Development of in Vitro Injury Models for Oligodendroglia

1996 ◽  
pp. 44-56e ◽  
Author(s):  
A. Espinosa ◽  
P. Zhao ◽  
J. de Vellis
Keyword(s):  
Injury Models

The Matrine Derivate MASM Inhibits Recruitment of Gr1hi Monocyte and Alleviates Liver Injury

Pharmacology ◽  
2019 ◽  
Vol 104 (5-6) ◽  
pp. 235-243 ◽  
Author(s):  
Wei-Heng Xu ◽  
Jing Xu ◽  
Fang-Yuan Xie ◽  
Ying-Hua Li ◽  
Zhen-Lin Hu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Protective Effect ◽  
Protective Role ◽  
Chronic Liver ◽  
Monocyte Chemoattractant Protein 1 ◽  
Nonparenchymal Cells ◽  
Hepatic Expression ◽  
Injury Models ◽  
Vitro Effect

Backgrounds: (6aS, 10S, 11aR, 11bR, 11cS)-10-methylaminododecahydro-3a, 7a-diaza-benzo (de) anthracene-8-thione (MASM), a novel derivative of matrine, exhibits better anti-inflammatory activity. This study was designed to evaluate the protective effect of MASM on acute and chronic liver injuries and explore the possible mechanisms. Methods: Acute and chronic liver injury models were established by the CCl4 intraperitoneal injection and the protective effect of MASM was assessed by biochemical and histological examination. The infiltration of different monocyte subsets into the liver was characterized and analyzed by flow cytometry. The in vitro effect of MASM on liver nonparenchymal cells was evaluated by real-time PCR and transwell chemotaxis assays. Results: Administration of MASM markedly attenuated acute liver injury and liver fibrosis induced by CCl4 injection. Meanwhile, the infiltrations of Gr1hi monocytes in injured livers and induced hepatic expression of monocyte chemoattractant protein-1 (MCP-1) were greatly inhibited. Cellular experiments demonstrated that MASM not only decreased the expression of MCP-1 but also inhibited its chemotactic activity. Conclusions: This study demonstrates that the protective effect of MASM on liver injury could be contributed to the suppression of Gr1hi monocyte infiltration to the liver and the inhibition of MCP-1 production and activity. These findings provide new insights into the protective role of MASM in liver injury.

scholarly journals Exosomal CCL2 from Tubular Epithelial Cells Is Critical for Albumin-Induced Tubulointerstitial Inflammation

2018 ◽  
Vol 29 (3) ◽  
pp. 919-935 ◽  
Author(s):  
Lin-Li Lv ◽  
Ye Feng ◽  
Yi Wen ◽  
Wei-Jun Wu ◽  
Hai-Feng Ni ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Cell ◽  
Kidney Injury ◽  
Tubular Epithelial Cells ◽  
Tail Vein Injection ◽  
Chronic Kidney Injury ◽  
Ccl2 Mrna ◽  
Injury Models ◽  
Tubulointerstitial Inflammation

Albuminuria is a key instigator of tubulointerstitial inflammation associated with CKD, but the mechanism through which filtered albumin propagates renal injury remains unclear. In this study, we explored the role in this process of exosome mRNA released from tubular epithelial cells (TECs). Compared with control mice, acute and chronic kidney injury models had more exosomes containing inflammatory cytokine mRNA, particularly the chemokine CCL2, in kidneys and urine. In vitro stimulation of TECs with BSA recapitulated this finding. Notably, the internalization of purified TEC exosomes by cultured macrophages increased if TECs were exposed to BSA. Macrophage internalization of exosomes from BSA-treated TECs led to an enhanced inflammatory response and macrophage migration, but CCL2 silencing in TECs prevented these effects. Using a GFP-CCL2 fusion mRNA construct, we observed direct transfer of CCL2 mRNA from TEC exosomes to macrophages. Mice subjected to tail vein injection of purified BSA-treated TEC exosomes developed tubular injury with renal inflammatory cell infiltration. However, injection of exosomes from BSA-treated CCL2-deficient TECs induced less severe kidney inflammation. Finally, in patients with IgA nephropathy, the increase of proteinuria correlated with augmented urinary excretion of exosomes with exaggerated expression of CCL2 mRNA. Moreover, the level of CCL2 mRNA in urinary exosomes correlated closely with levels of renal interstitial macrophage infiltration in these patients. Our studies demonstrate that the increasing release of exosomes that transfer CCL2 mRNA from TECs to macrophages constitutes a critical mechanism of albumin-induced tubulointerstitial inflammation.

