{'fraction_non_alphanumeric': 0.031001589825119236, 'fraction_numerical': 0.014308426073131956, 'mean_word_length': 4.938679245283019, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Colony-stimulating factor 1 (CSF-1) is involved in an autocrine growth control of rat myogenic cells.

Colony stimulating factor-1 (CSF-1) and the CSF-1 receptor (the c-fms proto-oncogene product) are expressed during the proliferation of the L6 alpha 1 rat myogenic cell line and both are down-regulated during the differentiation to myotubes. Biologically active CSF-1 was shown to be secreted into the culture medium by L6 alpha 1 myoblasts and while they could not bind CSF-1, evidence was obtained for cell surface receptor-CSF-1 complexes. It was not possible to block the L6 alpha 1 proliferation by incubation with anti-CSF-1 antiserum or suramin. However, in L6 alpha 1 myoblasts that were stably transfected with an inducible anti-fms antisense construct, both c-fms protein expression and cell proliferation were more rapidly inhibited under induction and differentiation conditions than parental cells. Furthermore, under these conditions, the c-fms antisense transfected cells also entered myogenic differentiation more rapidly. These results suggest that autocrine regulation by CSF-1 that is intracellular may play a role in the proliferation of muscle cells and that its down-regulation leads to, and may be an obligatory step in, myogenesis.