Mitochondria Research

Mitophagy plays a critical role in maintaining neuronal homeostasis by removing damaged mitochondria, which are essential for energy production and prevention of neurodegenerative diseases. In cancer cells, mitophagy can be a double-edged sword, either promoting survival by removing damaged mitochondria or contributing to cell death when over-activated. In senescent cells, impaired mitophagy leads to the accumulation of dysfunctional mitochondria, exacerbating cellular dysfunction and contributing to age-related pathologies. Thus, regulation of mitophagy is critical for maintaining cellular homeostasis in various cell types, with implications for health and disease.

Mitophagy and cancer: role of BNIP3/BNIP3L as energetic drivers of stemness features, ATP production, proliferation, and cell migration
Click here for the original article: Marta Mauro-Lizcano, et. al., Aging, 2024.

A neuron–glia lipid metabolic cycle couples daily sleep to mitochondrial homeostasis
Click here for the original article: Paula R. Haynes, et. al., Nature Neuroscience, 2024.

Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule
Click here for the original article: George Kelly, et. al., Developmental Cell, 2024.

Point of Interest

- BNIP3 and BNIP3L are mitochondrial outer membrane receptors that promote mitophagy.

- Cancer cells with high BNIP3/BNIP3L activity have increased lysosomal mass, high mitophagy activity and exhibit greater cancer stem cell (CSC) characteristics.

- High levels of basal mitophagy in CSCs lead to increased levels of both ATP and antioxidant capacity, ultimately contributing to improved mitochondrial function as OCR.

Point of Interest

- Neurons undergo mitophagy and transfer lipid to glia to avoid oxidative mitochondria.

- Lipid droplet accumulation in glia contributes to neuroprotection and maintenance of neuronal mitochondrial activity (mmembrane potential).

- A full night's sleep is essential for glial lipid droplet clearance, neuronal and glial mitochondrial recovery.

Point of Interest

- Basal mitophagy in primary human cells is highly active compared to that in cell lines previously used in mitophagy studies.

- Mitochondria-derived ROS trigger mitophagy via superoxide production, influenced by mitochondrial dynamics, damage, and senescence processes.

- Loss of mitophagy drives cellular senescence phenotypes, whereas activation of mitophagy rescues senescence-related changes in cell function.

Co-staining of Lysosome and Mitophagy

We performed fluorescence imaging by stimulating mitophagy induction in SHSY-5Y cells stained with Mitophagy Detection(Code: MD01) and LysoPrime Green or existing products. The fluorescence signal of LysoPrime Green did not decrease and the lysosomal localization over time was confirmed. This means that the co-localization rate of the fluorescent spots of the Mtphagy Dye is higher than that of the existing product, and thus more accurate mitophagy analysis can be performed.

LysoPrime Green: Ex= 488 nm, Em= 500-570 nm
Mtphagy Dye: Ex= 561 nm, Em= 560-650 nm

Products in Use
   - LysoPrime Green
   - Mitophagy Detection Kit and Mtphagy Dye

Lysosomal Function and Mitochondrial ROS

CCCP and Antimycin are recognized inducers of mitochondrial ROS, linked to the loss of mitochondrial membrane potential. Recent studies have shown that CCCP induces not only mitochondrial ROS but also lysosomal dysfunction. To observe mitochondrial ROS, HeLa cells were labeled with MitoBright ROS Deep Red for Mitochondrial Superoxide Detection, and the lysosomal mass and pH were independently detected with LysoPrime Green and pHLys Red. Co-staining with MitoBright ROS and Lysosomal dyes revealed that CCCP, unlike Antimycin, triggers concurrent lysosomal neutralization and mitochondrial ROS induction.

Reference: Benjamin S Padman, et. al., Autophagy (2013)

Products in Use
   - LysoPrime Green
   - pHLys Red
   - Lysosomal Acidic pH Detection Kit
   - MitoBright ROS - Mitochondrial Superoxide Detection