title: Progesterone increases the expression of myelin basic protein and the number of cells showing NG2 immunostaining in the lesioned spinal cord.
abstract: It is now widely accepted that progesterone (PROG) brings neuroprotection in lesions of the peripheral and central nervous system. Spinal cord trauma leads to neuronal degeneration, astrogliosis, demyelination, and proliferation of oligodendrocyte-precursor cells (OPCs). In this work, we studied the effects of PROG on myelin-related parameters in rats with complete spinal cord transection (TRX). To this end, sham-operated controls and rats with TRX at thoracic level T10 received vehicle or PROG (4 mg/kg/day) during 3 days. Three variables were measured in the lumbar L4 region below the lesion: (1) expression of myelin basic protein (MBP) at the protein and mRNA levels; (2) density of NG2-immunopositive cells as markers for OPCs; and (3) number of cells immunopositive for RIP, an antibody staining mature oligodendrocytes. TRX decreased MBP immunostaining in the corticospinal tract (CST) and dorsal ascending tract (DAT) but not the ventral funiculus (VF). NG2+ cells, which were detected in low number in controls, increased after TRX in the gray and white matter. RIP-positive cell number, however, remained unchanged. PROG treatment of rats with TRX enhanced the expression of MBP protein and mRNA in CST and DAT, but not VF and highly stimulated the number of cells showing NG2 immunostaining over untreated lesioned rats. Instead, density of RIP positive cells was similar in the PROG-treated and untreated lesioned groups. We propose that PROG effects on expression of MBP and the number of NG2 immunopositive cells may contribute to neuroprotection, as they go in parallel with previous results showing enhanced biochemical and morphological parameters of motoneurons of animals with TRX receiving PROG treatment.
authors.affiliation: Laboratory of Neuroendocrine Biochemistry, Institute of Experimental Biology and Medicine, and Department of Human Biochemistry, Faculty of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
authors.forename: Florencia
authors.initials: F
authors.lastname: Labombarda
authors.forename: Susana
authors.initials: S
authors.lastname: Gonzalez
authors.forename: Maria Claudia
authors.initials: MC
authors.lastname: Gonzalez Deniselle
authors.forename: Laura
authors.initials: L
authors.lastname: Garay
authors.forename: Rachida
authors.initials: R
authors.lastname: Guennoun
authors.forename: Michael
authors.initials: M
authors.lastname: Schumacher
authors.forename: Alejandro F
authors.initials: AF
authors.lastname: De Nicola
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism*; D002452:Cell Count; D008297:Male; D004676:Myelin Basic Protein / Q000235:genetics / Q000378:metabolism*; D009836:Oligodendroglia / Q000378:metabolism*; D011374:Progesterone / Q000627:therapeutic use*; D011509:Proteoglycans / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D013234:Stem Cells; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D004676:Myelin Basic Protein; D011374:Progesterone; D011509:Proteoglycans; D012333:RNA, Messenger; D000099216:Chondroitin Sulfate Proteoglycan 4