pubmed-article:10495408 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10495408 | lifeskim:mentions | umls-concept:C0596995 | lld:lifeskim |
pubmed-article:10495408 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:10495408 | lifeskim:mentions | umls-concept:C0021665 | lld:lifeskim |
pubmed-article:10495408 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:10495408 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
pubmed-article:10495408 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
pubmed-article:10495408 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:10495408 | pubmed:dateCreated | 2000-5-1 | lld:pubmed |
pubmed-article:10495408 | pubmed:abstractText | Insulin-like growth factor-I (IGF-I) has been shown to stimulate myoblast proliferation for a limited time after which serum is required to reactivate IGF-I-stimulated myoblast proliferation. The aim of these studies was to determine whether IGF-I can stimulate myoblast proliferation and/or inhibit apoptosis alone or whether co-factors are necessary. This was achieved by investigating the proliferative response of L6 myoblasts to IGF-I and horse serum (HS) and by examining the status of cells in terms of cell number, substrate adherence, cell viability and DNA laddering following incubation with IGF-I and HS. L6 myoblasts proliferate in response to IGF-I after 36 h is not due to accumulation of waste products or lack of IGF-I. The addition of a low level (1% v/v) of HS restores the ability of myoblasts to proliferate in response to IGF-I and this supports the existence of a mitogenic competence factor. Furthermore, myoblasts failing to proliferate in response to IGF-I after 36 h regain the capacity to respond to IGF-I for a further period of 36 h when exposed to fetal bovine serum. Following the initial (36 h) phase of IGF-I-stimulated proliferation, removal of both IGF-I and HS led to a dramatic (60%) reduction in the number of cells fully attached to the culture vessel, with 60% of the completely detached cells dead. Agarose gel electrophoresis of extracts from these detached cells revealed higher levels of DNA laddering than extracts prepared from attached cells with IGF-I present. This suggests that IGF-I acts as a survival factor by protecting cells from apoptosis. In conclusion these experiments support the presence of a mitogenic competence factor in horse serum, which restores the ability of cells to proliferate in response to IGF-I. Unlike proliferation, protection against apoptosis is achieved by IGF-I or HS independently of each other. | lld:pubmed |
pubmed-article:10495408 | pubmed:language | eng | lld:pubmed |
pubmed-article:10495408 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10495408 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10495408 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10495408 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10495408 | pubmed:month | Oct | lld:pubmed |
pubmed-article:10495408 | pubmed:issn | 0022-0795 | lld:pubmed |
pubmed-article:10495408 | pubmed:author | pubmed-author:HodgkinsonS... | lld:pubmed |
pubmed-article:10495408 | pubmed:author | pubmed-author:BassJ JJJ | lld:pubmed |
pubmed-article:10495408 | pubmed:author | pubmed-author:SharmaMM | lld:pubmed |
pubmed-article:10495408 | pubmed:author | pubmed-author:ThomasM FMF | lld:pubmed |
pubmed-article:10495408 | pubmed:author | pubmed-author:NapierJ RJR | lld:pubmed |
pubmed-article:10495408 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10495408 | pubmed:volume | 163 | lld:pubmed |
pubmed-article:10495408 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10495408 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10495408 | pubmed:pagination | 63-8 | lld:pubmed |
pubmed-article:10495408 | pubmed:dateRevised | 2004-11-17 | lld:pubmed |
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pubmed-article:10495408 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10495408 | pubmed:articleTitle | Insulin-like growth factor-I protects myoblasts from apoptosis but requires other factors to stimulate proliferation. | lld:pubmed |
pubmed-article:10495408 | pubmed:affiliation | AgResearch Ltd, Private Bag 3123, Hamilton, New Zealand. | lld:pubmed |
pubmed-article:10495408 | pubmed:publicationType | Journal Article | lld:pubmed |