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Induction of negative hematopoietic regulators by neurokinin-A in bone
marrow stroma
P Rameshwar and P Gascon
Department of Medicine, UMDNJ-New Jersey Medical School, Newark 07103, USA.
The tachykinins are a family of neuropeptides that share a common carboxyl
terminus. Substance P (SP) and neurokinin-A (NK-A) are derived from the
preprotachykinin l gene. Although SP and NK-A can bind to either NK-1,
NK-2, or NK-3 receptors (R), they have preferences for NK- 1R and NK-2R,
respectively. We have reported that SP stimulates erythroid (E)
(burst-forming unit [BFU]-E and colony-forming unit [CFU]- E) and myeloid
(CFU-granulocyte-macrophage [GM]) progenitors partly through the induction
of growth factors. We have now investigated the hematopoietic effects of
NK-A using short-term bone marrow (BM) cultures and found that NK-A (10(-7)
to 10(-12) mol/L) inhibits CFU-GM proliferation but stimulates erythroid
progenitors. Release of soluble factors by the stroma appears to mediate
the inhibition because direct contact with the stroma was not required. We
have found that NK-A, through NK-2-like receptors induces increased levels
of macrophage inflammatory protein-1 alpha (MIP-1 alpha) and transforming
growth factor-beta (TGF-beta) (transcriptional and posttranscriptional) in
BM stroma. Clonogenic assays with NK-A (10(-9) mol/L) and either anti-MIP-
1 alpha or anti-TGF- beta 1 indicate that these cytokines partly contribute
to the inhibition, suggesting that these two negative hematopoietic
regulators exert part of the inhibition by NK-A on CFU- GM. The findings of
two closely related neuropeptides, derived from the same gene, exerting
opposite effects on myeloid colonies suggest that neuropeptides, by
themselves could be important factors in hematopoietic regulation.
Volume 88,
Issue 1,
pp. 98-106,
07/01/1996
Copyright © 1996 by The American Society of Hematology
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