Related Experiment Video

Updated: Feb 26, 2026

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
08:22

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

Published on: October 27, 2020

3.5K

A brain-specific isoform of apoptosis-inducing factor 2 attenuates ischemia-induced oxidative stress in HT22 cells

Yuanyang Xie1, Siyi Wanggou1, Qing Liu1

  • 1Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410012, China.

Neurochemistry International
|July 23, 2017
PubMed

Insights

Apoptosis-inducing factor 2 (AIF-2), a brain-specific protein, protects neurons from ischemic damage. Overexpressing AIF-2 reduces cell death and oxidative stress, suggesting its therapeutic potential for brain ischemia.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Apoptosis-inducing factor (AIF) proteins are mitochondrial flavoproteins with critical cellular roles.
  • While AIF-1 is well-studied, other AIF isoforms, including brain-specific AIF-2, remain largely uncharacterized.
  • Understanding AIF isoforms is crucial for cellular function and disease mechanisms.

Purpose of the Study:

  • To investigate the role of AIF-2 in an in vitro neuronal ischemia model.
  • To determine the protective effects of AIF-2 against oxygen and glucose deprivation (OGD)-induced neuronal injury.
  • To elucidate the molecular mechanisms underlying AIF-2's neuroprotective function.

Main Methods:

  • Utilized the HT22 neuronal cell line as an in vitro ischemia model.
  • Employed small interfering RNA (siRNA) to downregulate AIF-2 expression.
  • Overexpressed AIF-2 using lentivirus transfection.
  • Assessed cell viability, apoptosis, lactate dehydrogenase (LDH) release, mitochondrial membrane potential (MMP), reactive oxygen species (ROS) generation, and AIF-1 translocation.

Main Results:

  • AIF-2 is constitutively expressed in HT22 cells and its expression is unaffected by OGD.
  • AIF-2 downregulation exacerbated OGD-induced cell death and LDH release.
  • AIF-2 overexpression protected neurons against OGD, preserving MMP, inhibiting cytochrome c release, and reducing ROS and lipid peroxidation.
  • AIF-2 overexpression prevented OGD-induced translocation of AIF-1 to the nucleus.

Conclusions:

  • AIF-2 exhibits significant neuroprotective effects in an in vitro model of brain ischemia.
  • AIF-2 mitigates OGD-induced neuronal injury by preserving mitochondrial function and reducing oxidative stress.
  • AIF-2 may counteract AIF-1-mediated neurotoxicity, presenting a potential therapeutic target for brain ischemia.
Keywords:
Apoptosis-inducing factorBrain ischemiaMitochondrial dysfunctionOxygen and glucose deprivation

More Related Videos

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

17.9K
Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke11:32

Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke

Published on: January 3, 2025

1.7K

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...
8.8K
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...
9.0K
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
14.3K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
16.0K