Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNAi profiling by array of of Smad2 and Smad3 in mouse mammary epithelial cells treated with TGF-beta to induce epithelial-to-mesenchymal transition

ABSTRACT: Effects of Smad3 and Smad2 knock-down on TGFbeta-induced epithelial-to-mesenchymal transition (EMT) in mouse mammary epithelial (Nme) cells

ORGANISM(S): Mus musculus

SUBMITTER: Joanna Dzwonek

PROVIDER: E-MEXP-1342 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Smad3 is a key nonredundant mediator of transforming growth factor beta signaling in Nme mouse mammary epithelial cells.

Dzwonek Joanna J Preobrazhenska Olena O Cazzola Silvia S Conidi Andrea A Schellens Ann A van Dinther Maarten M Stubbs Andrew A Klippel Anke A Huylebroeck Danny D ten Dijke Peter P Verschueren Kristin K

Molecular cancer research : MCR 20090811 8

Smad2 and Smad3 are intracellular mediators of transforming growth factor beta (TGFbeta) signaling that share various biochemical properties, but data emerging from functional analyses in several cell types indicate that these two Smad proteins may convey distinct cellular responses. Therefore, we have investigated the individual roles of Smad2 and Smad3 in mediating the cytostatic and proapoptotic effects of TGFbeta as well as their function in epithelial-to-mesenchymal transition. For this pur ...[more]

PMID: 19671686

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Project description:Severe hyposalivation often results from Sjögren’s syndrome or radiation therapy for head and neck cancer. Devastating consequences of hyposalivation, such as rampant dental caries and persistent oral candidiasis, compromise the quality of life in those patients. Clinical management for dry mouth typically involves simple palliative methods or secretagogues, which are designed to stimulate saliva secretion from residual salivary acinar cells present in the glands. However, direct interventions in chronic dryness have yet to be employed in the clinical setting. Despite numerous studies on salivary gland regeneration, the molecular basis governing stem cell transdifferentiation into salivary epithelial precursors (SEP) is largely unknown. Our previously published study clearly indicated mouse bone marrow-derived mesenchymal stem cells (BM-MSCs) can be differentiated into SEP in vitro when co-cultured with isolated primary salivary gland cells without cell-to-cell contact. Our current study utilized iTRAQ-LS-MS/MS-based quantitative proteomics to profile key regulatory factors involved in mouse MSC-to-SEP conversion. We identified 280 differentially expressed proteins in BM-MSCs over the course of 7 days of co-culture. Interestingly, protein expression of salivary transcription factors (STFs), such as transcription factor E2a (TCF3), high mobility group protein 20B (HMG20b), and ankyrin repeat domain-containing protein 56 (ANKRD56) were increased in a time-dependent manner. Notably, pancreas specific transcription factor 1a (PTF1α), muscle, intestine and stomach expression-1 (MIST-1) and achaete-scute complex homolog 3(ASCL3) were newly induced over time in differentiated MSCs. We also identified the expression of Ptf1α in the mouse salivary glands for the first time and verified its expression in independent batches of co-cultured MSCs by western blotting. Furthermore, simulation of the molecular network involving the identified STFs has demonstrated evidence for their perspective roles in salivary gland development during glandular maturation. Thus, our study provides the first extensive proteomic profile of MSC-to-SEP transdifferentiation and identifies novel STFs that may be critical for this process.

Dataset Information

RNAi profiling by array of of Smad2 and Smad3 in mouse mammary epithelial cells treated with TGF-beta to induce epithelial-to-mesenchymal transition

Publications

Smad3 is a key nonredundant mediator of transforming growth factor beta signaling in Nme mouse mammary epithelial cells.

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