Mitochondria and calcium flux as targets of neuroprotection caused by minocycline in cerebellar granule cells

Abstract

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Minocycline Blocks Asthma-associated Inflammation in Part by Interfering with the T Cell Receptor-Nuclear Factor κB-GATA-3-IL-4 Axis without a Prominent Effect on Poly(ADP-ribose) Polymerase

“…These reports may suggest a general broader effect, especially given the potential antioxidant property of these drugs and, more importantly, the high dosages used by the aforementioned studies. Our results and those recently published by some of us (49) clearly show that at concentrations higher than 10 M, minocycline harbors anti-oxidant properties. Accordingly, it is plausible that some of the effects observed with minocycline or other tetracycline derivatives may be attributed to their anti-oxidant functions.…”

VDAC as a Potential Target in Huntingtons Disease Therapy: The State of the Art

“…It has been shown that VDAC contributes to the processes directly or indirectly by interacting with the involved proteins. On the other hand, VDAC may promote cytoprotection including neuroprotection [77,109]. Thus, VDAC may play a central role in mitochondria dysfunction detected in HD ( Figure 1) and its attenuation and consequently in HD treatment.…”

Cytoprotective activity of minocycline includes improvement of mitochondrial coupling: the importance of minocycline concentration and the presence of VDAC

“…Therefore, it can be speculated that VDAC may be involved in minocycline transport across the outer membrane as proposed by Cuenca-Lopez et al (2011). Accordingly, it is known that minocycline is able to interact with VDAC (Garcia- Martinez et al 2010). Therefore, it can be also suggested that minocycline interaction with VDAC results in changes of properties of minocycline and/or VDAC.…”

“…On the other hand, data shown by Gieseler et al (2009) and Antonenko et al (2010) indicate that minocycline prevents MPP activation because of a direct inhibitory interaction with MPP or due to dissipation of the inner membrane potential by ion channels formed by minocycline in the inner mitochondrial membrane, respectively. Minocycline could also result in MPP modulation by affecting the activity of the voltage-dependent anion-selective channel (VDAC) located in the outer membrane, as well as the mitochondrial respiratory chain at the level of complexes I and IV (Garcia-Martinez et al 2010), adenine nucleotide translocase and mitochondrial ATP synthase (FernandezGomez et al 2005).…”

“…The presence of only one channel-forming VDAC isoform in S. cerevisiae mitochondria simplifies studies of the channel. Accordingly, it has been recently shown that the minocycline cytoprotective effect depends on the presence of VDAC (Gałgańska et al 2010), and minocycline modulates conductance of VDAC reconstituted in artificial membranes (Garcia-Martinez et al 2010). Therefore, a detailed description of cellular and molecular mechanisms surrounding VDAC and triggered by minocycline appears to be timely and necessary.…”