The synthesis of glycoprotein Po and peripheral myelin protein 22 in sciatic nerve of male rats is modulated by testosterone metabolites

Magnaghi, Valerio; Ballabio, M.; González, Laura; Leonelli, Emanuela; Motta, Marcella; Melcangi, Roberto Cosimo

doi:10.1016/j.molbrainres.2004.03.009

Cited by 29 publications

(32 citation statements)

References 36 publications

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“…Effects of steroids on the expression of myelin proteins (D esarnaud et al, 1998, 2000Magnaghi et al, 2001Magnaghi et al, , 2004Melcangi et al, 1999bMelcangi et al, , 2000a and of transcription factors regulating the expression of myelin proteins Mercier et al, 2001) have been detected in Schwann cells and oligodendrocytes (Ghoumari et al, 2003;Ibanez et al, 2003;Jung-Testas et al, 1992). These effects are important for the regulation of myelin formation and myelin regeneration by steroids and will be discussed in detail later.…”

Section: Glial Cell Responses To Steroid Actionsmentioning

confidence: 96%

Steroids and glial cell function

Garcia-Segura¹,

Melcangi²

2006

Glia

176

131

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Hormonal and locally produced steroids act in the nervous system as neuroendocrine regulators, as trophic factors and as neuromodulators and have a major impact on neural development and function. Glial cells play a prominent role in the local production of steroids and in the mediation of steroid effects on neurons and other glial cells. In this review, we examine the role of glia in the synthesis and metabolism of steroids and the functional implications of glial steroidogenesis. We analyze the mechanisms of steroid signaling on glia, including the role of nuclear receptors and the mechanisms of membrane and cytoplasmic signaling mediated by changes in intracellular calcium levels and activation of signaling kinases. Effects of steroids on functional parameters of glia, such as proliferation, myelin formation, metabolism, cytoskeletal reorganization, and gliosis are also reviewed, as well as the implications of steroid actions on glia for the regulation of synaptic function and connectivity, the regulation of neuroendocrine events, and the response of neural tissue to injury. © 2006 Wiley‐Liss, Inc.

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Section: Glial Cell Responses To Steroid Actionsmentioning

confidence: 96%

Steroids and glial cell function

Garcia-Segura¹,

Melcangi²

2006

Glia

176

131

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“…In support of these findings in the male sciatic nerve, DHT and 3α-diol increase P0 and PMP22 mRNA levels, respectively, in cultured rat Schwann cells [30,52]. In confirmation of a role for AR in controlling P0 expression, in vivo treatment with an AR antagonist like flutamide decreases P0 synthesis in the rat sciatic nerve [53]. Interestingly, inhibition of AR influences P0 synthesis in adult animals only.…”

Section: Schwann Cell Responses To Neuroactive Steroidsmentioning

confidence: 74%

“…In further support of the effect of THP on the GABA A receptor is the finding that isopregnanolone, which does not interact with GABA A receptor, does not alter PMP22 expression. Moreover, among the T derivatives tested so far, only 3α-diol which binds to the GABA A receptor increases PMP22 mRNA levels [52,53]. Taken together, these data indicate that GABA A receptors are important mediators of the effects of THP on PMP22 expression.…”

Section: Schwann Cell Responses To Neuroactive Steroidsmentioning

confidence: 93%

“…In adult male rats, castration decreases the expression of P0 mRNA in the sciatic nerve, while subsequent treatment with DHT or 3α-diol restores P0 mRNA to precastration levels [30,53]. Castration also decreases PMP22 mRNA levels in the sciatic nerve, but only 3α-diol treatment restores PMP22 levels [53]. In support of these findings in the male sciatic nerve, DHT and 3α-diol increase P0 and PMP22 mRNA levels, respectively, in cultured rat Schwann cells [30,52].…”

Section: Schwann Cell Responses To Neuroactive Steroidsmentioning

confidence: 99%

See 1 more Smart Citation

Neuroactive Steroids and Peripheral Neuropathy

Melcangi

Giatti

Pesaresi

et al. 2011

Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis

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Peripheral neuropathy, either inherited or acquired, is a very common disorder for which effective clinical treatments are not yet available. Neuroactive steroids such as progesterone, testosterone, and their reduced metabolites represent a promising therapeutic option for peripheral neuropathy. Peripheral nerves are able to synthesize and metabolize neuroactive steroids and are a target for these molecules since they express classical and nonclassical steroid receptors. Neuroactive steroids modulate the expression of key transcription factors (TFs) for Schwann cell function, regulate Schwann cell proliferation, and promote the expression of myelin proteins. Interestingly, they are also able to counteract biochemical, morphological, and functional alterations of peripheral nerves in different experimental models of neuropathy, including the alterations caused by aging, diabetic neuropathy, and physical injury. Therefore, neuroactive steroids and pharmacological agents that are able to increase their local synthesis and the synthetic ligands for their receptors offer a promising potential for the treatment of different forms of peripheral neuropathy.

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“…Other gonadal steroids may also affect the synthesis of these myelin proteins. For instance, in adult male rats, castration decreases the expression of P0 and of PMP22 in the sciatic nerve [96,97]. These effects are counteracted by the treatment with neuroactive metabolites of testosterone, such as DHTor 3a-androstanediol (3a-diol) in case of P0 and by the treatment with 3a-diol in case of PMP22 [97].…”

Section: Figurementioning

confidence: 99%