Disease relevance of Ogn

• OBJECTIVE: We hypothesize that the mimecan gene expressed in the human pituitary and regulated by pituitary transcription factor-1 (Pit-1) might act as a marker for diagnosing pituitary tumors [1].

High impact information on Ogn

• Bone morphogenetic protein-1/tolloid-related metalloproteinases process osteoglycin and enhance its ability to regulate collagen fibrillogenesis [2].
• In addition, our data also show that almost all the ACTH- or GH-positive pituitary tumors likely express mimecan protein, and only a portion of prolactin-, TSH-, FSH-, and LH-positive pituitary tumors express mimecan protein [1].
• Expression of mimecan mRNA and protein is also observed in the human anterior pituitary gland [1].
• RESULTS: The mimecan gene was expressed at a moderate level in the mouse pituitary gland by Northern blot analysis [1].
• This indicates that, compared with lumican and keratocan, mimecan has a lesser role in the control of stromal architecture in mouse cornea [3].

Biological context of Ogn

• In this study, we have isolated from a mouse limb-bud library cDNA clones encoding a 298-aa OG [4].
• Microarray hybridization was used to determine gene expression differences between lenses isolated from mimecan-null and wild type mice [5].
• The 177 base pair DNA coding for this unique sequence shows 47% identity to an 189 base pair sequence between exons 4 and 5 of the bovine osteoglycin/mimecan gene [6].
• Recently we demonstrated the presence of eight mimecan mRNA transcripts generated by alternative transcription initiation, alternative polyadenylation, and differential splicing, all of which encode an identical protein [7].
• These results suggest that the increased expression of the osteoglycin gene by LLLI in the early proliferation stage of cultured osteoblastic cells may play an important role in the stimulation of bone formation in concert with matrix proteins and growth factors [8].

Anatomical context of Ogn

• RESULTS: The mean collagen fibril diameter in the corneas of mimecan-null mice, as an average throughout the whole thickness of the tissue, was not appreciably different from normal (35.6 +/- 1.1 nm vs. 35.9 +/- 1.0 nm) [3].
• This study was performed to investigate the fibrillar architecture of the corneal stroma in mice homozygous for a null mutation in the corneal KSPG, mimecan [3].
• Mimecan is a member of this gene family and is expressed in many connective tissues [5].
• Effect of low-level laser irradiation on osteoglycin gene expression in osteoblasts [8].
• As the OIFs of the parietal and frontal bones approach, but prior to any physical overlap, they lie in different planes dorsoventrally; the parietal OIF located dorsal to the frontal OIF, a pattern maintained throughout subsequent sutural morphogenesis [9].

Associations of Ogn with chemical compounds

• The deduced amino acid (aa) sequence from the cDNA analysis showed that a precursor of OG has consensus leucine-rich repeats [4].
• Osteoglycin (OG) is a glycoprotein that was first isolated from bovine bone [4].

Regulatory relationships of Ogn

• The results from gene expression profiling reveal the ability of mimecan to influence expression of biglycan and chondroadherin, thereby indicating possible novel regulatory interactions between these SLRP family members [5].

Other interactions of Ogn

• The validity of the microarray data was established with the increased expression of bone-related genes such as pleiotrophin, osteoglycin, and legumain upon four-point bending and confirmation of increased expression of selected genes by real-time PCR [10].
• Osteoglycin is a small leucine-rich proteoglycan (SLRP) of the extracellular matrix which was previously called the osteoinductive factor [8].

Analytical, diagnostic and therapeutic context of Ogn

• Molecular cloning of the mouse osteoglycin-encoding gene [4].
• The absence of mimecan transcripts was confirmed by Northern blot analysis [11].
• In mimecan-null mice lenses, microarray analysis of 5,002 mouse genes demonstrated a more than two fold increase in expression of 65 genes and a more than two fold decrease in expression of 76 genes [5].
• METHODS: Mimecan-deficient mice were generated by gene-targeting using standard techniques [11].
• Collagen morphology in cornea and skin preparations from mimecan-null and control wild-type mice was analyzed by transmission electron microscopy [11].

References