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Transcription profiling of human Human long-bone growth plate chondrocytes

ABSTRACT: This SuperSeries is composed of the following subset Series:; GSE1277: HGPC, in monolayer, 0.5 vs. 20% serum; GSE1278: HGPC, in monolayer, 0.5% serum Experiment Overall Design: Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Robert Olney

PROVIDER: E-GEOD-6429 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of human growth plate chondrocytes were isolated from the distal femoral growth plate from 3 different adolescents undergoing epiphysiodesis

Project description:Human growth plate chondrocytes were isolated from the distal femoral growth plate from 3 different adolescents undergoing epiphysiodesis. Cell were isolated and grown in monolayers, long term, in 20% serum. Cells were replated and cultured 48 h in 0.5% serum.

2008-06-12 | E-GEOD-1278 | biostudies-arrayexpress

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C-type natriuretic peptide facilitates autonomic Ca2+ entry in growth plate chondrocytes for stimulating bone growth.

Project description:The growth plates are cartilage tissues found at both ends of developing bones, and vital proliferation and differentiation of growth plate chondrocytes are primarily responsible for bone growth. C-type natriuretic peptide (CNP) stimulates bone growth by activating natriuretic peptide receptor 2 (NPR2) which is equipped with guanylate cyclase on the cytoplasmic side, but its signaling pathway is unclear in growth plate chondrocytes. We previously reported that transient receptor potential melastatin-like 7 (TRPM7) channels mediate intermissive Ca2+ influx in growth plate chondrocytes, leading to activation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) for promoting bone growth. In this report, we provide evidence from experiments using mutant mice, indicating a functional link between CNP and TRPM7 channels. Our pharmacological data suggest that CNP-evoked NPR2 activation elevates cellular cGMP content and stimulates big-conductance Ca2+-dependent K+ (BK) channels as a substrate for cGMP-dependent protein kinase (PKG). BK channel-induced hyperpolarization likely enhances the driving force of TRPM7-mediated Ca2+ entry and seems to accordingly activate CaMKII. Indeed, ex vivo organ culture analysis indicates that CNP-facilitated bone growth is abolished by chondrocyte-specific Trpm7 gene ablation. The defined CNP signaling pathway, the NPR2-PKG-BK channel-TRPM7 channel-CaMKII axis, likely pinpoints promising target proteins for developing new therapeutic treatments for divergent growth disorders.

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Valproic Acid Impacts the Growth of Growth Plate Chondrocytes.

Project description:A range of bone abnormalities including short stature have been reported to be associated with the use of antiepileptic drugs (AEDs) in children. Exactly how AEDs impact skeletal growth, however, is not clear. In the present study, rat growth plate chondrocytes were cultured to study the effects of AEDs, including valproic acid (VPA), oxcarbazepine (OXA), levetiracetam (LEV), lamotrigine (LTG), and topiramate (TPM) on the skeletal growth. VPA markedly reduced the number of chondrocytes by apoptosiswhile other AEDs had no effect. The apoptosis associated noncleaved and cleaved caspase 3, and caspases were increased by exposure to VPA, which up-regulated cyclooxygenase 2 (COX-2) mRNA and protein levels likely through histone acetylation. The COX-2 inhibitor NS-398 attenuated the effects of VPA up-regulating COX-2 expression and decreased VPA-induced caspase 3 expression. The use of VPA in children should be closely monitored or replaced, where appropriate, by AEDs which do not apparently affect the growth plate chondrocytes.

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Long-Term Storage of Human Cells at Ambient Temperature

Project description:This series represents the complete series of the human 293h media depleted storage on agarose / rehydration condition course analysis. Samples include Control, monolayer; Control, monolayer/full recovery, antibiotics; Spheroid, no storage; two week storage/0hr recovery; two week storage/full recovery; four week storage/0hr recovery; six week storage/0hr recovery. Keywords = 293h cells Keywords = desiccation Keywords = rehydration Keywords = spheroid Keywords = stabilization Keywords = ambient temperature Keywords: other

2005-08-01 | GSE1364 | GEO

Transcription profiling of human growth plate chrondrocytes grown in monolayer, 0.5 vs. 20% serum

Project description:Human growth plate chondrocytes were isolated from the distal femoral growth plate from a single adolescent undergoing epiphysiodesis. Cell were isolated and grown in monolayers, long term. Cells were replated and cultured in 0.5% or 20% serum.

2008-06-12 | E-GEOD-1277 | biostudies-arrayexpress

Bovine Hypertrophic Growth Plate Chondrocytes vs. Reserve Zone Chondrocytes

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2009-10-27 | GSE18738 | GEO

Genes uniquely expressed in human growth plate chondrocytes uncover a distinct regulatory network.

Project description:BACKGROUND:Chondrogenesis is the earliest stage of skeletal development and is a highly dynamic process, integrating the activities and functions of transcription factors, cell signaling molecules and extracellular matrix proteins. The molecular mechanisms underlying chondrogenesis have been extensively studied and multiple key regulators of this process have been identified. However, a genome-wide overview of the gene regulatory network in chondrogenesis has not been achieved. RESULTS:In this study, employing RNA sequencing, we identified 332 protein coding genes and 34 long non-coding RNA (lncRNA) genes that are highly selectively expressed in human fetal growth plate chondrocytes. Among the protein coding genes, 32 genes were associated with 62 distinct human skeletal disorders and 153 genes were associated with skeletal defects in knockout mice, confirming their essential roles in skeletal formation. These gene products formed a comprehensive physical interaction network and participated in multiple cellular processes regulating skeletal development. The data also revealed 34 transcription factors and 11,334 distal enhancers that were uniquely active in chondrocytes, functioning as transcriptional regulators for the cartilage-selective genes. CONCLUSIONS:Our findings revealed a complex gene regulatory network controlling skeletal development whereby transcription factors, enhancers and lncRNAs participate in chondrogenesis by transcriptional regulation of key genes. Additionally, the cartilage-selective genes represent candidate genes for unsolved human skeletal disorders.

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