scholarly journals Characteristic and Otopathogenic Analysis of a Vibrio alginolyticus Strain Responsible for Chronic Otitis Externa in China

2021 ◽  
Vol 12 ◽  
Author(s):  
Ke Zhou ◽  
Ke-yong Tian ◽  
Xin-qin Liu ◽  
Wei Liu ◽  
Xin-yu Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Otitis Externa ◽  
Flow Cytometric Analysis ◽  
Vibrio Alginolyticus ◽  
Cell Counting ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Characteristic Analysis ◽  
Ear Infections ◽  
Ganglion Neurons

Vibrio alginolyticus, a Gram-negative rod bacterium found in marine environments, is known to cause opportunistic infections in humans, including ear infections, which can be difficult to diagnose. We investigated the microbiological and otopathogenic characteristics of a V. alginolyticus strain isolated from an ear exudate specimen obtained from a patient with chronic otitis externa to provide a basis for the future diagnosis of V. alginolyticus-associated infections. The identification of V. alginolyticus was accomplished using a combination of matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS), classical biochemical identification methods, and the use of Vibrio-selective media and advanced molecular identification methodologies. Antimicrobial susceptibility testing revealed that the strain was resistant to ampicillin and sensitive to β-lactam, aminoglycosides, fluoroquinolones, and sulfonamide antibiotics. The potential otopathogenic effects of V. alginolyticus were determined through the performance of cell viability, cell apoptosis, and cell death assays in tympanic membrane (TM) keratinocytes and HEI-OC1 cells treated with V. alginolyticus-conditioned medium using cell-counting kit (CCK)-8 assay, a wound-healing migration assay, Annexin V/propidium iodide (PI) flow cytometric analysis, and terminal deoxynucleotidyl transferase deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL staining). The results indicated that the identified V. alginolyticus strain exerts cytotoxic effects on keratinocytes and HEI-OC1 cells by inhibiting cell proliferation and migration and inducing apoptosis and cell death. To evaluate the ototoxicity of V. alginolyticus, the cell density and morphological integrity of hair cells (HCs) and spiral ganglion neurons (SGNs) were analyzed after exposing cochlear organotypic explants to the bacterial supernatant, which revealed the pre-dominant susceptibility and vulnerability of HCs and SGNs in the basal cochlear region to the ototoxic insults exerted by V. alginolyticus. Our investigation highlights the challenges associated with the identification and characteristic analysis of the Vibrio strain isolated in this case and ultimately aims to increase the understanding and awareness of clinicians and microbiologists for the improved diagnosis of V. alginolyticus-associated ear infections and the recognition of its potential otopathogenic and ototoxic effects.

Increased cell death in osteopontin-deficient cardiac fibroblasts occurs by a caspase-3-independent pathway

2004 ◽  
Vol 287 (4) ◽  
pp. H1730-H1739 ◽  
Author(s):  
Ron Zohar ◽  
Baoqian Zhu ◽  
Peter Liu ◽  
Jaro Sodek ◽  
C. A. McCulloch
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Cardiac Fibroblasts ◽  
Chromatin Condensation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Wild Type ◽  
Nuclear Fragmentation ◽  
A Cell

