Rgs19 regulates mouse palatal fusion by modulating cell proliferation and apoptosis in the MEE.

Palatal development is one of the critical events in craniofacial morphogenesis. During fusion of the palatal shelves, removal of the midline epithelial seam (MES) is a fundamental process for achieving proper morphogenesis of the palate. The reported mechanisms for removing the MES are the processes of apoptosis, migration or general epithelial-to-mesenchymal transition (EMT) through modulations of various signaling molecules including Wnt signaling.

Proteome analysis of developing mice diastema region.

Different from humans, who have a continuous dentition of teeth, mice have only three molars and one incisor separated by a toothless region called the diastema in the hemi mandibular arch. Although tooth buds form in the embryonic diastema, they regress and do not develop into teeth. In this study, we evaluated the proteins that modulate the diastema formation through comparative analysis with molar-forming tissue by liquid chromatography-tandem mass spectroscopy (LC-MS/MS) proteome analysis.

FGF2 stimulates SDF-1 expression through the Erm transcription factor in Sertoli cells.

Ets-related molecule (Erm) is a member of the Ets transcription factor family. Erm is known to be an important factor for the self-renewal of Spermatogonial stem cells (SSCs) and the maintenance of spermatogenesis. We investigated the molecular mechanism of Erm regulation on SDF-1 in TM4 Sertoli cells.

Upregulation of smpd3 via BMP2 stimulation and Runx2.

Deletion of smpd3 induces osteogenesis and dentinogenesis imperfecta in mice. smpd3 is highly elevated in the parietal bones of developing mouse calvaria, but not in sutural mesenchymes. Here, we examine the mechanism of smpd3 regulation, which involves BMP2 stimulation of Runx2.

Suppression of mesangial cell proliferation and extracellular matrix production in streptozotocin-induced diabetic rats by Sp1 decoy oligodeoxynucleotide in vitro and in vivo.

Transcription factor Sp-1 is an important fibrogenic factor that is involved in the pathogenesis of diabetic nephropathy. In this study, we examined the effect of Sp1 decoy oligodeoxynucleotides (ODNs) on the extracellular matrix (ECM) gene expression in cultured rat mesangial cells (RMC) and streptozotocin (STZ)-induced diabetic rats. The ring-type Sp1 decoy ODNs significantly decreased ECM mRNA expression and Sp1 binding to the promoter region of these PDGF-induced genes in RMC.

The inhibitory effect of siRNAs on the high glucose-induced overexpression of TGF-beta1 in mesangial cells.

Diabetic nephropathy is characterized by an expansion of the glomerular mesangium, caused by mesangial cell proliferation and an excessive accumulation of extracellar matrix (ECM) proteins, which eventually leading to glomerulosclerosis. TGF-beta1 was found to play an important role in the accumulation of ECM in the kidney. In this study, TGF-beta1 RNA interference was used as an effective therapeutic strategy.

TGF-beta1 siRNA suppresses the tubulointerstitial fibrosis in the kidney of ureteral obstruction.

TGF-beta1 has been known as an important factor in tubulointerstitial fibrosis which is a common process in most progressive renal diseases. We hypothesized that the interstitial fibrosis could be prevented by abolishing TGF-beta1 function in unilateral ureteral obstruction (UUO)-induced renal fibrosis. shRNA vectors were generated to suppress TGF-beta1 expression at a high glucose concentration which allowed the maximal induction of TGF-beta1 in primary rat mesangial cells.

Sp1-decoy oligodeoxynucleotide inhibits high glucose-induced mesangial cell proliferation.

Mesangial expansion caused by cell proliferation and glomerular extracellular matrix accumulation is one of the earliest renal abnormalities observed at the onset of hyperglycemia in diabetes mellitus. Transcription factor Sp1 is implicated in the transcriptional regulation of a wide range of genes participating in cell proliferation, and is assumed to play an essential role in mesangial expansion. We have generated a phosphorothioated double-stranded Sp1-decoy oligodeoxynucleotide that effectively blocks Sp1 binding to the promoter region for transcriptional regulation of transforming growth factor-beta1 and plasminogen activator inhibitor-1.

Inhibitory effects of novel E2F decoy oligodeoxynucleotides on mesangial cell proliferation by coexpression of E2F/DP.

Proliferation of glomerular mesangial cells (MCs) is an important feature of several forms of glomerulonephritis. The transcription factor E2F coordinately regulates expression of genes required for cell proliferation, thereby mediating cell growth control. Here we investigated the role of E2F1 and E2F4 expression, with or without co-expression of DP1 or DP2, on cell proliferation in transiently transfected primary rat MCs.