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Blood, Vol. 96 No. 3 (August 1), 2000:
pp. 917-924
Expression of connexin 43 (Cx43) is critical for normal
hematopoiesis
Encarnacion Montecino-Rodriguez,
Hyosuk Leathers, and
Kenneth Dorshkind
From the Department of Pathology and Laboratory Medicine and the
Jonsson Comprehensive Cancer Center, UCLA School of Medicine, Los
Angeles, CA.
Gap junctions are intercellular channels, formed by individual
structural units known as connexins (Cx), that allow the intercellular exchange of various messenger molecules. The finding that numbers of
Cx43-type gap junctions in bone marrow are elevated during establishment and regeneration of the hematopoietic system has led to
the hypothesis that expression of Cx43 is critical during the
initiation of blood cell formation. To test this hypothesis, lymphoid
and myeloid development were examined in mice with a targeted
disruption of the gene encoding Cx43. Because Cx43 / mice die
perinatally, initial analyses were performed on Cx43/, Cx43+/, and Cx43+/+ embryos and newborns. The data
indicate that lack of Cx43 expression during embryogenesis compromises
the terminal stages of primary T and B lymphopoiesis. Cx43/
embryos and neonates had a reduced frequency of CD4+ and
T-cell receptor-expressing thymocytes and surface IgM+
cells compared to their Cx43+/+ littermates. Surprisingly,
Cx43+/ embryos/neonates also showed defects in B- and T-cell
development similar to those observed in Cx43/ littermates, but
their hematopoietic system was normal at 4 weeks of age. However, the
regeneration of lymphoid and myeloid cells was severely impaired in the
Cx43+/ mice after cytoablative treatment. Taken together, these
data indicate that loss of a single Cx43 allele can affect blood cell formation. Finally, the results of reciprocal bone marrow transplants between Cx43+/+ and Cx43+/ mice and examination of
hematopoietic progenitors and stromal cells in vitro indicates that the
primary effects of Cx43 are mediated through its expression in the
hematopoietic microenvironment.
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