Reperfusion-induced oxidative injury to the myocardium promotes activation and proliferation of cardiac fibroblasts and repair by scar formation. Osteopontin (OPN) is a proinflammatory cytokine that is upregulated after reperfusion. To determine whether OPN enhances fibroblast survival after exposure to oxidants, cardiac fibroblasts from wild-type (WT) or OPN-null (OPN−/−) mice were treated in vitro with H2O2to model reperfusion injury. Within 1 h, membrane permeability to propidium iodide (PI) was increased from 5 to 60% in OPN−/−cells but was increased to only 20% in WT cells. In contrast, after 1–8 h of treatment with H2O2, the percent of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-stained cells was more than twofold higher in WT than OPN−/−cells. Electron microscopy of WT cells treated with H2O2showed chromatin condensation, nuclear fragmentation, and cytoplasmic and nuclear shrinkage, which are consistent with apoptosis. In contrast, H2O2-treated OPN−/−cardiac fibroblasts exhibited cell and nuclear swelling and membrane disruption that are indicative of cell necrosis. Treatment of OPN−/−and WT cells with a cell-permeable caspase-3 inhibitor reduced the percentage of TUNEL staining by more than fourfold in WT cells but decreased staining in OPN−/−cells by ∼30%. Although the percentage of PI-permeable WT cells was reduced threefold, the percent of PI-permeable OPN−/−cells was not altered. Restoration of OPN expression in OPN−/−fibroblasts reduced the percentage of PI-permeable cells but not TUNEL staining after H2O2treatment. Thus H2O2-induced cell death in OPN-deficient cardiac fibroblasts is mediated by a caspase-3-independent, necrotic pathway. We suggest that the increased expression of OPN in the myocardium after reperfusion may promote fibrosis by protecting cardiac fibroblasts from cell death.

Oxidative Stress Is Associated With Cell Death, Wall Degradation, and Increased Risk of Rupture of the Intracranial Aneurysm Wall

Neurosurgery ◽  
2012 ◽  
Vol 72 (1) ◽  
pp. 109-117 ◽  
Author(s):  
Elisa Laaksamo ◽  
Riikka Tulamo ◽  
Arto Liiman ◽  
Marc Baumann ◽  
Robert M. Friedlander ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Caspase 9 ◽  
Tissue Samples ◽  
Aneurysm Wall ◽  
Increased Risk ◽  
Risk Of Rupture ◽  
High Oxidative Stress

Abstract BACKGROUND: The cause of rupture of intracranial aneurysms (IA) is not well understood. We previously demonstrated that loss of cells from the IA wall is associated with wall degeneration and rupture. OBJECTIVE: To investigate the mechanisms mediating cell death in the IA wall. METHODS: Snap-frozen tissue samples from aneurysm fundi were studied with terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and immunostaining (14 unruptured and 20 ruptured), as well as with Western blot (12 unruptured and 12 ruptured). RESULTS: Ruptured IA walls had more TUNEL-positive cells than unruptured walls (P < .001). Few cells positive for cleaved caspase-3 were detected. Cleaved caspase-9 (intrinsic activation of apoptosis) was significantly increased in ruptured IA walls, whereas cleaved caspase-8 (extrinsic activation of apoptosis) was not detected. Increased expression of hemeoxygenase-1, a marker for oxidative stress, was associated with IA wall degeneration and rupture. CONCLUSION: Our results show that programmed cell death is activated in the IA wall via the intrinsic pathway. High oxidative stress in the IA wall is probably a significant cause of the intrinsic activation of cell death.

Glutathione S-transferase overexpression protects against anthracycline-induced H9C2 cell death

2004 ◽  
Vol 286 (6) ◽  
pp. H2057-H2064 ◽  
Author(s):  
Thomas L'Ecuyer ◽  
Zuhair Allebban ◽  
Ronald Thomas ◽  
Richard Vander Heide
Keyword(s):  
Cell Death ◽  
Trypan Blue ◽  
Oxidant Stress ◽  
Hematologic Malignancies ◽  
Model System ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
H9c2 Cell ◽  
Significant Activity ◽  
Glutathione S Transferase

