Difference between revisions of "Kopitar-Jerala 2017 Abstract MITOEAGLE Barcelona"

Revision as of 11:02, 27 February 2017

Link: MITOEAGLE

(2017)

Event: MITOEAGLE Barcelona 2017

The mitochondrion plays a critical role in cell survival, most prominently by generating the vast majority of a cell’s supply of adenosine triphosphate (ATP), but also by influencing apoptosis, cell cycle, and metabolism. Mitochondria generate ATP through aerobic respiration, whereby glucose, pyruvate, and NADH are oxidized, thus generating ROS as a byproduct. Several recent publications showed that mitochondrial ROS (mtROS) act as signaling molecules to trigger pro-inflammatory cytokine production (Nakahira et al., 2011; Zhou et al., 2011). A recent study implicated mitochondrial complex I in LPS induction of cytokines in macrophages. It was reported that metformin, mitochondria complex I inhibitor, decreased production of the pro-form of the inflammatory cytokine IL-1β and increased the expression of the anti-inflammatory cytokine IL-10, in response to LPS in macrophages (Kelly et al., 2015).

Stefin B (cystatin B) is an endogenous cysteine cathepsin inhibitor, and the loss-of-function mutations in the stefin B gene were reported in patients with Unverricht-Lundborg disease (EPM1). Recently, several studies implicated increased oxidative stress and inflammation in the pathology of the disease (Kopitar-Jerala et al., 2005, Lehtinen et al., 2009, Maher et al, 2014, Joensuu et al. 2014, Korber et al., 2016, Kopitar-Jerala, 2015, Okuneva et al. 2016). In stefin B deficient macrophages we reported decreased IL-10 expression upon LPS stimulation and increased NLRP3 inflammasome activation Upon LPS stimulation, stefin B was targeted into the mitochondria, and the lack of stefin B resulted in the increased destabilization of mitochondrial membrane potential and mitochondrial superoxide generation (Maher et al., 2014). The possible role of stefin B in mitochondria will be discussed.

• Bioblast editor: Kandolf G

Labels: Pathology: Inherited Stress:Oxidative stress;RONS

Regulation: Inhibitor

Event: B2

Affiliations

Dept Biochem, Molecular Structural Biol, Ljubljana, Slovenia.

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 |title=[[File:MITOEAGLE-representation.jpg|left|60px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
 |info=[[MITOEAGLE]]
-|authors=
 |year=2017
 |event=MITOEAGLE Barcelona 2017
 |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MITOEAGLE]]
+The mitochondrion plays a critical role in cell survival, most prominently by generating the vast majority of a cell’s supply of adenosine triphosphate (ATP), but also by influencing apoptosis, cell cycle, and metabolism. Mitochondria generate ATP through aerobic respiration, whereby glucose, pyruvate, and NADH are oxidized, thus generating ROS as a byproduct. Several recent publications showed that mitochondrial ROS (mtROS) act as signaling molecules to trigger pro-inflammatory cytokine production (Nakahira et al., 2011; Zhou et al., 2011). A recent study implicated mitochondrial complex I in LPS induction of cytokines in macrophages. It was reported that metformin, mitochondria complex I inhibitor, decreased production of the pro-form of the inflammatory cytokine IL-1β and increased the expression of the anti-inflammatory cytokine IL-10, in response to LPS in macrophages (Kelly et al., 2015).
+Stefin B (cystatin B) is an endogenous cysteine cathepsin inhibitor, and the loss-of-function mutations in the stefin B gene were reported in patients with Unverricht-Lundborg disease (EPM1).  Recently, several studies implicated increased oxidative stress and inflammation in the pathology of the disease (Kopitar-Jerala et al., 2005, Lehtinen et al., 2009, Maher et al, 2014, Joensuu et al. 2014, Korber et al., 2016, Kopitar-Jerala, 2015, Okuneva et al. 2016). In stefin B deficient macrophages we reported decreased IL-10 expression upon LPS stimulation and increased NLRP3 inflammasome activation Upon LPS stimulation, stefin B was targeted into the mitochondria, and the lack of stefin B resulted in the increased destabilization of mitochondrial membrane potential and mitochondrial superoxide generation (Maher et al., 2014). The possible role of stefin B in mitochondria will be discussed.
+|editor=[[Kandolf G]],
+}}
+{{Labeling
+|diseases=Inherited
+|injuries=Oxidative stress;RONS
+|topics=Inhibitor
+|event=B2
 }}
 == Affiliations ==
-:::: (1)
+:::: Dept Biochem,  Molecular Structural Biol, Ljubljana, Slovenia.
-::::#
-== Figure 1 ==
-== References ==
-:::#