Document Detail


Expression of retinoic acid receptor mRNA in hematopoietic cells.
MedLine Citation:
PMID:  2167405     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Retinoic acid (RA) has profound effects upon the proliferation and differentiation of many hematopoietic cells. The mechanism by which RA acts is unclear. Recently, several retinoic acid receptors (RAR) have been cloned. We studied expression of RAR-alpha mRNA by RNA blots in hematopoietic cells blocked at different stages of differentiation. All hematopoietic cells expressed RAR-alpha mRNA (3.4, 4.5 kb) including KG-1 (myeloblasts); HL-60 (promyelocytes); ML3, THP-1, U937 (myelomonoblasts and monoblasts); K562 (erythroblasts); and S-LB1 (T-lymphocytes). In addition, transformed cells from four non-hematopoietic tissues also expressed RAR-alpha mRNA. Steady-state levels of RAR-alpha mRNA were not affected by induction of terminal differentiation of HL-60 cells to either granulocytes or macrophages. Furthermore, both actively proliferating and resting lymphocytes from the same individuals expressed equal concentrations of RAR-alpha mRNA. Taken together, data suggest that level of expression of RAR-alpha mRNA is not related to cellular proliferation. We also showed that exposure to ligand (all-trans retinoic acid) did not change levels of RAR-alpha mRNA in three different cell types. Half-life of RAR-alpha mRNA was short (0.7 h) as determined by measuring decay of message after addition of actinomycin D. Consistent with this finding, accumulation of RAR-alpha mRNA increased in cells of three lines as their protein synthesis was inhibited. In summary, hematopoietic cells of different lineages and stages of differentiation constitutively express RAR-alpha mRNA. This expression is unaffected either by terminal differentiation or cell cycle. The RAR-alpha mRNA is short-lived and super-inducible by a protein synthesis inhibitor.
Authors:
M Kizaki; H P Koeffler; C W Lin; C W Miller
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Leukemia research     Volume:  14     ISSN:  0145-2126     ISO Abbreviation:  Leuk. Res.     Publication Date:  1990  
Date Detail:
Created Date:  1990-09-24     Completed Date:  1990-09-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7706787     Medline TA:  Leuk Res     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  645-55     Citation Subset:  IM    
Affiliation:
UCLA Department of Medicine 90024.
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MeSH Terms
Descriptor/Qualifier:
Carrier Proteins / genetics*
Cell Differentiation
Cell Line
Cycloheximide / pharmacology
Half-Life
Hematopoietic Stem Cells / analysis*
Humans
Leukemia / metabolism
Lymphocytes / analysis
RNA, Messenger / analysis*
Receptors, Retinoic Acid
Chemical
Reg. No./Substance:
0/Carrier Proteins; 0/RNA, Messenger; 0/Receptors, Retinoic Acid; 66-81-9/Cycloheximide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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