DEGs in the bone marrow of Esr1Nkx2-1Cre females
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE122055 | GEO | 2018/11/02
REPOSITORIES: GEO
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Project description:DEGs in the bone marrow of Esr1Nkx2-1Cre females
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Project description:During lactation, mothers initiate cycles of bone formation followed by significant bone loss to meet the high calcium (Ca2+) demand by progeny. While estrogen functions typically as an anabolic driver of bone remodeling, this sex steroid is absent in postpartum females. Here, we report that a brain-derived secreted from neurons of the arcuate nucleus (ARC) fills this void and functions as a potent osteogenic factor to promote bone mass in lactating females. We previously reported an extraordinarily sex-specific high bone mass phenotype in female mice that persists with aging and is central in origin after eliminating estrogen receptor alpha signaling in ARCKISS1 neurons. Parabiosis and bone transplant studies established that a humoral factor in mutant females accounts for this unusual skeletal phenotype. High bone mass in mutant females could be traced back to the skeletal stem cell (SSC) level, reflected by their increased frequency and osteochondrogenic potential. Based on ex-vivo, in vivo, and in vitro assays, one protein emerged as the most promising secreted pro-osteogenic factor from the ARC, acting in mice and human SSCs at low concentrations (<nM) independent of age and sex. The role of this brain-derived factor in bone formation was confirmed by in vivo gain and loss of function studies. Unexpectedly, in wild-type females, a transient spike of this protein appears in ARCKISS1 neurons coincident with lactation when bone remodeling and high calcium demand intensify in estrogen-depleted mothers. Our findings establish a potentially new therapeutic anabolic bone hormone that functions in a novel female-specific brain-bone axis to ensure mammalian species survival.
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Project description:During lactation, mothers initiate cycles of bone formation followed by significant bone loss to meet the high calcium (Ca2+) demand by progeny. While estrogen functions typically as an anabolic driver of bone remodeling, this sex steroid is absent in postpartum females. Here, we report that a brain-derived secreted from neurons of the arcuate nucleus (ARC) fills this void and functions as a potent osteogenic factor to promote bone mass in lactating females. We previously reported an extraordinarily sex-specific high bone mass phenotype in female mice that persists with aging and is central in origin after eliminating estrogen receptor alpha signaling in ARCKISS1 neurons. Parabiosis and bone transplant studies established that a humoral factor in mutant females accounts for this unusual skeletal phenotype. High bone mass in mutant females could be traced back to the skeletal stem cell (SSC) level, reflected by their increased frequency and osteochondrogenic potential. Based on ex-vivo, in vivo, and in vitro assays, one protein emerged as the most promising secreted pro-osteogenic factor from the ARC, acting in mice and human SSCs at low concentrations (<nM) independent of age and sex. The role of this brain-derived factor in bone formation was confirmed by in vivo gain and loss of function studies. Unexpectedly, in wild-type females, a transient spike of this protein appears in ARCKISS1 neurons coincident with lactation when bone remodeling and high calcium demand intensify in estrogen-depleted mothers. Our findings establish a potentially new therapeutic anabolic bone hormone that functions in a novel female-specific brain-bone axis to ensure mammalian species survival.
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Project description:We found that mesenchymal stem cells isolated from colonic tissue express significantly increased expression of Ptgs2 or cox-2 compared to that of mesenchymal stem cells isolated from the bone marrow, one of the most common tissues from which this cell type is derived. We hypothesized that the localization of these cells in the colon exposes them to specific environmental factors that induce and/or maintain increased constitutive levels of cox-2 uniquely in this cell type. In order to identify possible candidate molecules regulating cox-2 in these cells, we decided to compare the transcriptomes of colonic mesenchymal stem cells and bone marrow-derived mesenchymal stem cells. Mesenchymal stem cells were isolated by fast plastic adherence after collagenase type I-mediated dissociation of the tissue of origin. Cells were maintained in culture in low glucose DMEM with 10mM HEPES and 10% FBS. Cells were passaged at 90-100% confluency. Approximately 4 million cells from four MSC lines, two from colon and two from bone marrow, were lysed between passages 5 and 10. Total RNA was isolated, amplified, and hybridized to Affymetrix MOE230.2 chips.
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