Multipotent Schwann cell precursors generate steroid-producing cells of the adrenal cortex and chromaffin cells of the adrenal medulla
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PROVIDER: PRJNA589040 | ENA |
REPOSITORIES: ENA
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Project description:Multipotent stem cells are considered as promising biological tools for regenerative medicine, and transcriptome analysis of these cells is fundamental for identifying new factors controlling proliferation versus differentiation. To obtain a comprehensive characterization of adrenal progenitors, we have developed an analytical pipeline relying on flow cytometric sorting of living cells followed by RNA sequencing. This analysis showed that two distinct populations of Nestin-positive progenitors are located in the adrenal cortex and medulla, respectively. Though 1039 genes were differentially regulated, both populations showed Schwann cell precursor properties suggesting both populations to be neural crest-derived.
2023-01-04 | GSE140247 | GEO
Project description:Renewal of the catecholamine-secreting chromaffin cell population of the adrenal medulla is necessary for physiological homeostasis throughout life. Definitive evidence for the presence or absence of an adrenomedullary stem cell has been enigmatic. In this work, we show that a subpopulation of uncommitted sustentacular cells, previously thought to be support cells, are in fact adrenomedullary stem cells. These postnatal cells express the transcription factor SOX2, and give rise to chromaffin cells of both the adrenaline and noradrenaline lineages in vivo and in vitro. We present comprehensive transcriptomic data of the mouse adrenal medulla as well as of purified SOX2+ adrenomedullary stem cell populations. Through genetic tracing, we show that postnatal stem cells specialise from embryonic Schwann Cell Precursors and identify this population in the normal adult human adrenal medulla.
2024-07-13 | GSE237125 | GEO
Project description:Pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNFalpha) and interleukin-1beta/alpha (IL1beta/alpha) modulate catecholamine secretion, and long-term gene regulation, in chromaffin cells of the adrenal medulla. Interleukin-6 (IL6), also released during inflammation, affects transcriptional responses in primary chromaffin cells, and may coordinate immune and autonomic adrenomedullary responses via an autocrine mechanism, as TNFalpha itself strongly induces IL6 expression in chromaffin cells, which in turn express receptors responsive to IL6. We have examined the signaling mechanisms employed by IL6 to affect tyrosine hydroxylase (TH) enzymatic activation, and adrenomedullary gene transcription, in cultured bovine chromaffin cells. IL6 caused acute tyrosine/threonine phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), and serine phosphorylation of signal transducer and activator of transcription 3 (STAT3), as do several other first messengers acting on the chromaffin cell, including histamine, nicotine and angiotensin II. IL6 uniquely activated tyrosine phosphorylation of STAT3. Consistent with a short-term ERK1/2 activation, IL6 treatment caused prompt regulation of TH phosphorylation, and up-regulation of genes encoding secreted proteins of the adrenal medulla including galanin, vasoactive intestinal peptide (VIP), gastrin releasing peptide (GRP) and parathyroid hormone-like hormone (PTHLH). We further examined the effects of IL6 treatment on the entire bovine chromaffin cell transcriptome. Of 90 genes up-regulated by IL6, only 16 of which are known targets of IL6 in the immune system. The remaining genes likely represent a combination of novel IL6/STAT3 targets, targets of ERK1/2 shared by other first messengers, and, potentially, IL6-dependent genes activated in a secondary cascade via transcription mediated by IL6-induced transcription factors, such as HIF-1alpha. Notably, genes induced by IL6 represent a cohort with a profile that includes both neuroendocrine-specific genes, including several that are activated by G-protein couple receptor (GPCR) signaling pathways initiated by histamine and pituitary adenylate cyclase-activating polypeptide (PACAP), and some transcripts also activated by cytokines including interferon-alpha (INFalpha and TNFalpha. These results suggest an integrative role for IL6 in overall fine-tuning of the chromaffin cell response to a wide range of physiological and paraphysiological stressors, particularly when immune and endocrine stimuli converge in the adrenal medulla.
