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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2002-7-31
pubmed:abstractText
This study aims to investigate the expression of heparin-binding epidermal growth factor-like growth factor (HB-EGF) and its role in regulating apoptosis of human luteinized granulosa cells (LGC). By using RT-PCR and immunocytochemistry, the expression of HB-EGF and the EGF receptor family was demonstrated. HER4, one of the two cognate receptors for HB-EGF, was found translocated into the nucleus. HB-EGF exists in two forms, the precursor membrane-anchored form and the mature secreted form. Addition of recombinant HB-EGF, which acts as the secreted form, into the cell culture inhibited apoptosis and appeared to stimulate mitosis, indicating that the secreted form is potentially an anti-apoptotic factor and a mitogen for LGC. In contrast, CRM197, a specific inhibitor for the interaction between HB-EGF and the EGF receptor, inhibited rather than enhanced apoptosis, suggesting that the membrane-anchored form constitutively functions as a pro-apoptotic factor for LGC. Furthermore, the finding that apoptosis inhibition by CRM197 in the aggregate cells was much more pronounced than in the single cells indicates that pro-apoptotic activity was carried out in a juxtacrine fashion, as would be expected for the membrane-anchored form of HB-EGF. These data suggest that HB-EGF may be a unique regulator of LGC apoptosis, with two functionally opposing products arising from the same gene.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1360-9947
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
734-41
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
The soluble and membrane-anchored forms of heparin-binding epidermal growth factor-like growth factor appear to play opposing roles in the survival and apoptosis of human luteinized granulosa cells.
pubmed:affiliation
Department of Obstetrics and Gynecology, Asahikawa Medical College, Midorigaoka Higashi 2-1-1-1, Japan. pan@mail.asahikawa-med.ac.jp
pubmed:publicationType
Journal Article