cd contamination. Macroautophagy/autophagy has been proposed to play a pivotal role in Cd-mediated bone toxicity. However, the mechanisms that underlie Cd-induced autophagy are not yet completely understood. We demonstrated that Cd treatment increased autophagic flux and inhibition of the autophagic process using Atg7 gene silencing blocked the Cd-induced mesenchymal stem cell death. Mechanistically, Cd activated nuclear translocation of TFE3 but not that of TFEB or MITF, which contributed to the expression of autophagy-related genes and lysosomal biogenesis. Specifically, Cd decreased expression of phospho-AKT (Ser473). The reduction in AKT activity led to dephosphorylation of cytosolic TFE3 at Ser565 and promoted TFE3 nuclear translocation independently of MTORC1. Notably, Cd treatment increased the activity of PPP3/calcineurin, and pharmacological inhibition of PPP3/calcineurin with FK506 suppressed AKT dephosphorylation and TFE3 activity. These results suggest that PPP3/calcineurin negatively regulates AKT phosphorylation and is involved in Cd-induced TFE3-dependent autophagy. Modulation of the PPP3/calcineurin-AKT-TFE3 autophagic-lysosomal machinery may offer novel therapeutic approaches for the treatment of Cd-induced bone damage. Abbreviations: ACTB: actin: beta; AKT: thymoma viral proto-oncogene; AMPK: AMP-activated protein kinase; ATG: autophagy related; Baf A1: bafilomycin A1; Cd: cadmium; FOXO3: forkhead box O3; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MITF: melanogenesis associated transcription factor; MSC: mesenchymal stem sell; MTORC1: mechanistic target of rapamycin kinase complex 1; RPS6KB1: ribosomal protein S6 kinase: polypeptide 1; SGK1: serum/glucocorticoid regulated kinase 1; SQSTM1/p62: sequestosome 1;TFE3: transcription factor E3; TFEB: transcription factor EB; TFEC: transcription factor EC [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

36. Melatonin antagonizes cadmium‐induced neurotoxicity by activating the transcription factor EB‐dependent autophagy–lysosome machinery in mouse neuroblastoma cells

Author

Li, Min, primary, Pi, Huifeng, additional, Yang, Zhiqi, additional, Reiter, Russel J., additional, Xu, Shangcheng, additional, Chen, Xiaowei, additional, Chen, Chunhai, additional, Zhang, Lei, additional, Yang, Min, additional, Li, Yuming, additional, Guo, Pan, additional, Li, Gaoming, additional, Tu, Manyu, additional, Tian, Li, additional, Xie, Jia, additional, He, Mindi, additional, Lu, Yonghui, additional, Zhong, Min, additional, Zhang, Yanwen, additional, Yu, Zhengping, additional, and Zhou, Zhou, additional

Published
2016
Full Text
View/download PDF

38. Extremely Low-Frequency Electromagnetic Fields Promote In Vitro Neuronal Differentiation and Neurite Outgrowth of Embryonic Neural Stem Cells via Up-Regulating TRPC1

Author

Ma, Qinlong, primary, Chen, Chunhai, additional, Deng, Ping, additional, Zhu, Gang, additional, Lin, Min, additional, Zhang, Lei, additional, Xu, Shangcheng, additional, He, Mindi, additional, Lu, Yonghui, additional, Duan, Weixia, additional, Pi, Huifeng, additional, Cao, Zhengwang, additional, Pei, Liping, additional, Li, Min, additional, Liu, Chuan, additional, Zhang, Yanwen, additional, Zhong, Min, additional, Zhou, Zhou, additional, and Yu, Zhengping, additional

Published
2016
Full Text
View/download PDF

39. SIRT3-SOD2-mROS-dependent autophagy in cadmium-induced hepatotoxicity and salvage by melatonin

Author

Pi, Huifeng, primary, Xu, Shangcheng, additional, Reiter, Russel J, additional, Guo, Pan, additional, Zhang, Lei, additional, Li, Yuming, additional, Li, Min, additional, Cao, Zhenwang, additional, Tian, Li, additional, Xie, Jia, additional, Zhang, Ruiqi, additional, He, Mindi, additional, Lu, Yonghui, additional, Liu, Chuan, additional, Duan, Weixia, additional, Yu, Zhengping, additional, and Zhou, Zhou, additional

Published
2015
Full Text
View/download PDF

42. Exposure to 1800 MHz radiofrequency radiation impairs neurite outgrowth of embryonic neural stem cells

Author

Chen, Chunhai, Ma, Qinlong, Liu, Chuan, Deng, Ping, Zhu, Gang, Zhang, Lei, He, Mindi, Lu, Yonghui, Duan, Weixia, Pei, Liping, Li, Min, Yu, Zhengping, Zhou, Zhou, Chen, Chunhai, Ma, Qinlong, Liu, Chuan, Deng, Ping, Zhu, Gang, Zhang, Lei, He, Mindi, Lu, Yonghui, Duan, Weixia, Pei, Liping, Li, Min, Yu, Zhengping, and Zhou, Zhou

Abstract

A radiofrequency electromagnetic field (RF-EMF) of 1800 MHz is widely used in mobile communications. However, the effects of RF-EMFs on cell biology are unclear. Embryonic neural stem cells (eNSCs) play a critical role in brain development. Thus, detecting the effects of RF-EMF on eNSCs is important for exploring the effects of RF-EMF on brain development. Here, we exposed eNSCs to 1800 MHz RF-EMF at specific absorption rate (SAR) values of 1, 2, and 4 W/kg for 1, 2, and 3 days. We found that 1800 MHz RF-EMF exposure did not influence eNSC apoptosis, proliferation, cell cycle or the mRNA expressions of related genes. RF-EMF exposure also did not alter the ratio of eNSC differentiated neurons and astrocytes. However, neurite outgrowth of eNSC differentiated neurons was inhibited after 4 W/kg RF-EMF exposure for 3 days. Additionally, the mRNA and protein expression of the proneural genes Ngn1 and NeuroD, which are crucial for neurite outgrowth, were decreased after RF-EMF exposure. The expression of their inhibitor Hes1 was upregulated by RF-EMF exposure. These results together suggested that 1800 MHz RF-EMF exposure impairs neurite outgrowth of eNSCs. More attention should be given to the potential adverse effects of RF-EMF exposure on brain development.

Published
2014

46. Dynamin 1-like-dependent mitochondrial fission initiates overactive mitophagy in the hepatotoxicity of cadmium

Author

Pi, Huifeng, primary, Xu, Shangcheng, additional, Zhang, Lei, additional, Guo, Pan, additional, Li, Yuming, additional, Xie, Jia, additional, Tian, Li, additional, He, Mindi, additional, Lu, Yonghui, additional, Li, Min, additional, Zhang, Yanwen, additional, Zhong, Min, additional, Xiang, Yang, additional, Deng, Linhong, additional, Zhou, Zhou, additional, and Yu, Zhengping, additional

Published
2013
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results