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Human marrow stromal precursors are α1 integrin subunit‐positive
Author(s) -
Deschaseaux Frédéric,
Charbord Pierre
Publication year - 2000
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/1097-4652(200009)184:3<319::aid-jcp5>3.0.co;2-n
Subject(s) - stromal cell , haematopoiesis , cd34 , bone marrow , integrin , alpha (finance) , lymph node stromal cell , biology , microbiology and biotechnology , cell culture , protein subunit , immunology , cancer research , stem cell , cell , medicine , biochemistry , gene , genetics , construct validity , nursing , patient satisfaction
In this work we studied the expression of adhesion molecules on primate human and non‐human marrow stromal cells (primary cultures and lines) and on human CD34 + hematopoietic normal and leukemic precursors. Differential expression of α1 integrin subunit was observed, since this molecule was intensely expressed by marrow stroma but not detected on CD34 + cells. We used this difference to select, in fresh bone marrow samples, α1‐positive cells. We found that all stromal precursors giving rise to colony‐forming units‐fibroblasts (CFU‐F) were present in the α1‐positive fraction. No colonies were detected in the α1‐negative fraction even after 2 weeks of culture. Phenotypic studies of stromal cells derived from α1‐positive cells and grown in long‐term marrow culture indicated that these cells were similar to stromal cells from primary cultures. We also observed early upregulation of α4 and α2 integrin subunits in cultures derived from α1‐positive cells with maximal expression by day 10 (26 and 51%, respectively) preceding a gradual decline to low to nil values at day 30 (4.5 and 12%). These data indicate that α1 integrin subunit is a marker for both mature stromal cells and stromal precursors, while α2 and α4 integrin subunits are expressed primarily by immature cells. J. Cell. Physiol. 184:319–325, 2000. © 2000 Wiley‐Liss, Inc.