Retinoic acid enhances growth of human early erythroid progenitor cells in vitro.

نویسندگان

  • D Douer
  • H P Koeffler
چکیده

We studied the effect of retinoic acid on the clonal proliferation of normal human early erythroid progenitor cells in vitro. Normal peripheral blood cells were cultured in methylcellulose with erythropoietin and the number of burst-forming units-erythroid (BFU-E) colonies were scored on day 12 of culture. All-trans retinoic acid increased the number of colonies in a dose-response fashion. Maximal stimulation occurred at 30 nM retinoic acid, which increased the number of BFU-E by a mean of 225 +/- 25% (+/- SE) over plates containing erythropoietin alone. Colony formation increased even in the presence of maximally stimulating concentrations of erythropoietin. The 13-cis retinoic acid stimulated BFU-E proliferation in a parallel manner as the trans analogue, while retinol (vitamin A) did not affect clonal growth. This data supports further the thesis that retinoic acid, in addition to its known effect on epithelial cells, may be involved in the growth of normal hematopoietic cells.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

A New Two Step Induction Protocol for Neural Differentiation of Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells

Background: In this study, we examined a new two step induction protocol for improving the differentiation of human umbilical cord blood-derived mesenchymal stem cells into neural progenitor cells. Materials and Methods: Human umbilical cord blood-derived mesenchymal stem cells were first cultured in Dulbecco’s modified eagle medium supplemented with 10% fetal bovine serum in a humidified incu...

متن کامل

Effect of a New Retinoidal Benzoic Acid Derivative on Normal Human Hematopoietic Progenitor Cell Growth in Vitro1

13-cis-Retinoic acid (RA) has been demonstrated to alter hemopoiesis in vitro. We compared proliferation and differentiation effects of RA to a synthetic retinoid, (E)-4-|2-(5,6,7,8-tetrahydro-5,5,8,8-terrainethyl-2naphthalenyl-l-propenyl|benzoicacid (TTNPB), on human normal bone marrow cells. TTNPB stimulated the in vitro growth of erythroidgranulocyte-macrophage progenitors and erythroid prog...

متن کامل

A hepatitis B virus pre-S-retinoic acid receptor beta chimera transforms erythrocytic progenitor cells in vitro.

In this report, we investigated the transforming properties of retinoic acid receptor beta (RAR beta). The v-erbA protein, which is the viral oncogenic homologue of the thyroid hormone receptor, was replaced by either the complete RAR beta (beta R) or a hepatitis B virus pre-S-RAR beta (H beta R) hybrid product in an avian erythroblastosis virus-based vector. In chicken hematopoietic cells, the...

متن کامل

Analysis of Promyelocytic Leukemia in Human Embryonic Carcinoma Stem Cells During Retinoic Acid-Induced Neural Differentiation

Background: Promyelocytic leukemia protein (PML) is a tumor suppressor protein that is involved in myeloid cell differentiation in response to retinoic acid (RA). In addition, RA acts as a natural morphogen in neural development. Objectives: This study aimed to examine PML gene expression in different stages of in vitro neural differentiation of NT2 cells, and to investigate the possible role o...

متن کامل

The RAR-RXR as well as the RXR-RXR pathway is involved in signaling growth inhibition of human CD34+ erythroid progenitor cells.

Previous studies have shown that retinoic acid (RA), similar to tumor necrosis factor-alpha (TNF-alpha), can act as a bifunctional regulator of the growth of bone marrow progenitors, in that it can stimulate granulocyte-macrophage colony-stimulating factor (GM-CSF)- or interleukin-3 (IL-3)-induced GM colony formation, but potently inhibit G-CSF-induced growth. The present study, using highly en...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • The Journal of clinical investigation

دوره 69 4  شماره 

صفحات  -

تاریخ انتشار 1982