In Situ Detection of Apoptosis by the TUNEL Assay: An Overview of Techniques

Loo, Deryk

doi:10.1007/978-1-60327-409-8_1

Cited by 199 publications

(132 citation statements)

References 23 publications

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“…In situ detection of apoptosis by using TUNEL assay is a commonly used method to analyze the existence of apoptosis (21). Our present results demonstrate that DB can induce hepatocyte apoptosis, whereas FA can prevent DB-induced apoptosis in liver.…”

Section: Discussionmentioning

confidence: 54%

Ferulic acid prevents liver injury induced by Diosbulbin B and its mechanism

Niu

Sheng

Zhu

et al. 2016

BST

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Section: Discussionmentioning

confidence: 54%

Ferulic acid prevents liver injury induced by Diosbulbin B and its mechanism

Niu

Sheng

Zhu

et al. 2016

BST

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“…Sections (3 mm) of liver were cut and stained with H&E. Detection of apoptosis by TUNEL assay was according to the protocol (Millipore S7100; Billerica, MA) (17). Liver H&E sections were graded for CCl 4 injury under Leica DM4000 B Upright Research Microscope (2003 and 4003) using the system devised by Suzuki et al (18) and as described previously.…”

Section: Microscopic Investigation and Tunel Assaymentioning

confidence: 99%

IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation

Tan

Qian

Jiang

et al. 2013

The Journal of Immunology

258

202

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Liver fibrosis is a severe, life-threatening clinical condition resulting from nonresolving hepatitis of different origins. IL-17A is critical in inflammation, but its relation to liver fibrosis remains elusive. We find increased IL-17A expression in fibrotic livers from HBV-infected patients undergoing partial hepatectomy because of cirrhosis-related early-stage hepatocellular carcinoma in comparison with control nonfibrotic livers from uninfected patients with hepatic hemangioma. In fibrotic livers, IL-17A immunoreactivity localizes to the inflammatory infiltrate. In experimental carbon tetrachloride–induced liver fibrosis of IL-17RA–deficient mice, we observe reduced neutrophil influx, proinflammatory cytokines, hepatocellular necrosis, inflammation, and fibrosis as compared with control C57BL/6 mice. IL-17A is produced by neutrophils and T lymphocytes expressing the Th17 lineage–specific transcription factor Retinoic acid receptor–related orphan receptor γt. Furthermore, hepatic stellate cells (HSCs) isolated from naive C57BL/6 mice respond to IL-17A with increased IL-6, α-smooth muscle actin, collagen, and TGF-β mRNA expression, suggesting an IL-17A–driven fibrotic process. Pharmacologic ERK1/2 or p38 inhibition significantly attenuated IL-17A–induced HSC activation and collagen expression. In conclusion, IL-17A+ Retinoic acid receptor–related orphan receptor γt+ neutrophils and T cells are recruited into the injured liver driving a chronic, fibrotic hepatitis. IL-17A–dependent HSC activation may be critical for liver fibrosis. Thus, blockade of IL-17A could potentially benefit patients with chronic hepatitis and liver fibrosis.

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“…This detects DNA fragmentation resulting from apoptotic signaling and may also label cells undergoing other types of cell death, as well as active DNA repair and gene transcription (28,29). However, TUNEL labeling is too crude and very limited in sensitivity for detecting repairable DNA damage (30,31). 3-Week ethanol exposure significantly increased the density of TUNEL-labeled neurons in the mouse cerebral cortex (Fig.…”

Section: -Week Ethanol Consumption Induces Neuronal Death In Thementioning

confidence: 99%

Alcohol-induced One-carbon Metabolism Impairment Promotes Dysfunction of DNA Base Excision Repair in Adult Brain

Fowler

Hewetson

Agrawal

et al. 2012

Journal of Biological Chemistry

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Background: DNA repair dysfunction leads to genomic instability and neuron death. Results: Long term alcohol exposure results in reduced DNA repair, increased DNA damage, and neuron death in adult brain. Conclusion: Long term alcohol exposure in adult brain promotes genomic instability mediated by impairment in one-carbon metabolism. Significance: This is the first demonstration of alcohol-induced genomic instability in brain.The brain is one of the major targets of chronic alcohol abuse. Yet the fundamental mechanisms underlying alcohol-mediated brain damage remain unclear. The products of alcohol metabolism cause DNA damage, which in conditions of DNA repair dysfunction leads to genomic instability and neural death. We propose that one-carbon metabolism (OCM) impairment associated with long term chronic ethanol intake is a key factor in ethanol-induced neurotoxicity, because OCM provides cells with DNA precursors for DNA repair and methyl groups for DNA methylation, both critical for genomic stability. Using histological (immunohistochemistry and stereological counting) and biochemical assays, we show that 3-week chronic exposure of adult mice to 5% ethanol (Lieber-Decarli diet) results in increased DNA damage, reduced DNA repair, and neuronal death in the brain. These were concomitant with compromised OCM, as evidenced by elevated homocysteine, a marker of OCM dysfunction. We conclude that OCM dysfunction plays a causal role in alcohol-induced genomic instability in the brain because OCM status determines the alcohol effect on DNA damage/repair and genomic stability. Short ethanol exposure, which did not disturb OCM, also did not affect the response to DNA damage, whereas additional OCM disturbance induced by deficiency in a key OCM enzyme, methylenetetrahydrofolate reductase (MTHFR) in Mthfr ؉/؊ mice, exaggerated the ethanol effect on DNA repair. Thus, the impact of long term ethanol exposure on DNA repair and genomic stability in the brain results from OCM dysfunction, and MTHFR mutations such as Mthfr 677C3 T, common in human population, may exaggerate the adverse effects of ethanol on the brain.Nearly 100 million people worldwide have alcohol use disorders. Brain damage is a common and potentially severe consequence of alcohol abuse (1). It is estimated that 50 -75% of long term alcoholics exhibit cognitive impairment and structural damage to the brain. It is also known that chronic alcohol abuse is associated with cerebral cortical atrophy (1). Neuropathological analyses have provided evidence for loss of neurons in certain brain regions such as frontal lobes, which are highly affected in the alcoholic brain (1, 2). This region is essential for executive functions, whose loss may lead to a progressive loss of these functions, as seen in people addicted to alcohol as well as in individuals with frontal cortical damage (2, 3). These structural and cognitive changes have been suggested as the primary consequence of alcohol toxicity (4).Alcohol consumption is associated with generation of genotoxic metabolit...

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In Situ Detection of Apoptosis by the TUNEL Assay: An Overview of Techniques

Cited by 199 publications

References 23 publications

Ferulic acid prevents liver injury induced by Diosbulbin B and its mechanism

Ferulic acid prevents liver injury induced by Diosbulbin B and its mechanism

IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation

Alcohol-induced One-carbon Metabolism Impairment Promotes Dysfunction of DNA Base Excision Repair in Adult Brain

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