Anthracyclines (AC) are antitumor antibiotics with significant activity against solid and hematologic malignancies. One problem preventing more widespread use has been the development of cardiac toxicity. Experimental evidence supports oxidant stress as an important trigger and/or mediator of AC-induced cardiotoxicity (ACT). Therefore, reducing oxidant stress should be protective against ACT. To determine whether antioxidant protein overexpression can reduce ACT, we developed a cell culture model system using the H9C2 cardiac cell line exhibiting controlled overexpression of the α4-isoform of glutathione- S-transferase (GST). Treatment with the AC doxorubicin (DOX) produced both oncosis, manifested by an increase in the number of cells staining positive for Trypan blue, and apoptosis, indicated by the presence of positive terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. In both cases, the loss of cell viability was preceded by an AC-induced increase in fluorescence with carboxy-2′,7′-dichlorofluorescein diacetate, demonstrating the presence of high levels of reactive oxygen species (ROS). The DOX-induced increase in ROS was reduced to control levels by maximal GST overexpression. Coincident with this elimination of oxidative stress, there was a reduction in both Trypan blue and TUNEL-positive cells, indicating that GST overexpression reduced both ROS and cell death in this model system. We conclude that GST overexpression may be an important part of a protective strategy against ACT and that this model system will aid in defining steps in the pathway(s) leading to AC-induced cell death that can be therapeutically manipulated.

scholarly journals Transgenic Overexpression of IL-37 Protects Against Atherosclerosis and Strengthens Plaque Stability

2018 ◽  
Vol 45 (3) ◽  
pp. 1034-1050 ◽  
Author(s):  
Jing Liu ◽  
Jibin Lin ◽  
Shaolin He ◽  
Chun Wu ◽  
Boyuan Wang ◽  
...  
Keyword(s):  
Immunohistochemical Staining ◽  
Intracellular Cytokine Staining ◽  
Flow Cytometric Analysis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Atherosclerotic Plaques ◽  
Plaque Stability ◽  
Atherosclerotic Burden

Background/Aims: Recently, studies have shown that interleukin-37 (IL-37) is involved in atherosclerosis-related diseases. However, the regulatory mechanisms of IL-37 in atherosclerosis remain unknown. This study aims to determine the role of IL-37 in atherosclerosis and to investigate the underlying mechanisms involved. Methods: IL-37 expression in human atherosclerotic plaques was detected by immunohistochemical staining and real-time reverse transcription polymerase chain reaction (RT-PCR). Oil Red O staining was used to measure the size of plaques. Cell apoptosis in vitro and in vivo was tested by flow cytometric analysis and terminal deoxynucleotidyl-transferase mediated dUTP nick-end labeling (TUNEL) staining, respectively. Protein expression levels of IL-37, IL-18Rα and p-Smad3 were measured by Weston blotting. Results: Immunohistochemical staining revealed that IL-37 was highly expressed in human atherosclerotic plaques. Intracellular cytokine staining revealed that infiltrated CD4+ T lymphocytes and vascular smooth muscle cells (VSMCs), but not macrophages, were the major sources of IL-37. Mice that overexpressed IL-37 exhibited significant improvements in their atherosclerotic burden, as demonstrated by reduced plaque size, increased collagen levels, and reduced numbers of apoptotic cells in vivo. Subsequently, mechanistic studies showed that IL-37 played an anti-atherosclerotic role, at least partially, through reducing inflammation by promoting the differentiation of the T helper cell anti-inflammatory phenotype, and through increasing plaque stability by decreasing matrix metalloproteinase (MMP)-2/13-mediated degradation of collagen and inhibiting VSMCs apoptosis. Conclusion: IL-37 may be a novel potential therapeutic target in patients with atherosclerotic heart disease.

scholarly journals Do TUNEL and Other Apoptosis Assays Detect Cell Death in Preclinical Studies?

