Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-1-12
pubmed:abstractText
Colony-stimulating factor-1 (CSF-1) is the principal regulator of cells of the mononuclear phagocytic lineage that includes monocytes, tissue macrophages, microglia, and osteoclasts. Macrophages are found throughout the reproductive tract of both males and females and have been proposed to act as regulators of fertility at several levels. Mice homozygous for the osteopetrosis mutation (csfm[op]) lack CSF-1 and, consequently, have depleted macrophage numbers. Further analysis has revealed that male csfm(op)/csfm(op) mice have reduced mating ability, low sperm numbers, and 90% lower serum testosterone levels. The present studies show that this low serum testosterone is due to reduced testicular Leydig cell steroidogenesis associated with severe ultrastructural abnormalities characterized by disrupted intracellular membrane structures. In addition, the Leydig cells from csfm(op)/ csfm(op) males have diminished amounts of the steroidogenic enzyme proteins P450 side chain cleavage, 3beta-hydroxysteroid dehydrogenase, and P450 17alpha-hydroxylase-lyase, with associated reductions in the activity of all these steroidogenic enzymes, as well as in 17beta-hydroxysteroid dehydrogenase. The CSF-1-deficient males also have reduced serum LH and disruption of the normal testosterone negative feedback response of the hypothalamus, as demonstrated by the failure to increase LH secretion in castrated males and their lack of response to exogenous testosterone. However, these males are responsive to GnRH and LH treatment. These studies have identified a novel role for CSF-1 in the development and/or regulation of the male hypothalamic-pituitary-gonadal axis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1636-50
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9328346-17-Hydroxysteroid Dehydrogenases, pubmed-meshheading:9328346-3-Hydroxysteroid Dehydrogenases, pubmed-meshheading:9328346-Adrenal Glands, pubmed-meshheading:9328346-Adrenal Hyperplasia, Congenital, pubmed-meshheading:9328346-Animals, pubmed-meshheading:9328346-Chorionic Gonadotropin, pubmed-meshheading:9328346-Female, pubmed-meshheading:9328346-Follicle Stimulating Hormone, pubmed-meshheading:9328346-Genotype, pubmed-meshheading:9328346-Gonadotropin-Releasing Hormone, pubmed-meshheading:9328346-Hypothalamo-Hypophyseal System, pubmed-meshheading:9328346-Infertility, Male, pubmed-meshheading:9328346-Intracellular Membranes, pubmed-meshheading:9328346-Leydig Cells, pubmed-meshheading:9328346-Luteinizing Hormone, pubmed-meshheading:9328346-Macrophage Colony-Stimulating Factor, pubmed-meshheading:9328346-Macrophages, pubmed-meshheading:9328346-Male, pubmed-meshheading:9328346-Mice, pubmed-meshheading:9328346-Mice, Mutant Strains, pubmed-meshheading:9328346-Osteopetrosis, pubmed-meshheading:9328346-Testis, pubmed-meshheading:9328346-Testosterone
pubmed:year
1997
pubmed:articleTitle
Colony-stimulating factor-1 plays a major role in the development of reproductive function in male mice.
pubmed:affiliation
Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't