PMID- 16632872
OWN - NLM
STAT- MEDLINE
DCOM- 20060627
LR  - 20211020
IS  - 0895-8696 (Print)
IS  - 0895-8696 (Linking)
VI  - 28
IP  - 1
DP  - 2006
TI  - Progesterone treatment of spinal cord injury: Effects on receptors, 
      neurotrophins, and myelination.
PG  - 3-15
AB  - 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.
FAU - De Nicola, Alejandro F
AU  - De Nicola AF
AD  - Laboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina 
      Experimental, Buenos Aires, Argentina. denicola@dna.uba.ar
FAU - Gonzalez, Susana L
AU  - Gonzalez SL
FAU - Labombarda, Florencia
AU  - Labombarda F
FAU - Gonzalez Deniselle, Maria Claudia
AU  - Gonzalez Deniselle MC
FAU - Garay, Laura
AU  - Garay L
FAU - Guennoun, Rachida
AU  - Guennoun R
FAU - Schumacher, Michael
AU  - Schumacher M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Receptors, Progesterone)
RN  - 4G7DS2Q64Y (Progesterone)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Cyclic AMP Response Element-Binding Protein/*metabolism
MH  - Myelin Basic Protein/metabolism
MH  - Myelin Sheath/*metabolism
MH  - Neurons/cytology/metabolism
MH  - Neuroprotective Agents/metabolism/therapeutic use
MH  - Oligodendroglia/cytology/metabolism
MH  - Progesterone/metabolism/*therapeutic use
MH  - Receptors, Progesterone/metabolism
MH  - Spinal Cord/cytology/metabolism
MH  - Spinal Cord Injuries/*drug therapy/pathology
MH  - Stem Cells/cytology/physiology
RF  - 93
EDAT- 2006/04/25 09:00
MHDA- 2006/06/28 09:00
CRDT- 2006/04/25 09:00
PHST- 2005/06/21 00:00 [received]
PHST- 1999/11/30 00:00 [revised]
PHST- 2005/06/28 00:00 [accepted]
PHST- 2006/04/25 09:00 [pubmed]
PHST- 2006/06/28 09:00 [medline]
PHST- 2006/04/25 09:00 [entrez]
AID - JMN:28:1:3 [pii]
AID - 10.1385/jmn:28:1:3 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2006;28(1):3-15. doi: 10.1385/jmn:28:1:3.