2017-08-01 | GSE85901 | GEO
Project description:Cells producing adrenalin are largely derived from nerve-associated Schwann cell precursors via an intermediate progenitor “bridge” cell. We demonstrate that large numbers of chromaffin cells arise from peripheral glial stem cells, termed Schwann cell precursors (SCPs)
2017-07-10 | GSE99933 | GEO
Project description:Adrenal chromaffin cells and sympathetic neuron are derived from neural crest precursors and both cell types can give rise to childhood cancer, neuroblastoma. However only limited is known about the mechanism of their development. Better understanding of their transcriptomic profiles during development could gives an insight into the cell fates acquisition as well as the origin of neuroblastoma. Yellow fluorescent protein expressing sympathetic neuroblasts and adrenal chromaffin cells were isolated from E12.5 TH-IRES-Cre;ROSA26-EYFP mouse embryos by fluorescence-activated cell sorting. Transcriptomic profiles of sympathetic neuroblasts and adrenal chromaffin cells from embryonic age (E)12.5 TH-IRES-Cre;ROSA26-EYFP mice were generated by RNA sequencing, in four paired biological replicates.
2019-05-24 | E-MTAB-7086 | biostudies-arrayexpress
Project description:Characterization of postnatal mouse adrenal chromaffin cells
| PRJNA824412 | ENA
Project description:Transcriptom analysis of microdissect adrenal medulla after 8 weeks of cardiac pressure overload caused by transverse aortic constriction. Comparative transcriptome analysis was determined using the GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA, USA). Six microarrays from microdissected adrenal medulla of mice were performed 8 weeks after transverse aortic constriction or sham operation.
2011-05-03 | E-GEOD-21829 | biostudies-arrayexpress
Project description:Adrenal gland is the major organ releasing catecholamines and regulating our stress response. The mechanisms balancing adrenal hormone-producing cells and protecting against neuroblastoma or other tumors are still enigmatic. Here we revealed that adrenergic chromaffin cells release serotonin (5HT), which acts upon their immediate progenitor “bridge” cells via 5-hydroxytryptamine receptor 3A (HTR3A). Consistently, the aggressive HTR3Ahigh human neuroblastoma cell lines reduce proliferation in response to HTR3A-specific agonists, suggesting the mechanism of anti-tumor protection. Physiological increase of 5HT in vivo caused prolongation of a cell cycle length in “bridge” progenitors leading to smaller chromaffin population and changing the balance of hormones and behavioral patterns in resulting adult rodents. These behavioral effects and smaller adrenals were mirrored in a progeny of pregnant females subjected to experimental stress, suggesting novel maternal-fetal link controlling developmental adaptations. Finally, these findings corresponded to a size-distribution of adrenals found in wild rodents with different coping strategies.
2021-07-28 | GSE180861 | GEO
Project description:Transcriptom analysis of microdissect adrenal medulla after 8 weeks of cardiac pressure overload caused by transverse aortic constriction.
2011-05-03 | GSE21829 | GEO
Project description:Adrenal glands are the major organs releasing catecholamines and regulating our stress response. The mechanisms balancing generation of adrenergic chromaffin cells and protecting against neuroblastoma tumors are still enigmatic. Here we revealed that serotonin (5HT) controls the numbers of chromaffin cells by acting upon their immediate progenitor “bridge” cells via 5-hydroxytryptamine receptor 3A (HTR3A), and the aggressive HTR3Ahigh human neuroblastoma cell lines reduce proliferation in response to HTR3A-specific agonists. In embryos (in vivo), the physiological increase of 5HT caused a prolongation of the cell cycle in “bridge” progenitors leading to a smaller chromaffin population and changing the balance of hormones and behavioral patterns in adulthood. These behavioral effects and smaller adrenals were mirrored in the progeny of pregnant female mice subjected to experimental stress, suggesting a novel maternal-fetal link that controls developmental adaptations. Finally, these results corresponded to a size-distribution of adrenals found in wild rodents with different coping strategies.
2022-04-04 | GSE195929 | GEO