Drosophila melanogaster mitochondrial Hsp22: a role in resistance to oxidative stress, aging and the mitochondrial unfolding protein response

Abstract

Aging is characterized by the accumulation of dysfunctional mitochondria. Since these organelles are involved in many important cellular processes, different mechanisms exist to maintain their integrity. Among them is the mitochondrial unfolding protein response, which triggers the expression of a set of proteins aimed at re-establishing mitochondrial homeostasis. The induction of mitochondrial chaperones expression, particularly of Hsp60 and Hsp70, is a hallmark of this pathway. In Drosophila melanogaster, Hsp22 is also up-regulated by mitochondrial stress. This small heat shock protein is one of the members of the family to be localized inside mitochondria. One characteristic of Drosophila Hsp22 is its preferential up-regulation during aging and in oxidative stress conditions. It is a beneficial protein since its over-expression increases lifespan and resistance to stress while its down-regulation is detrimental. This review focuses on Drosophila Hsp22 and its links with the mitochondrial unfolding protein response and the aging process, in addition to highlight the important role of this sHSP in mitochondrial homeostasis.

Tat-HSP22 inhibits oxidative stress-induced hippocampal neuronal cell death by regulation of the mitochondrial pathway

“…Tat-HSP22 protein significantly prevented mitochondrial dysfunction and inhibited the release of cytochrome c from mitochondria to cytosol as well as inhibited cell death via regulation of the expression of the apoptotic proteins Bax, Bcl-2, and active caspase-3. Corroborating our results, other studies have demonstrated that overexpression of HSP22 protein increase resistance to oxidative stress and prevents mitochondrial dysfunction by reducing ROS production during the aging process of flies [14]. Also, overexpression of HSP22 protein inhibits the mitochondria dependent apoptosis through regulation of pro-apoptotic and anti-apoptotic proteins expression in myocardial infarction [41].…”

“…The mitochondria play an important role in multiple cellular processes including apoptosis [14]. Mitochondria are known as one of the major sources of reactive oxygen species (ROS) production as a by-product of cellular processes.…”

“…Mitochondria are known as one of the major sources of reactive oxygen species (ROS) production as a by-product of cellular processes. Excessive ROS causes damage to macromolecules, subsequently leading to mitochondria dysfunction and cell death [14–16]. Other studies have showed that mitochondrial dysfunction is associated with ROS production and mitochondria as well as with ischemic damage [12–16].…”

MicroRNA miR-1002 enhances NMNAT-mediated stress response by modulating alternative splicing

“…The modest reduction in thermotolerance suggests that miR-1002 is one of the key players in the complex stress response network. Many other genes and proteins including heat shock proteins (HSPs) have been found to contribute to stress resistance (Bartelt-Kirbach et al, 2016;Jo et al, 2017;Kawasaki et al, 2016;Morrow et al, 2016;Shukla et al, 2014).…”

Phenotypic and transcriptomic responses to stress differ according to population geography in an invasive species

“…Exposure to paraquat leads to the production of ROS (reactive oxygen species) and has often been used in the lab as a proxy to study oxidative stress [31][32][33][34]. Resistance to oxidative stress has been associated with extended lifespan [34][35][36], a trait possibly under selection during invasion of a new area. Furthermore, paraquat has been banned since 2007 in Europe but is still used in the U.S.A and Japan.…”