Related Experiment Video

Updated: May 18, 2026

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells
10:00

Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells

Published on: December 11, 2020

PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression

Duk-Soo Kim1, Eun Jeong Sohn, Dae Won Kim

  • 1Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan 330-090, Korea.

BMB Reports
|September 27, 2012
PubMed

Insights

PEP-1-p18, a tumor suppressor, protected against oxidative stress in Parkinson

Area of Science:

  • Molecular Biology
  • Neuroscience
  • Oncology

Background:

  • P18, an INK4 family cyclin-dependent kinase inhibitor, functions as a tumor suppressor and promotes cell survival in cancers.
  • INK4 proteins are implicated in neuronal diseases and oxidative stress, key factors in Parkinson's disease (PD) pathogenesis.
  • Oxidative stress contributes significantly to the loss of dopaminergic neurons observed in PD.

Purpose of the Study:

  • To investigate the protective effects of PEP-1-p18 against oxidative stress in neuronal cells.
  • To evaluate PEP-1-p18's efficacy in a mouse model of Parkinson's disease.

Main Methods:

  • Utilized SH-SY5Y cells exposed to oxidative stress induced by 1-methyl-4-phenyl pyridinium (MPP+).
  • Administered PEP-1-p18 to assess its impact on cell viability and apoptosis markers (Bax expression, DNA fragmentation).
  • Employed a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP)-induced PD mouse model to evaluate neuroprotection in vivo.

Main Results:

  • PEP-1-p18 significantly inhibited MPP+-induced SH-SY5Y cell death by reducing Bax expression and DNA fragmentation.
  • Transduced PEP-1-p18 treatment prevented dopaminergic neuronal cell loss in the substantia nigra of MPTP-treated mice.
  • Demonstrated a neuroprotective effect of PEP-1-p18 in a relevant Parkinson's disease model.

Conclusions:

  • PEP-1-p18 exhibits significant protective effects against oxidative stress-induced neuronal cell death.
  • PEP-1-p18 demonstrates therapeutic potential for Parkinson's disease by preserving dopaminergic neurons.
  • PEP-1-p18 may serve as a valuable therapeutic agent for various diseases involving oxidative stress.

Related Concept Videos

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...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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 Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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...
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.