Related Experiment Video

Updated: May 8, 2026

Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice
09:50

Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice

Published on: April 24, 2013

Ethanol induces cell cycle arrest and triggers apoptosis via Sp1-dependent p75NTR expression in human neuroblastoma

Hang Do1, Hey-Jin Park, Eun-Hwa Sohn

  • 1School of Medicine, Tan Tao University, Tan Duc ECity, Long An Province, Viet Nam.

Cell Biology and Toxicology
|September 13, 2013
PubMed

Insights

Ethanol exposure increases neurotrophin receptor (p75NTR) expression, driving neuronal cell death. Inhibiting p75NTR or Sp1 protects against ethanol-induced apoptosis, revealing key signaling pathways in neurotoxicity.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Toxicology

Background:

  • Ethanol causes central nervous system damage, but mechanisms of neuronal cell death are unclear.
  • The p75 neurotrophin receptor (p75NTR) is implicated in neuronal survival regulation.
  • Understanding ethanol's impact on neuronal signaling is crucial for neuroprotection.

Purpose of the Study:

  • To investigate the role of p75NTR in ethanol-induced apoptotic signaling in neuroblastoma cells.
  • To elucidate the regulatory pathways of p75NTR expression under ethanol exposure.
  • To identify molecular targets for mitigating ethanol's neurotoxic effects.

Main Methods:

  • Utilized small interfering RNA (siRNA) to inhibit p75NTR expression.
  • Assessed DNA binding activity of Sp1 transcription factor.
  • Employed inhibitors for casein kinase 2 (CK2) and extracellular signal-regulated kinase (ERK).
  • Analyzed p75NTR promoter activity and expression of cell cycle regulators (p21, p53, Bax, Puma, Bcl-2).

Main Results:

  • Ethanol significantly increased p75NTR expression and induced cell cycle arrest and apoptosis.
  • Inhibition of p75NTR or Sp1 attenuated ethanol-induced apoptosis and cell cycle arrest.
  • Ethanol increased Sp1 DNA binding activity, which was crucial for p75NTR expression.
  • ERK and CK2 signaling pathways inversely regulate Sp1-mediated p75NTR expression.
  • Ethanol increased p21 expression, contributing to cell cycle arrest and apoptosis.

Conclusions:

  • Ethanol-induced neurotoxicity involves the upregulation of p75NTR.
  • Sp1 transcription factor mediates ethanol-induced p75NTR expression.
  • ERK and CK2 signaling pathways modulate Sp1-dependent p75NTR expression.
  • Targeting p75NTR or Sp1 may offer therapeutic strategies against ethanol neurotoxicity.

More Related Videos

Neurogenesis Using P19 Embryonal Carcinoma Cells07:46

Neurogenesis Using P19 Embryonal Carcinoma Cells

Published on: April 27, 2019

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...