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Progesterone Treatment of Spinal Cord Injury: Effects on Receptors, Neurotrophins, and Myelination
Open accessAbstract
In addition to its traditional role in reproduction, progesterone (PROG) has demonstrated neuroprotective and promyelinating effects in lesions of the peripheral and central nervous systems, including the spinal cord. The latter is a target of PROG, as nuclear receptors, as well as membrane receptors, are expressed by neurons and/or glial cells. When spinal cord injury (SCI) is produced at the thoracic level, several genes become sensitive to PROG in the region caudal to the lesion site. Although the cellular machinery implicated in PROG neuroprotection is only emerging, neurotrophins, their receptors, and signaling cascades might be part of the molecules involved in this process. In rats with SCI, a 3-d course of PROG treatment increased the mRNA of brain-derived neurotrophic factor (BDNF) and BDNF immunoreactivity in perikaryon and processes of motoneurons, whereas chromatolysis was strongly prevented. The increased expression of BDNF correlated with increased immunoreactivity for the BDNF receptor TrkB and for phosphorylated cAMP-responsive element binding in motoneurons. In the same SCI model, PROG restored myelination, according to measurements of myelin basic protein (MBP) and mRNA levels, and further increased the density of NG2+-positive oligodendrocyte progenitors. These cells might be involved in remyelination of the lesioned spinal cord. Interestingly, similarities in the regulation of molecular parameters and some cellular events attributed to PROG and BDNF (i.e., choline acetyltransferase, Na,K-ATPase, MBP, chromatolysis) suggest that BDNF and PROG might share intracellular pathways. Furthermore, PROG-induced BDNF might regulate, in a paracrine or autocrine fashion, the function of neurons and glial cells and prevent the generation of damage.
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“…failure of repair in chronic lesions are not fully understood, although several possible mechanisms, including expression of inhibitory molecules and alterations in hormone levels, have been described (Back et al. 2005; De Nicola et al. 2006; Fernandez et al. 2004; Warrington and Rodriguez 2008).”
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“…neurodegeneration, progesterone increases myelination, sustains neuronal viability, and reduces the inflammatory response (Azcoitia et al. 2003; De Nicola et al. 2006; Desarnaud et al. 1998; Ghoumari et al. 2003; Gonzalez et al. 2005; Gonzalez Deniselle et al. 2003; Grossman et al. 2004; Ibanez…”
Self-citationMyelin Pathogenesis and Functional Deficits Following SCI are Age-Associated
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“…a role in the marked decrease in repair mechanisms following injury, such as remyelination (Arsenijevic and Weiss, 1998; Cheng and Mattson, 1994; De Nicola et al., 2006; Du et al., 2003; Ibanez et al., 2003; Koenig et al., 1995; Kokaia et al., 1994; Larsson et al., 1999; Lindvall et al., 1994;…”
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“…vascular endothelial growth factor (VEGF; Swiatek-De Lange et al., 2007), brain-derived neurotrophic factor (BDNF; Gonzalez et al., 2004, 2005; De Nicola et al., 2006; Gonzalez Deniselle et al., 2007; Kaur et al., 2007), and insulin/insulin-like growth factor-I (IGF-I; Dueñas et al., 1994;…”
BackgroundInfluentialProgress in progestin-based therapies for neurological disorders
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Self-citationEstrogen induced changes in uterine brain-derived neurotrophic factor and its receptors
Wessels, J. M., Leyland, N. A., Agarwal, S. K., & Foster, W. G. (2015) · Human Reproduction · doi:10.1093/humrep/dev018 · Cited by 35
“…(Kaur et al., 2007; Jodhka et al., 2009; Meyer et al., 2012; Su et al., 2012; Atif et al., 2013) and nervous system (Gonzalez et al., 2004, 2005; De Nicola et al., 2006; Gonzalez Deniselle et al., 2007; Cekic et al., 2012), and BDNF is expressed in luteinized granulosa cells (Dominguez et al.,…”
BackgroundEffects of progesterone on glucose uptake in neurons of Alzheimer's disease animals and cell models
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Self-citationPak, M. E., Jung, D. H., Lee, H. J., Shin, M., Kim, S.-Y., Shin, Y. B., Yun, Y.-J., Shin, H. K., & Choi, B. T. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.11.014 · Cited by 32
“These paracrine or autocrine functions effectively cause neuroregeneration, promoting the activation of endogenous neural stem/ progenitor cells (De Nicola et al., 2006; Shin et al., 2017; Zhao et al., 2004).”
