Translocator protein (TSPO 18kDa) is expressed by neural stem and neuronal precursor cells

Varga, Balázs; Markó, Károly; Hádinger, Nóra; Jelitai, Márta; Demeter, Kornél; Tihanyi, Károly; Vas, Ádám; Madarász, Emı́lia

doi:10.1016/j.neulet.2009.06.051

Cited by 47 publications

(40 citation statements)

References 27 publications

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“…However, in developing or damaged neural regions, TSPO appears in differentiating/regenerating neurons similar to nestin. TSPO mRNA and protein, while missing from mature neurons, are present in neural stem cells and also in postmitotic neuronal precursors [47]. Further studies are needed to clarify how abundant TSPO expression is in our dedifferentiated melanocytes and how it translates to protein expression.…”

Section: Discussionmentioning

confidence: 99%

In Vitro Dedifferentiation of Melanocytes from Adult Epidermis

et al. 2011

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In previous work we described a novel culture technique using a cholera toxin and PMA-free medium (Mel-mix) for obtaining pure melanocyte cultures from human adult epidermis. In Mel-mix medium the cultured melanocytes are bipolar, unpigmented and highly proliferative. Further characterization of the cultured melanocytes revealed the disappearance of c-Kit and TRP-1 and induction of nestin expression, indicating that melanocytes dedifferentiated in this in vitro culture. Cholera toxin and PMA were able to induce c-Kit and TRP-1 protein expressions in the cells, reversing dedifferentiation. TRP-1 mRNA expression was induced in dedifferentiated melanocytes by UV-B irradiated keratinocyte supernatants, however direct UV-B irradiation of the cells resulted in further decrease of TRP-1 mRNA expression. These dedifferentiated, easily accessible cultured melanocytes provide a good model for studying melanocyte differentiation and possibly transdifferentiation. Because melanocytes in Mel-mix medium can be cultured with human serum as the only supplement, this culture system is also suitable for autologous cell transplantation.

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Section: Discussionmentioning

confidence: 99%

In Vitro Dedifferentiation of Melanocytes from Adult Epidermis

et al. 2011

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“…According to this study, the increase in [ 3 H] PK11195 binding in the spinal cord seems to occur in microglial cells. TSPO is strongly expressed in activated microglia (Benavides et al, 1983; Moynagh et al, 1991; Itzhak et al, 1993; Park et al, 1996; Karchewski et al, 2004; Hernstadt et al, 2009; Varga et al, 2009). Microglial TSPO requires a particular attention due the key role of this cell type in the initiation and maintenance of chronic pain states (Tsuda et al, 2005).…”

Section: Tspo Expression Possible Cell Cooperation and Signaling Mecmentioning

confidence: 99%

Analgesic strategies aimed at stimulating the endogenous production of allopregnanolone

Poisbeau

Keller

Aouad

et al. 2014

Front. Cell. Neurosci.

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A growing number of studies indicate that 3-alpha reduced neurosteroids are remarkable analgesics in various pain states. This is the case for allopregnanolone (AP), one of the most potent endogenous positive allosteric modulators of GABAA receptor function. From the pioneering work of Hans Selye, who described the sedative properties of steroids, synthetic compounds resembling the progesterone metabolite AP have been developed. If some of them have been used as anesthetics, it seems difficult to propose them as a therapeutic option for pain since they display several adverse side effects such as sedation, amnesia and functional tolerance. An alternative strategy, chosen by few laboratories around the world, is aimed at stimulating the local production of 3-alpha reduced neurosteroids in order to limit these well-known side effects. This pharmacological approach has the advantage of targeting specific structures, fully equipped with the necessary biosynthetic enzymatic machinery, where neurosteroids already act as endogenous pain modulators. The various pharmacological trials which attempted to treat pain symptoms by stimulating the production of 3-alpha reduced neurosteroids are reviewed here, as well as novel neurotransmitter systems possibly regulating their endogenous production.

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“…TSPO, which is ubiquitously expressed throughout the peripheral tissues although at various levels 8 is almost absent in healthy adult brain, 9 to instead accumulate in age-related degenerative disorders 10 and traumatic stress. 11 …”

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confidence: 99%

A role for TSPO in mitochondrial Ca2+ homeostasis and redox stress signaling

et al. 2017

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The 18 kDa translocator protein TSPO localizes on the outer mitochondrial membrane (OMM). Systematically overexpressed at sites of neuroinflammation it is adopted as a biomarker of brain conditions. TSPO inhibits the autophagic removal of mitochondria by limiting PARK2-mediated mitochondrial ubiquitination via a peri-organelle accumulation of reactive oxygen species (ROS). Here we describe that TSPO deregulates mitochondrial Ca2+ signaling leading to a parallel increase in the cytosolic Ca2+ pools that activate the Ca2+-dependent NADPH oxidase (NOX) thereby increasing ROS. The inhibition of mitochondrial Ca2+ uptake by TSPO is a consequence of the phosphorylation of the voltage-dependent anion channel (VDAC1) by the protein kinase A (PKA), which is recruited to the mitochondria, in complex with the Acyl-CoA binding domain containing 3 (ACBD3). Notably, the neurotransmitter glutamate, which contributes neuronal toxicity in age-dependent conditions, triggers this TSPO-dependent mechanism of cell signaling leading to cellular demise. TSPO is therefore proposed as a novel OMM-based pathway to control intracellular Ca2+ dynamics and redox transients in neuronal cytotoxicity.

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Translocator protein (TSPO 18kDa) is expressed by neural stem and neuronal precursor cells

Cited by 47 publications

References 27 publications

In Vitro Dedifferentiation of Melanocytes from Adult Epidermis

In Vitro Dedifferentiation of Melanocytes from Adult Epidermis

Analgesic strategies aimed at stimulating the endogenous production of allopregnanolone

A role for TSPO in mitochondrial Ca2+ homeostasis and redox stress signaling

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