Abstract:
:Retinoic acid (RA) affects the response of many cells to growth factors, including the bone morphogenetic proteins (BMPs). The BMPs are members of the TGF-beta, family of growth factors, originally identified by their bone-inducing activities. Their widespread expression suggests many roles other than that in osteogenesis. Because RA modulates the cell's response to growth factors, this may be a means by which the retinoids exert some of their known teratogenic effects. One such cellular response may be apoptosis. While apoptosis is required for normal development, the location and timing of its induction must be carefully controlled. Recently, several TGF-beta family members have been implicated in the induction of apoptosis in certain cell types. We show here, using P19 embryonal carcinoma cells, that the combination of RA and BMP2 or BMP4 synergistically induces apoptosis in 40% of the population within 24 hr. In contrast, RA alone induces apoptosis in only 10-15% of the population and each of the BMPs alone minimally induces apoptosis. Apoptosis depends on the dose of both the RA and the BMP as well as on new protein synthesis. Further, the induction of apoptosis prevents the formation of fully differentiated neurons and glial cells and instead leads to primarily smooth muscle cell differentiation. These results suggest that some of the malformations caused by retinoids may be due to the induction of inappropriate apoptosis in cells exposed to BMPs.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Glozak MA,Rogers MBdoi
10.1006/dbio.1996.0275subject
Has Abstractpub_date
1996-11-01 00:00:00pages
458-70issue
2eissn
0012-1606issn
1095-564Xpii
S0012-1606(96)90275-4journal_volume
179pub_type
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journal_title:Developmental biology
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journal_title:Developmental biology
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journal_title:Developmental biology
pub_type: 杂志文章
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pub_type: 杂志文章
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