Organic dust exposure induces stress response and mitochondrial dysfunction in monocytic cells.
Histochem Cell Biol
; 155(6): 699-718, 2021 Jun.
Article
en En
| MEDLINE
| ID: mdl-33755775
ABSTRACT
Exposure to airborne organic dust (OD), rich in microbial pathogen-associated molecular patterns (PAMPs), is shown to induce lung inflammation. A common manifestation in lung inflammation is altered mitochondrial structure and bioenergetics that regulate mitochondrial ROS (mROS) and feed a vicious cycle of mitochondrial dysfunction. The role of mitochondrial dysfunction in other airway diseases is well known. However, whether OD exposure induces mitochondrial dysfunction remains elusive. Therefore, we tested a hypothesis that organic dust extract (ODE) exposure induces mitochondrial stress using a human monocytic cell line (THP1). We examined whether co-exposure to ethyl pyruvate (EP) or mitoapocynin (MA) could rescue ODE exposure induced mitochondrial changes. Transmission electron micrographs showed significant differences in cellular and organelle morphology upon ODE exposure. ODE exposure with and without EP co-treatment increased the mtDNA leakage into the cytosol. Next, ODE exposure increased PINK1, Parkin, cytoplasmic cytochrome c levels, and reduced mitochondrial mass and cell viability, indicating mitophagy. MA treatment was partially protective by decreasing Parkin expression, mtDNA and cytochrome c release and increasing cell viability.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Monocitos
/
Polvo
/
Exposición a Riesgos Ambientales
/
Mitocondrias
Límite:
Humans
Idioma:
En
Revista:
Histochem Cell Biol
Asunto de la revista:
CITOLOGIA
/
HISTOCITOQUIMICA
Año:
2021
Tipo del documento:
Article
País de afiliación:
Estados Unidos