In vitro requirement for periostin in B lymphopoiesis

Siewe, Basile; Kalis, Susan L.; Le, Phong T.; Witte, Pamela L.; Choi, Sangdun; Conway, Simon J.; Druschitz, Laurel; Knight, Katherine L.

doi:10.1182/blood-2010-08-301119

Cited by 13 publications

(16 citation statements)

References 54 publications

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“…The loss of transcripts associated with osteoblastoid differentiation was of interest, because osteoblastoid stroma may support B-lymphoid differentiation in vivo. 32 Using quantitative PCR, we confirmed decreased accumulation in Smo-depleted OP9 cells of transcripts for periostin (Postn), the expression of which in OP9 cells is essential for B lymphopoiesis 33 ; IL-7, a cytokine essential for B lymphopoiesis in adult mice that was present in the ex vivo differentiation systems used herein; adiponectin (Adipoq), asporin (Aspn), and osteomodulin (Omd), 26,27 was performed on 264 genes (206 down-regulated, 58 up-regulated) displaying a 2-fold or greater change with P Ͻ .001. *General DAVID functional category.…”

Section: B-lymphoid Differentiation Promoted By Hh Signaling In Strommentioning

confidence: 81%

“…Of the transcripts reduced in Smo-deficient cells, several encode proteins that stimulate B lymphopoiesis. Transcripts encoding periostin (Postn), an ECM protein required by OP9 cells to support B lymphopoiesis, 33 were reduced by 20-fold, whereas transcripts for the B-lymphopoietic factor IL-7 were reduced by nearly 4-fold. These reductions may be related, because depletion of periostin from OP9 cells is accompanied by reduced expression of IL-7.…”

Section: Hedgehog Signaling In B-cell Development 5445mentioning

confidence: 99%

“…These reductions may be related, because depletion of periostin from OP9 cells is accompanied by reduced expression of IL-7. 33 Because exogenous IL-7 was present in the culture systems used herein, it is unlikely that the effects of Smo depletion are exerted through decreased stromal expression of IL-7; rather, one or more additional factors is likely to be limiting. In addition to periostin, candidates include SC1/ECM2, which promotes B lymphopoiesis 44 and the expression of which is reduced after Smo depletion.…”

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confidence: 99%

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Non–cell-autonomous hedgehog signaling promotes murine B lymphopoiesis from hematopoietic progenitors

Cooper

Hardy

Reth

et al. 2012

Blood

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The role of hedgehog (Hh) signaling in B lymphopoiesis has remained unclear. We observed that the proliferation of pro-B cells in stromal cocultures was impaired by interruption of Hh signaling, prompting us to investigate whether the target of Hh antagonism was intrinsic or extrinsic to the B-lymphoid compartment. In the present study, using conditional deletion of the pathway activator gene Smo, we found that cell-autonomous Hh signaling is dispensable for B-cell development, B-lymphoid repopulation of the BM, and humoral immune function. In contrast, depletion of the Smo protein from stromal cells was associated with impaired generation of B-lymphoid cells from hematopoietic stem progenitor cells, whereas reciprocal removal of Smo from these cells had no effect on the production of B-cell progenitors. Depletion of Smo from stromal cells was associated with coordinate down-regulation of genes for which expression is associated with osteoblastoid identity and Blymphopoietic activity. The results of the present study suggest that activity of the Hh pathway within stromal cells promotes B lymphopoiesis in a non-cellautonomous fashion. (Blood. 2012; 119(23):5438-5448) IntroductionThe major pathway of B lymphopoiesis from hematopoietic stem progenitor cells has been described in some detail previously. 1 The earliest identifiable B-cell progenitors, termed pro-B cells, arise initially in the fetal liver and subsequently in the BM, carrying partial D-to-J H rearrangements of both Ig alleles. Subsequent, productive V H -to-DJ H joining triggers the transition to the pre-B stage, at which time the Ig heavy chain associates with surrogate light chains to form the pre-BCR. Signals emanating from the pre-BCR suppress further heavy-chain rearrangement, activate Ig light-chain rearrangement, promote proliferation, inhibit apoptosis, and increase sensitivity to IL-7. After productive Ig light-chain rearrangement, counterselection of self-reactive specificities, and receptor editing, nascent B cells leave the marrow for peripheral lymphoid tissues.In the BM, B-cell development occurs in essential association with stromal cells. 2 Some effects of stromal cells on B-cell development are mediated by direct contact, such as the interaction of c-Kit on pro-B cells with SCF on stromal cells. 3 Other effects are mediated by soluble products of stromal cells, such as IL-7, which supports maturation beyond the pro-B stage. 4 However, the contributions of the stromal environment to B-lymphoid differentiation remain poorly defined, as evident from the requirement for stromal cells in addition to soluble factors in systems that support B lymphopoiesis ex vivo.The Hedgehog (Hh) signaling pathway serves several developmental functions, including establishment of tissue polarity, embryonic patterning, and stem cell maintenance. 5 Hh signaling is initiated by a family of ligands that includes Sonic Hh (Shh), Indian Hh (Ihh), and Desert Hh (Dhh). In the absence of ligand, the receptor Patched (Ptch) inhibits the activator Smoothened (Smo); t...