2020 ◽  
Vol 21 (23) ◽  
pp. 9090
Author(s):  
Razmik Mirzayans ◽  
David Murray
Keyword(s):  
Cell Death ◽  
Genomic Dna ◽  
Apoptotic Cell ◽  
Tunel Assay ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Caspase Activation ◽  
Dna Breaks ◽  
Tissue Samples ◽  
Dna Breakage

The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay detects DNA breakage by labeling the free 3ʹ-hydroxyl termini. Given that genomic DNA breaks arise during early and late stages of apoptosis, TUNEL staining continues to be widely used as a measure of apoptotic cell death. The advantages of the assay include its relative ease of performance and the broad availability of TUNEL assay kits for various applications, such as single-cell analysis of apoptosis in cell cultures and tissue samples. However, as briefly discussed herein, aside from some concerns relating to the specificity of the TUNEL assay itself, it was demonstrated some twenty years ago that the early stages of apoptosis, detected by TUNEL, can be reversed. More recently, compelling evidence from different biological systems has revealed that cells can recover from even late stage apoptosis through a process called anastasis. Specifically, such recovery has been observed in cells exhibiting caspase activation, genomic DNA breakage, phosphatidylserine externalization, and formation of apoptotic bodies. Furthermore, there is solid evidence demonstrating that apoptotic cells can promote neighboring tumor cell repopulation (e.g., through caspase-3-mediated secretion of prostaglandin E2) and confer resistance to anticancer therapy. Accordingly, caution should be exercised in the interpretation of results obtained by the TUNEL and other apoptosis assays (e.g., caspase activation) in terms of apoptotic cell demise.

scholarly journals Expression of Fas ligand by human gastric adenocarcinomas: a potential mechanism of immune escape in stomach cancer

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 156-162 ◽  
Author(s):  
M W Bennett ◽  
J O’Connell ◽  
G C O’Sullivan ◽  
D Roche ◽  
C Brady ◽  
...  
Keyword(s):  
Cell Death ◽  
Stomach Cancer ◽  
Fas Ligand ◽  
Immune Escape ◽  
Immune Privilege ◽  
Lymphoid Cells ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Gastric Adenocarcinomas

BackgroundDespite being immunogenic, gastric cancers overcome antitumour immune responses by mechanisms that have yet to be fully elucidated. Fas ligand (FasL) is a molecule that induces Fas receptor mediated apoptosis of activated immunocytes, thereby mediating normal immune downregulatory roles including immune response termination, tolerance acquisition, and immune privilege. Colon cancer cell lines have previously been shown to express FasL and kill lymphoid cells by Fas mediated apoptosis in vitro. Many diverse tumours have since been found to express FasL suggesting that a “Fas counterattack” against antitumour immune effector cells may contribute to tumour immune escape.AimTo ascertain if human gastric tumours express FasL in vivo, as a potential mediator of immune escape in stomach cancer.SpecimensThirty paraffin wax embedded human gastric adenocarcinomas.MethodsFasL protein was detected in gastric tumours using immunohistochemistry; FasL mRNA was detected in the tumours using in situ hybridisation. Cell death was detected in situ in tumour infiltrating lymphocytes using terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL).ResultsPrevalent expression of FasL was detected in all 30 resected gastric adenocarcinomas examined. In the tumours, FasL protein and mRNA were co-localised to neoplastic gastric epithelial cells, confirming expression by the tumour cells. FasL expression was independent of tumour stage, suggesting that it may be expressed throughout gastric cancer progression. TUNEL staining disclosed a high level of cell death among lymphocytes infiltrating FasL positive areas of tumour.ConclusionsHuman gastric adenocarcinomas express the immune downregulatory molecule, FasL. The results suggest that FasL is a prevalent mediator of immune privilege in stomach cancer.

scholarly journals Visualization of Cell Death in MICE with Focal Cerebral Ischemia using Fluorescent Annexin A5, Propidium Iodide, and Tunel Staining

2011 ◽  
Vol 31 (5) ◽  
pp. 1311-1320 ◽  
Author(s):  
Peyman Bahmani ◽  
Eyk Schellenberger ◽  
Jan Klohs ◽  
Jens Steinbrink ◽  
Ryan Cordell ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Propidium Iodide ◽  
Ex Vivo ◽  
Focal Cerebral Ischemia ◽  
High Specificity ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Annexin A5 ◽  
Cell Integrity