Olfactory ensheathing glia: Repairing injury to the mammalian visual system
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“It could be argued that the appropriate culture conditions were not achieved; for example recent evidence has suggested that progesterone has promyelinating effects (De Nicola et al., 2006).”
Gender differences in the histopathology of MS?
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“Recent reports suggest that one potential mechanism is via the upregulation of endogenous BDNF (De Nicola et al., 2006; Gonzalez Deniselle et al., 2007; Gonzalez et al., 2004, 2005; Kaur et al., 2007).”
BackgroundResultInfluentialLimiting spinal cord injury by pharmacological intervention
Priestley, J. V., Michael-Titus, A. T., & Tetzlaff, W. (2012) · Handbook of clinical neurology · doi:10.1016/b978-0-444-52137-8.00029-2 · Cited by 23
“…hormone, progesterone is also synthesized in the CNS. Endogenous PH progesterone expression increases after SCI, and exogenous treatment upregulated brain-derived neurotrophic factor (BDNF) in motor neurons and appeared to prevent their SCI-induced atrophy (for review, see De Nicola et al., 2006).”
Regulatory role of cytochrome P450scc and pregnenolone in myelination by rat Schwann cells
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“steroid hormones and their roles in the regulation of myelin synthesis and repair in both the central and peripheral nervous systems have been investigated [7–16].”
BackgroundProgesterone improves neurocognitive outcomes following therapeutic cranial irradiation in mice
Yousuf, S., Brat, D. J., Shu, H. G., Wang, Y., Stein, D. G., & Atif, F. (2017) · Hormones and Behavior · doi:10.1016/j.yhbeh.2017.08.004 · Cited by 20
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Self-citationTitle : Novel perspectives for progesterone in HRT, with special reference to the nervous system
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Metadata
- Authors
- De Nicola, A. F., Gonzalez, S. L., Labombarda, F., Deniselle, M. C. G., Garay, L., Guennoun, R., & Schumacher, M.
- Affiliations
- Universidad de Buenos Aires (AR)
- Inserm (FR)
- Venue
- Journal of Molecular Neuroscience
- Published
- 2006
- Volume
- 28
- Issue
- 1
- Pages
- 3-16
- ISSN
- 0895-8696 (ISSN-L)
- OpenAlex
- W153328306
- Semantic Scholar
- 8ca69c844ba5b9c038c308d3f8e1aa7ece651fa0
- Cited by
- 92
- References
- 93
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 4 · 2018: 3 · 2017: 6 · 2016: 6 · 2015: 3 · 2014: 2 · 2013: 7 · 2012: 5
- FWCI
- 8.39
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-sa
- Locations
- Journal of Molecular Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
- Funders
- Consejo Nacional de Investigaciones Científicas y Técnicas
- Universidad de Buenos Aires (CONICET)
- Fondo para la Investigación Científica y Tecnológica
- Topics
- Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Keywords
- progesterone, spinal cord injury, neuroprotection, brain-derived neurotrophic factor, TrkB receptor, myelination, remyelination, oligodendrocyte progenitors, motor neurons, chromatolysis, myelin basic protein, nuclear receptors, paracrine signaling
- MeSH terms
- Animals, Myelin Basic Protein, Myelin Sheath, Neurons, Oligodendroglia, Progesterone, Receptors, Progesterone, Spinal Cord, Spinal Cord Injuries, Stem Cells, Cyclic AMP Response Element-Binding Protein, Neuroprotective Agents, Brain-Derived Neurotrophic Factor
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