Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Neonatal Skeletal Progenitors

ABSTRACT: Prospectively isolated and characerized skeletal progenitor lineages 3 repeats per FACS sorted population

ORGANISM(S): Mus musculus

SUBMITTER: Charles KF

PROVIDER: E-GEOD-64447 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Identification and specification of the mouse skeletal stem cell.

Chan Charles K F CK Seo Eun Young EY Chen James Y JY Lo David D McArdle Adrian A Sinha Rahul R Tevlin Ruth R Seita Jun J Vincent-Tompkins Justin J Wearda Taylor T Lu Wan-Jin WJ Senarath-Yapa Kshemendra K Chung Michael T MT Marecic Owen O Tran Misha M Yan Kelley S KS Upton Rosalynd R Walmsley Graham G GG Lee Andrew S AS Sahoo Debashis D Kuo Calvin J CJ Weissman Irving L IL Longaker Michael T MT

Cell 20150101 1-2

How are skeletal tissues derived from skeletal stem cells? Here, we map bone, cartilage, and stromal development from a population of highly pure, postnatal skeletal stem cells (mouse skeletal stem cells, mSSCs) to their downstream progenitors of bone, cartilage, and stromal tissue. We then investigated the transcriptome of the stem/progenitor cells for unique gene-expression patterns that would indicate potential regulators of mSSC lineage commitment. We demonstrate that mSSC niche factors can ...[more]

PMID: 25594184

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Project description:Melanocytes within benign human nevi are the paradigm for tumor suppressive senescent cells in a pre-malignant neoplasm. These cells typically contain mutations in either the BRAF or N-RAS oncogene and express markers of senescence, including p16. However, a nevus can contain 10s to 100s of thousands of clonal melanocytes and approximately 20-30% of melanoma are thought to arise in association with a pre-existing nevus. Neither observation is indicative of fail-safe senescence-associated proliferation arrest and tumor suppression. We set out to better understand the status of nevus melanocytes. Proliferation-promoting Wnt target genes, such as cyclin D1 and c-myc, were repressed in oncogene-induced senescent melanocytes in vitro, and repression of Wnt signaling in these cells induced a senescent-like state. In contrast, cyclin D1 and c-myc were expressed in many melanocytes of human benign nevi. Specifically, activated Wnt signalling in nevi correlated inversely with nevus maturation, an established dermatopathological correlate of clinical benignancy. Single cell analyses of lone epidermal melanocytes and nevus melanocytes showed that expression of proliferation-promoting Wnt targets correlates with prior proliferative expansion of p16-expressing nevus melanocytes. In a mouse model, activation of Wnt signaling delayed, but did not bypass, senescence of oncogene-expressing melanocytes, leading to massive accumulation of proliferation-arrested, p16-positive non-malignant melanocytes. We conclude that clonal hyperproliferation of oncogene-expressing melanocytes to form a nevus is facilitated by transient delay of senescence due to activated Wnt signaling. The observation that activation of Wnt signaling correlates inversely with nevus maturation, an indicator of clinical benignancy, supports the notion that persistent destabilization of senescence by Wnt signaling contributes to the malignant potential of nevi. We used microarrays to detail the global programme of gene expression after lentiviral infection of BRAF in 3 replicates. Primary human melanocytes were infected/uninfected with lentivirus containing either an Empty Vector or activated BRAFV600E mutant in three biological replicates

Dataset Information

Neonatal Skeletal Progenitors

Publications

Identification and specification of the mouse skeletal stem cell.

Similar Datasets

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