To monitor stroke-induced brain damage and assess neuroprotective therapies, specific imaging of cell death after cerebral ischemia in a noninvasive manner is highly desirable. Annexin A5 has been suggested as a marker for imaging cell death under various disease conditions including stroke. In this study, C57BL6/N mice received middle cerebral artery occlusion (MCAO) and were injected intravenously with either active or inactive Cy5.5-annexin A5 48 hours after reperfusion. Some mice also received propidium iodide (PI), a cell integrity marker. Only in mice receiving active Cy5.5-annexin A5 were fluorescence intensities significantly higher over the hemisphere ipsilateral to MCAO than on the contralateral side. This was detected noninvasively and ex vivo 4 and 8 hours after injection. The majority of cells positive for fluorescent annexin A5 were also positive for PI and fragmented DNA as detected by terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining. This study demonstrates the high specificity of annexin A5 for visualization of cell death in a mouse model of stroke. To our knowledge, this is the first study to compare the distribution of injected active and inactive annexin A5, PI, and TUNEL staining. It provides important information on the experimental and potential clinical applications of annexin A5-based imaging agents in stroke.

scholarly journals FUBP1 promotes neuroblastoma proliferation via enhancing glycolysis-a new possible marker of malignancy for neuroblastoma

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Ping Jiang ◽  
Mao Huang ◽  
Weiwei Qi ◽  
Fenghua Wang ◽  
Tianyou Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Flow Cytometric Analysis ◽  
Staging System ◽  
Cell Counting ◽  
Luciferase Assay ◽  
Tunel Staining ◽  
Mrna Levels ◽  
Atp Production ◽  
Von Hippel Lindau

Abstract Background Neuroblastoma (NB) is one of the deadliest paediatric solid tumours due to its rapid proliferative characteristics. Amplified copies of MYCN are considered the most important marker for the prediction of tumour relapse and progression in NB, but they were only detected in 20–30% of NB patients, indicating there might be other oncogenes in the development of NB. The far upstream element binding protein 1 (FUBP1) was first identified as a transcriptional regulator of the proto-oncogene MYC. However, the expression and role of FUBP1 in NB have not been documented. Methods FUBP1 expression was analysed from GEO database and verified by immunohistochemistry (IHC) and western blotting (WB) in NB tissues and cell lines. Cell proliferation and apoptosis were detected by Cell Counting Kit-8, Colony formation assay, EDU, TUNEL staining and flow cytometric analysis. Several glycolytic metabolites production was confirmed by ELISA and oxygen consuming rate (OCR). Luciferase assay, WB, chromatin immunoprecipitation (CHIP) were used to explore the mechanisms of the effect of FUBP1 on NB. Results FUBP1 mRNA levels were increased along with the increase in International Neuroblastoma Staging System (INSS) stages. High expression of FUBP1 with low N-Myc expression accounted for 44.6% of NB patient samples (n = 65). In addition, FUBP1 protein levels were remarkably increased with NB malignancy in the NB tissue microarray (NB: n = 65; ganglioneuroblastoma: n = 31; ganglioneuroma: n = 27). Furthermore, FUBP1 expression was negatively correlated with patient survival rate but positively correlated with ki67 content. In vitro experiments showed that FUBP1 promotes NB cell proliferation and inhibits cell apoptosis via enhancing glycolysis and ATP production. Mechanistically, FUBP1 inhibited the degradation of HIF1α via downregulation of Von Hippel-Lindau (VHL), the E3 ligase for HIF1α, resulting in upregulation of lactate dehydrogenase isoform B (LDHB) expression to enhance glycolysis. Overexpressed or silenced N-Myc could not regulate FUBP1 or LDHB levels. Conclusions Taken together, our findings demonstrate for the first time that elevated FUBP1 promotes NB glycolysis and growth by targeting HIF1α rather than N-Myc, suggesting that FUBP1 is a novel and powerful oncogene in the development of NB independent of N-Myc and may have potential in the diagnosis and treatment of NB.

