Identification of a subunit of NADH-dehydrogenase as a p49/STRAP-binding protein

Background  

The p49/STRAP (or SRFBP1) protein was recently identified in our laboratory as a cofactor of serum response factor that contributes to the regulation of SRF target genes in the heart.     

Effects of nerve growth factor (NGF) on blood vessels area and expression of the angiogenic factors VEGF and TGFbeta1 in the rat ovary

Background  

Angiogenesis is a crucial process in follicular development and luteogenesis. The nerve growth factor (NGF) promotes angiogenesis in various tissues. An impaired production of this neurotrophin has been associated with delayed wound healing. A variety of ovarian functions are regulated by NGF, but its effects on ovarian angiogenesis remain unknown. The aim of this study was to elucidate if NGF modulates 1) the amount of follicular blood vessels and 2) ovarian expression of two angiogenic factors: vascular endothelial growth factor (VEGF) and transforming growth factor beta 1 (TGFbeta1), in the rat ovary.     

Serum response factor mRNA induction in the hypertrophying chicken patagialis muscle

Gene expression inthe stretched chicken patagialis (Pat) muscle has not been extensivelyexamined. This study's purpose was to determine the Pat muscle'sexpression pattern of serum response factor (SRF), skeletal -actin,and MyoD mRNAs after 3 days (onset of stretch), 6 days (end of firstweek of rapid growth), and 14 days (slowed rate of stretch-inducedgrowth) of stretch. SRF mRNA demonstrated two species (B1 and B2), withB2 being more prevalent in the predominantly fast-twitch Pat muscle,compared with the slow-tonic muscle. Stretch overload increased B1 andB2 SRF mRNA concentrations, and the increase in B1 SRF mRNAconcentration was greater at day 6 compared with days 3 or14. MyoD mRNA concentration wasgreater in 3-day-stretched Pat muscles, compared withdays 6 or14 . Skeletal -actin mRNAconcentration was not changed during the study. Gel mobility shiftassays demonstrated that SRF binding with serum response element 1 ofthe skeletal -actin promoter had no altered binding patterns from6-day-stretched Pat nuclear extracts. It appears that SRF and MyoDmRNAs are induced in the stretch-overloaded Pat muscle but at differenttime points.

     

Angiotensin II upregulates the expression of placental growth factor in human vascular endothelial cells and smooth muscle cells

Background  

Atherosclerosis is now recognized as a chronic inflammatory disease. Angiotensin II (Ang II) is a critical factor in inflammatory responses, which promotes the pathogenesis of atherosclerosis. Placental growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family cytokines and is associated with inflammatory progress of atherosclerosis. However, the potential link between PlGF and Ang II has not been investigated. In the current study, whether Ang II could regulate PlGF expression, and the effect of PlGF on cell proliferation, was investigated in human vascular endothelial cells (VECs) and smooth muscle cells (VSMCs).     

Proof-of-principle investigation of an algorithmic model of adenosine-mediated angiogenesis

Background  

We investigated an algorithmic approach to modelling angiogenesis controlled by vascular endothelial growth factor (VEGF), the anti-angiogenic soluble VEGF receptor 1 (sVEGFR-1) and adenosine (Ado). We explored its feasibility to test angiogenesis-relevant hypotheses. We illustrated its potential to investigate the role of Ado as an angiogenesis modulator by enhancing VEGF activity and antagonizing sVEGFR-1.     

A mathematical model of venous neointimal hyperplasia formation

Background  

In hemodialysis patients, the most common cause of vascular access failure is neointimal hyperplasia of vascular smooth muscle cells at the venous anastomosis of arteriovenous fistulas and grafts. The release of growth factors due to surgical injury, oxidative stress and turbulent flow has been suggested as a possible mechanism for neointimal hyperplasia.     

Adiponectin may contribute to synovitis and joint destruction in rheumatoid arthritis by stimulating vascular endothelial growth factor, matrix metalloproteinase-1, and matrix metalloproteinase-13 expression in fibroblast-like synoviocytes more than proinflammatory mediators

Introduction  

The role of adiponectin in the pathogenesis of arthritis is still controversial. This study was performed to examine whether adiponectin is involved in joint inflammation and destruction in rheumatoid arthritis (RA) in relation to the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs).     

Adenosine infusion increases plasma levels of VEGF in humans

Background  

Many in vitro studies have shown that adenosine (Ado) can induce vascular endothelial growth factor (VEGF) mRNA and protein expression and stimulate endothelial proliferation. In the present study, we seek to determine whether Ado can increase circulating levels of VEGF protein in the intact human.