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Section: B-lymphoid Differentiation Promoted By Hh Signaling In Strommentioning

confidence: 81%

Section: Hedgehog Signaling In B-cell Development 5445mentioning

confidence: 99%

mentioning

confidence: 99%

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Non–cell-autonomous hedgehog signaling promotes murine B lymphopoiesis from hematopoietic progenitors

Cooper

Hardy

Reth

et al. 2012

Blood

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“…Comparative microarray analysis of the Med1 +/+ p53 −/− and Med1 −/− p53 −/− MEFs has revealed that Postn expression is also attenuated in Med1 −/− MEFs (GEO accession number GSE22471) [8]. These findings and the proposed role for POSTN as a niche factor for rabbit and mouse B lymphopoiesis [13], prompted us to investigate whether POSTN also acts as a niche factor for other lineages of hematopoiesis.…”

Section: Resultsmentioning

confidence: 99%

“…POSTN, produced by OP-9 cells, has recently been reported to be required for optimal B lymphopoiesis in vitro [13], suggesting that POSTN, as well as CXCL12, are B cell-specific niche factors within the BM microenvironment. Moreover, increased expression of POSTN within BM stromal cells might correlate with myelofibrosis, leading to the interesting hypothesis that POSTN might be a niche factor for clonal expansion in some form of chronic myeloproliferative diseases [reviewed in 14].…”

Section: Introductionmentioning

confidence: 99%

Periostin supports hematopoietic progenitor cells and niche-dependent myeloblastoma cells in vitro

Tanaka

Maekawa

Matsubara

et al. 2016

Biochemical and Biophysical Research Communications

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The expression of extracellular matrix protein periostin (POSTN) was attenuated in Med1−/− mouse embryonic fibroblasts (MEFs), which exhibited a decreased capability to support hematopoietic progenitor cells (HPCs) in vitro. When bone marrow (BM) cells were cocultured with mitomycin C-treated Med1+/+ MEFs, or OP-9 or MS-5 BM stromal cells, in the presence of anti-POSTN antibody, the growth of BM cells and number of long-term culture-initiating cells (LTC-ICs) were attenuated. When BM cells were cocultured with Med1−/− MEFs in the presence of recombinant POSTN, the growth of BM cells and the number of LTC-ICs were restored. Moreover, antibody-mediated blockage of stromal cells-derived POSTN markedly reduced the growth and cobblestone formation, a leukemic stem cell feature, of stromal cell-dependent MB-1 myeloblastoma cells. POSTN was expressed both in BM cells and variably in different BM stromal cells. Expression in the latter cells was increased by physical interaction with hematopoietic cells. The receptor for POSTN, integrin αvβ3, was expressed abundantly in BM stromal cells. The addition of recombinant POSTN to BM stromal cells induced intracellular signaling downstream of integrin αvβ3. These results suggest that stromal cell POSTN supports both normal HPCs and leukemia-initiating cells in vitro, at least in part, indirectly by acting on stromal cells in an autocrine or paracrine manner.

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