MDM2 inhibition improves cisplatin-induced renal injury in mice via inactivation of Notch/hes1 signaling pathway

2020 ◽  
pp. 096032712095215
Author(s):  
X Luo ◽  
L Zhang ◽  
G-D Han ◽  
P Lu ◽  
Y Zhang
Keyword(s):  
Signaling Pathway ◽  
Renal Injury ◽  
Cell Apoptosis ◽  
Renal Tissue ◽  
Tunel Staining ◽  
Acute Renal Injury ◽  
Renal Tubular ◽  
Injury Models

Objective: To explore the potential function of MDM2-mediated Notch/hes1 signaling pathway in cisplatin-induced renal injury. Methods: The acute renal injury models of mice after intraperitoneal injection of cisplatin in vivo, and the apoptotic models of human renal tubular epithelial (HK-2) cells induced by cisplatin in vitro, were conducted respectively. The renal function-related parameters were measured. The renal tissue pathological changes and apoptosis were observed by PAS staining and TUNEL staining, respectively. Cell viability and apoptosis were detected by MTT and flow cytometry. Notch/hes1 pathway-related proteins were tested by Western blotting. Results: After mice injected by cisplatin, the levels of Cr, BUN, urine cystatin C, urine NGAL and urine ACR were increased and GFR was decreased with the elevation of renal tubular injury scores, the upregulation of the expressions of MDM2, N1ICD, Hes1 and Cleaved caspase-3, as well as the enhancement of cell apoptosis accompanying decreased ratio of Bcl-2/Bax. However, these cisplatin-induced renal injuries of mice have been improved by MDM2 inhibition. Besides, the declined viability, increased cytotoxicity, and enhanced apoptosis were observed in cisplatin-induced HK-2 cells, with the activated Notch/hes1 pathway. Notably, the phenomenon was alleviated in cisplatin-induced HK-2 cells transfected with MDM2 shRNA, but was severer in those co-treated with AdMDM2. Moreover, Notch1 siRNA can reverse the injury of AdMDM2 on HK-2 cells. Conclusion: Inhibiting MDM2 could reduce cell apoptosis through blocking Notch/hes1 signaling pathway, thus alleviating the acute renal injury caused by cisplatin.

scholarly journals Promoting axon regeneration by enhancing the non-coding function of the injury-responsive coding gene Gpr151

2021 ◽  
Author(s):  
Bohm Lee ◽  
Jinyoung Lee ◽  
Yewon Jeon ◽  
Hyemin Kim ◽  
Minjae Kwon ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Rna Binding ◽  
Axon Regeneration ◽  
Rna Binding Proteins ◽  
Nerve Repair ◽  
Coding Regions ◽  
Protein Functions ◽  
Injury Models

AbstractGene expression profiling in response to nerve injury has been mainly focused on protein functions of coding genes to understand mechanisms of axon regeneration and to identify targets of potential therapeutics for nerve repair. However, the protein functions of several highly injury-induced genes including Gpr151 for regulating the regenerative ability remain unclear. Here we present an alternative approach focused on non-coding functions of the coding genes, which led to the identification of the non-coding function of Gpr151 RNA interacting with RNA-binding proteins such as CSDE1. Gpr151 promotes axon regeneration by the function of its 5’-untranslated region (5’UTR) and expression of an engineered form of the 5’UTR improves regenerative capacity in vitro and in vivo in both sciatic nerve and optic nerve injury models. Our data suggest that searching injury-induced coding genes potentially functioning by their non-coding regions is required for the RNA-based gene therapy for improving axon regeneration.

