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Expression data from WT and BMPR2 knockout hematopoietic stem cells extracted from mice.

ABSTRACT: Expression data from WT and BMPR2 knockout hematopoietic stem cells extracted from mice.

PROVIDER: PRJNA862726 | ENA |

REPOSITORIES: ENA

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Expression data from WT and BMPR2 knockout hematopoietic stem cells extracted from mice.

Project description:Abstract copied in below, from Warsi et al. 2021 BMP signaling is required for postnatal murine hematopoietic stem cell self-renewal, published in Haematologica. DOI 10.3324/haematol.2019.236125 Life-long production of blood from hematopoietic stem cells (HSCs) is a process of strict modulation. Intrinsic and extrinsic signals govern fate options like self-renewal - a cardinal feature of HSCs. Bone morphogenetic proteins (BMP) have an established role in embryonic hematopoiesis, but less is known about its functions in adulthood. Previously, SMAD-mediated BMP signaling has been proven dispensable for HSCs. However, the BMP Type II receptor (BMPR-II) is highly expressed in HSCs, leaving the possibility that BMPs function via alternative pathways. Here, we establish that BMP signaling is required for self-renewal of adult HSCs. Through conditional knockout we show that BMPR-II deficient HSCs have impaired self-renewal and regenerative capacity. BMPR-II deficient cells have reduced p38 activation, implying that non-SMAD pathways operate downstream of BMPs in HSCs. Indeed, a majority of primitive hematopoietic cells do not engage in SMAD-mediated responses downstream of BMPs in vivo. Furthermore, deficiency of BMPR-II results in increased expression of TJP1, a known regulator of self-renewal in other stem cells, and knockdown of TJP1 in primitive hematopoietic cells partly rescues the BMPR-II null phenotype. This suggests TJP1 may be a universal stem cell regulator. In conclusion, BMP signaling, in part mediated through TJP1, is required endogenously by adult HSCs to maintain self-renewal capacity and proper resilience of the hematopoietic system during regeneration.

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Effect of tail domain and kinase domain mutations in BMPR2 on gene expression in rat Hc92 cells studied by RNA-Seq

Project description:We sequenced RNA from rat Hc92 cells transformed with empty vector, tail domain BMPR2 and kinase domain BMPR2 knockout vectors Comparison of Hc92 cells lacking BMPR2 tail domain vs those lacking BMPR2 kinase domain, using empty vector treated cells as control for both.

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Project description:We sequenced RNA from rat Hc92 cells transformed with empty vector, tail domain BMPR2 and kinase domain BMPR2 knockout vectors

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Expression data from WT and Elektra (Slfn2 mutant, loss of function) homozygous hematopoietic stem cells extracted from mice.

Project description:Expression data from WT and Elektra (Slfn2 mutant, loss of function) homozygous hematopoietic stem cells extracted from mice.

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Effect of BMPR2 mutation on vascular smooth muscle gene expression

Project description:BMPR2 mutation is the cause of most hereditary pulmonary arterial hypertension, but the common molecular consequence of different types of BMPR2 mutation is still not known. The goal of this study was to determine the common molecular consequences of three different classes of patient-derived BMPR2 mutation in vascular smooth muscle gene expression. Three different classes of BMPR2 mutation, wild-type BMPR2, or empty vector were stably transfected into A7R5 vascular smooth muscle cells, and expression compared.

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Bmpr2 mutation in murine PMVEC

Project description:Pulmonary arterial hypertension (PAH) is thought to be driven by dysfunction of pulmonary vascular microendothelial cells (PMVEC). Most hereditary PAH is associated with BMPR2 mutations. However, the physiologic and molecular consequences of expression of BMPR2 mutations in PMVEC are unknown. PMVEC were isolated from triple transgenic mice carrying the immortomouse gene, a transactivator, and either control, Bmpr2delx4+ or Bmpr2R899X mutation

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Effect of BMPR2 mutation on vascular smooth muscle gene expression

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