Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Abnormal marrow fibroblasts in aplastic anemia.

H S Juneja, F H Gardner, J J Minguell

    Experimental Hematology
    |May 1, 1984
    PubMed
    Summary
    This summary is machine-generated.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    Editorial Expression of Concern: Estrogen receptor, calcium mobilization and rat sperm motility.

    Molecular and cellular biochemistry·2024
    Same author

    Adhesion of B-Cell Chronic Lymphocytic Leukemia Cells to Marrow Stromal Cells is Mediated by α4β1 but not β2αL Integrin: MSC also Prevent Apoptosis of B-CLL Cells.

    Hematology (Amsterdam, Netherlands)·2016
    Same author

    G-CSF Regulates the Expression of mRNA for Collagen Type VI and Collagen VI Production in Human Bone Marrow Stromal Cells.

    Hematology (Amsterdam, Netherlands)·2016
    Same author

    Combination cell therapy for the treatment of acute myocardial infarction.

    International journal of cardiology·2012
    Same author

    Mechanism delineating differential effect of an antiestrogen, tamoxifen, on the serum LH and FSH in adult male rats.

    Journal of endocrinological investigation·2006
    Same author

    Aspirin and salicylate inhibit colon cancer medium- and VEGF-induced endothelial tube formation: correlation with suppression of cyclooxygenase-2 expression.

    Journal of thrombosis and haemostasis : JTH·2003

    Human bone marrow fibroblasts from aplastic anemia patients exhibit faster growth and lack cell-to-cell inhibition compared to normal fibroblasts. These abnormal fibroblasts show a paradoxical response to dexamethasone, indicating distinct cellular characteristics.

    Area of Science:

    • Cell Biology
    • Hematology
    • Fibroblast Research

    Background:

    • Aplastic anemia (AA) is a rare but serious condition where the bone marrow doesn't produce enough blood cells.
    • Bone marrow fibroblasts (BMF) play a crucial role in the bone marrow microenvironment.
    • Understanding BMF behavior in AA is essential for elucidating disease mechanisms.

    Purpose of the Study:

    • To investigate the in vitro growth characteristics of human bone marrow fibroblasts (BMF) from normal (N) subjects and aplastic anemia (AA) patients.
    • To compare the response of N-BMF and AA-BMF to hormonal stimulation, specifically focusing on dexamethasone.
    • To analyze dexamethasone binding in both N-BMF and AA-BMF to understand potential regulatory differences.

    Main Methods:

    • In vitro culture of BMF from normal and aplastic anemia subjects.

    Related Experiment Videos

  • Growth studies to determine population doubling time and cell proliferation.
  • Hormonal stimulation assays using testosterone, etiocholanolone, and dexamethasone.
  • Dexamethasone binding assays to quantify specific binding sites (Bmax) and dissociation constants (Kd).

    • Main Results:

    • A subgroup of AA-BMF demonstrated significantly faster growth rates and increased cell numbers compared to N-BMF.
    • AA-BMF exhibited a lack of normal cell-to-cell inhibition, growing in multiple layers, unlike N-BMF which grew as monolayers.
    • Dexamethasone stimulated N-BMF growth but suppressed AA-BMF growth, with AA-BMF showing significantly lower dexamethasone binding sites (Bmax) and a different dissociation constant (Kd).

    Conclusions:

    • Human bone marrow fibroblasts from aplastic anemia patients display abnormal growth patterns and a lack of contact inhibition.
    • The paradoxical response of AA-BMF to dexamethasone, coupled with altered receptor binding, suggests intrinsic cellular abnormalities.
    • These findings indicate that BMF from AA patients are fundamentally different from normal BMF, potentially contributing to the pathophysiology of aplastic anemia.