Measurement of In Vitro Single Cell Temperature by Novel Thermocouple Nanoprobe in Acute Lung Injury Models

2017 ◽  
Vol 13 (1) ◽  
pp. 54-60 ◽  
Author(s):  
Xing Wang ◽  
Qiuhua Chen ◽  
Wenjuan Tian ◽  
Jianqing Wang ◽  
Lu Cheng ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Single Cell ◽  
Cell Temperature ◽  
Injury Models

Comparison of microRNA expressions for the identification of chemical hazards in in vivo and in vitro hepatic injury models

2018 ◽  
Vol 39 (2) ◽  
pp. 333-342 ◽  
Author(s):  
So-Ryeon Hwang ◽  
Nga Thi Thu Tham ◽  
Soo-ho Lee ◽  
Ji-Hyun Bang ◽  
Hee Yi ◽  
...  
Keyword(s):  
Hepatic Injury ◽  
Chemical Hazards ◽  
Injury Models

scholarly journals Sphingolipids as a Novel Therapeutic Target in Radiation-Induced Lung Injury

2021 ◽  
Author(s):  
Jeffrey R. Jacobson
Keyword(s):  
Lung Injury ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Small Animal ◽  
Protective Effects ◽  
Sphingosine 1 Phosphate ◽  
Radiation Induced ◽  
Injury Models

AbstractRadiation-induced lung injury (RILI) is a potential complication of thoracic radiotherapy that can result in pneumonitis or pulmonary fibrosis and is associated with significant morbidity and mortality. The pathobiology of RILI is complex and includes the generation of free radicals and DNA damage that precipitate oxidative stress, endothelial cell (EC), and epithelial cell injury and inflammation. While the cellular events involved continue to be elucidated and characterized, targeted and effective therapies for RILI remain elusive. Sphingolipids are known to mediate EC function including many of the cell signaling events associated with the elaboration of RILI. Sphingosine-1-phosphate (S1P) and S1P analogs enhance EC barrier function in vitro and have demonstrated significant protective effects in vivo in a variety of acute lung injury models including RILI. Similarly, statin drugs that have pleiotropic effects that include upregulation of EC S1P receptor 1 (S1PR1) have been found to be strongly protective in a small animal RILI model. Thus, targeting of EC sphingosine signaling, either directly or indirectly, to augment EC function and thereby attenuate EC permeability and inflammatory responses, represents a novel and promising therapeutic strategy for the prevention or treatment of RILI.

scholarly journals Minocycline Increases in-vitro Cortical Neuronal Cell Survival after Laser Induced Axotomy

2020 ◽  
Vol 15 (2) ◽  
pp. 105-109 ◽  
Author(s):  
Burak Yulug ◽  
Mehmet Ozansoy ◽  
Merve Alokten ◽  
Muzaffer B.C. Ozansoy ◽  
Seyda Cankaya ◽  
...  
Keyword(s):  
Cell Survival ◽  
Cortical Neurons ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Neuroprotective Effects ◽  
Therapeutic Trials ◽  
Trauma Model ◽  
Injury Models ◽  
Translational Block

Background: Antibiotic therapies targeting multiple regenerative mechanisms have the potential for neuroprotective effects, but the diversity of experimental strategies and analyses of non-standardised therapeutic trials are challenging. In this respect, there are no cases of successful clinical application of such candidate molecules when it comes to human patients. Methods: After 24 hours of culturing, three different minocycline (Sigma-Aldrich, M9511, Germany) concentrations (1 μM, 10 μM and 100 μM) were added to the primary cortical neurons 15 minutes before laser axotomy procedure in order to observe protective effect of minocycline in these dosages. Results: Here, we have shown that minocycline exerted a significant neuroprotective effect at 1 and 100μM doses. Beyond confirming the neuroprotective effect of minocycline in a more standardised and advanced in-vitro trauma model, our findings could have important implications for future studies that concentrate on the translational block between animal and human studies. Conclusion: Such sophisticated approaches might also help to conquer the influence of humanmade variabilities in critical experimental injury models. To the best of our knowledge, this is the first study showing that minocycline increases in-vitro neuronal cell survival after laser-axotomy.

In Vitro Cartilage Explant Injury Models

2015 ◽  
pp. 29-40 ◽  
Author(s):  
Christopher T. Chen ◽  
Peter A. Torzilli
Keyword(s):  
Cartilage Explant ◽  
Injury Models
Sign in / Sign up

Export Citation Format

Share Document