Activation of extracellular signal-regulated kinases is essential for pressure-induced proliferation of vascular smooth muscle cells.

In hypertension, increased transmural pressure directly influences vascular smooth muscle cells and causes cell proliferation. However, the mechanisms of transmural pressure-induced proliferation of vascular smooth muscle cells are unknown. We investigated the role of various protein kinases in pressure-induced proliferation of vascular smooth muscle cells.

Association between plasma lipoprotein(a) and endothelial dysfunction in normocholesterolemic and non-diabetic patients with angiographically normal coronary arteries.

The present study was designed to examine whether elevated levels of lipoprotein(a) (Lp(a)) are related to the impairment of the endothelium-dependent vasoresponse to acetylcholine (ACh) in normocholesterolemic and non-diabetic human normal coronary arteries. ACh (30 microg) was injected into the left main coronary artery of 31 patients (serum low-density cholesterol <160mg/dl and fasting plasma glucose <126mg/dl) with angiographically normal coronary arteries, and the relation between diameter change and lipid levels was analyzed. The mean diameter change of all coronary segments examined (segments 6, 8, 11 and 13) was reduced by 14.

Expression of profilin, an actin-binding protein, in rat experimental glomerulonephritis and its upregulation by basic fibroblast growth factor in cultured rat mesangial cells.

Profilin binds to actin monomer to regulate actin polymerization, and to phosphatidylinositol 4,5-bisphosphate to inhibit hydrolysis by phospholipase Cgamma1. This study investigated the expression of profilin in rat anti-Thy-1.1 mesangial proliferative glomerulonephritis (GN) and examined the effect of growth factors on its expression in cultured rat mesangial cells.