scholarly journals Hemoglobin and Iron Handling in Brain after Subarachnoid Hemorrhage and the Effect of Deferoxamine on Early Brain Injury

2010 ◽  
Vol 30 (11) ◽  
pp. 1793-1803 ◽  
Author(s):  
Jin-Yul Lee ◽  
Richard F Keep ◽  
Yangdong He ◽  
Oren Sagher ◽  
Ya Hua ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Cell Death ◽  
Iron Concentration ◽  
Neuronal Cell ◽  
Nonheme Iron ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Heme Oxygenase 1

The purpose of this study was to investigate hemoglobin and iron handling after subarachnoid hemorrhage (SAH), examine the relationship between iron and neuroglial cell changes, and determine whether deferoxamine (DFX) can reduce SAH-induced injury. The SAH was induced in Sprague-Dawley rats ( n=110) using an endovascular perforation technique. Animals were treated with DFX (100 mg/kg) or vehicle 2 and 6 hours after SAH induction followed by every 12 hours for 3 days. Rats were killed at 6 hours, Days 1 and 3 to determine nonheme iron and examine iron-handling proteins using Western blot and immunohistochemistry. 8-Hydroxyl-2′-deoxyguanosine and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining were performed to assess oxidative DNA damage and neuronal cell death. After SAH, marked heme-oxygenase-1 (HO-1) upregulation at Day 3 ( P<0.01) was accompanied by elevated nonheme iron ( P<0.01), transferrin (Tf) ( P<0.01), Tf receptor ( P<0.05), and ferritin levels ( P<0.01). Deferoxamine treatment reduced SAH-induced mortality (12% versus 29%, P<0.05), brain nonheme iron concentration, iron-handling protein expression, oxidative stress, and neuronal cell death at Day 3 ( P<0.01) after SAH. These results suggest that iron overload in the acute phase of SAH causes oxidative injury leading to neuronal cell death. Deferoxamine effectively reduced oxidative stress and neuronal cell death, and may be a potential therapeutic agent for SAH.

scholarly journals Endoplasmic reticulum stress is involved in spiral ganglion neuron apoptosis following chronic kanamycin-induced deafness

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Yaqin Tu ◽  
Guorun Fan ◽  
Haiying Sun ◽  
Xiong Cai ◽  
Wen Kong
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Time Course ◽  
Morphological Changes ◽  
Spiral Ganglion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Spiral Ganglion Neuron ◽  
Tunel Staining ◽  
Caspase 12 ◽  
Ganglion Neurons

Abstract Aminoglycoside antibiotics-induced hearing loss is a common sensorineural impairment. Spiral ganglion neurons (SGNs) are first-order neurons of the auditory pathway and are critical for the maintenance of normal hearing. In the present study, we investigated the time-course of morphological changes and the degeneration process of spiral ganglion cells (SGCs) following chronic kanamycin-induced deafness and determined whether the endoplasmic reticulum (ER) stress was involved in the degeneration of SGNs. We detected density changes in SGCs and the expressions of Bip, inositol requirement 1 (IRE1)α, activating transcription factor-6α, p-PERK, p-eIF2α, CHOP, and caspase-12 at each time point after kanamycin treatment. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was also performed. The number of SGC deletions reached ∼50% at the 70th day after kanamycin administration and the ER of most SGCs were dilated. The expression of p-PERK, p-eIF2α, p-IRE1α, Bip, caspase-12, and Chop was significantly unregulated after kanamycin treatment. The number of SGCs that were positive for both TUNEL and caspase-12 increased from day 7 to 28. Taken together, these data demonstrate that ER stress was involved in kanamycin-induced apoptosis of SGNs. Kanamycin-induced SGN apoptosis is mediated, at least in part, by ER stress-induced upregulation of CHOP and caspase-12.

Sign in / Sign up

Export Citation Format

Share Document