http://barf.jcowboy.org Matrix Biology recent publications en-us http://barf.jcowboy.org/pubmed.gif http://barf.jcowboy.org http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=23747796 Publication Date: 2013 Jun 4 PMID: 23747796<br/>Authors: Stahl, J. - Nakano, Y. - Kim, S. O. - Gibson, C. W. - Le, T. - Den Besten, P.<br/>Journal: Matrix Biol<br/><br/>Highly mineralized tooth enamel develops from an extracellular matrix chiefly comprised of amelogenins formed by splicing of 7 (human) or 9 (rodent) exons secreted from specialized epithelial cells known as ameloblasts. Here we examined the role of the 59 amino acid alternatively spliced amelogenin known as leucine rich amelogenin peptide (LRAP) on enamel formation, using transgenic murine models in which LRAP overexpression is driven by an amelogenin promotor (TgLRAP). Beginning in the secretory stage of mouse amelogenesis, we found a reduced thickness of enamel matrix and a loss of Tomes' processes, followed by upregulated amelogenin mRNA expression, inhibited amelogenin secretion and loss of cell polarity. In the presecretory stage (P0) amelogenin m180 mRNA expression was increased 58 fold along with a 203 fold increase in MMP-20 expression and 3.5 and 3.2 fold increased in respectively enamelin and ameloblastin. When LRAP was overexpressed on an amelogenin knockout mouse model, the ameloblasts were not affected. Further, expression of the global chromatin organizer and transcription factor SATB1 was reduced in secretory stage TgLRAP ameloblasts. These findings identify a cellular role for LRAP in enamel formation that is not directly related to directing enamel crystal formation as is reported to be the primary function of full length amelogenins. The effect of LRAP overexpression in upregulating amelogenins, MMP-20 and SATB1, suggests a role in protein regulation critical to ameloblast secretion and matrix processing, to form a mineralized enamel matrix.<br/><br/>post to: <a href = "http://www.citeulike.org/posturl?url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DRetrieve%26db%3DPubMed%26dopt%3DAbstract%26list_uids%3D23747796&title=Entrez+Pubmed">CiteULike</a> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=23727079 Publication Date: 2013 May 29 PMID: 23727079<br/>Authors: Duncan, M. B.<br/>Journal: Matrix Biol<br/><br/>The extracellular matrix undergoes extensive remodeling during hepatocellular carcinoma and functions as a critical component of the tumor microenvironment by providing a substratum for cell adhesion and serving as a reservoir for a variety of cytokines and growth factors. Despite the clinical correlation between ECM deposition and hepatocellular carcinoma progression, it remains unclear how global extracellular matrix gene expression is altered in hepatocellular carcinoma and the molecular pathways that govern this change. Herein, a comprehensive analysis of the extracellular matrix transcriptome using an RNA-sequencing dataset provided by The Cancer Genome Atlas consortium was conducted and indicates substantial differential gene expression of key extracellular matrix collagens, glycoproteins, and proteoglycans in hepatocellular carcinoma. This analysis also reveals alternative expression of extracellular matrix gene transcript variants that could impact biological activity and serves as a framework for exploring the dynamic nature of the extracellular matrix transcriptome in cancer and identifying candidate genes for future exploration.<br/><br/>post to: <a href = "http://www.citeulike.org/posturl?url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DRetrieve%26db%3DPubMed%26dopt%3DAbstract%26list_uids%3D23727079&title=Entrez+Pubmed">CiteULike</a> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=23721659 Publication Date: 2013 May 27 PMID: 23721659<br/>Authors: Iiozzo, R.<br/>Journal: Matrix Biol<br/><br/><br/><br/>post to: <a href = "http://www.citeulike.org/posturl?url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DRetrieve%26db%3DPubMed%26dopt%3DAbstract%26list_uids%3D23721659&title=Entrez+Pubmed">CiteULike</a>