The effects of colony-stimulating factor 1 (CSF-1), the primary regulator of mononuclear phagocyte production, are thought to be mediated by the CSF-1 receptor (CSF-1R), encoded by the c-fms proto-oncogene. To investigate the in vivo specificity of CSF-1 for the CSF-1R, the mouse IntroductionColony-stimulating factor 1 (CSF-1) regulates the survival, proliferation, and differentiation of mononuclear phagocytic cells and is the primary regulator of mononuclear phagocyte production in vivo. 1,2 However, CSF-1 also regulates cells of the female reproductive tract and plays an important role in fertility. 3,4 The effects of CSF-1 are mediated by a high-affinity receptor tyrosine kinase (CSF-1R) [5][6][7][8] encoded by the c-fms proto-oncogene. 9 The CSF-1R is expressed on primitive multipotent hematopoietic cells, 10,11 mononuclear phagocyte progenitor cells, 12 monoblasts, promonocytes, monocytes, 5,6 tissue macrophages, 6,13-15 osteoclasts, 16 B cells, 17,18 smooth muscle cells, 19 and neurons. 20,21 CSF-1R messenger RNA (mRNA) is expressed in Langerhans cells, 22 in the female reproductive tract, in oocytes and embryonic cells of the inner cell mass and trophectoderm, 23 in decidual cells, [24][25][26] and in cells of the trophoblast. 24,25 The expression of the CSF-1R on primitive hematopoietic cells that are unable to proliferate in vitro in response to CSF-1 alone 10,11 but are able to proliferate and differentiate if stimulated with combinations of CSF-1 and other hematopoietic growth factors 10,11,27 suggests that CSF-1R is involved in the regulation of more primitive hematopoietic cells than those that form macrophage colonies in vitro in response to CSF-1 alone.Mice homozygous for the mutation osteopetrotic 28 possess an inactivating mutation in the coding region of the CSF-1 gene and are devoid of detectable CSF-1. 29,30 These Csf1 op /Csf1 op mice are osteopetrotic because of an early and marked deficiency of osteoclasts 28 that spontaneously recovers with age, 31,32 probably because of the action of vascular endothelial growth factor. 33 However, the phenotype of these mice is pleiotropic. 3 They are toothless; have low body weight, low growth rate, and skeletal abnormalities; and are deficient in tissue macrophages. 2,28,30,34,35 They have defects in both male and female fertility, neural development, the dermis, and synovial membranes. 3 The pleiotropic phenotype of the Csf1 op /Csf1 op mouse may be due to a reduction in trophic and/or scavenger functions of the tissue macrophages regulated by CSF-1, secondary to the reduction of their concentration in tissues, 2 because outside the female reproductive tract the CSF-1R is primarily expressed in mononuclear phagocytes. 1,3 However, it is possible that some of these effects may also be due to loss of function of other cells such as neuronal cells and muscle precursors, which have also been reported to express the CSF-1R. 20,36 To address the questions of whether CSF-1 activates other receptors besides the CSF-1R and, conversely, whether the CSF-1R me...

No abstract

In skeletal muscle isoenzymes of CK were determined by immunprecipitation and chromatography. The activity of CK-MB was between 17 and 47 U/g muscle, corresponding to a quota between 2,1 and 4,2% of the total activity. In sera of patients with muscular dystrophy, polymyositis, hypothyroidism, after arterial embolism, epilepsy, hyperventilation, operations and polytrauma with and without injury to the thorax isoenzymes were measure by immune precipitation- and immune inhibition-test. The percentage of CK-MB in all sera was less than 6% of the total CK-activity (range: 0 to 6%). Only patients in the first day after neurosurgical operations showed a quota till to 6.5% CK-MB. In serum of patients after polytrauma without injury to the thorax the percentage of CK-MB ranged from 0-5.7% while after polytrauma with injury to the thorax and a reasonable suspicion of a damage to the myocardium this quota was between 5.1 and 23.6% of the total activity. CK-BB activity was not detectable in any cases. Therefore a disease or damage of the skeletal muscle is more probable, if the percentage of CK-MB in less than 6%, because in sera of patients with myocardial infarction in the first 48 h after beginning of the symptoms this quota of CK-MB in the most cases in more than 6%.

No abstract