The immunohistopathology of glomerular antigens. III. Increased mesangial actomyosin in experimental diabetes in the rat.
Antisera to rat smooth muscle actomyosin (AMY) and myosin localize in the rat glomercular mesangium. The width of mesangial staining for AMY is increased in rats diabetic for four months (p less than 0.01) and seven months (p less than 0.0005) compared with age-matched controls. Mesangial AMY staining of unilaterally nephrectomized control animals was moderately increased after seven months, whereas unilaterally nephrectomized diabetic rats had prominently increased AMY mesangial width at four months, when they were compared with intact diabetic animals (p less than 0.05). Thus, a distinctive alteration that is found in human diabetic nephropathy also occurs in experimental (streptozotocin) diabetes in the rat. Further, this alteration appears to be accelerated by the changes in nephron hemodynamics resulting from unilateral nephrectomy. While the function of mesangial AMY is unknown, it may be related to intrarenal regulation of glomerular ultrafiltration, which appears to be altered in diabetic nephropathy in man.
D000205:Actomyosin / Q000378:metabolism*; D000375:Aging; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D003928:Diabetic Nephropathies / Q000378:metabolism; D007668:Kidney / Q000473:pathology / Q000502:physiology; D007678:Kidney Glomerulus / Q000378:metabolism*; D008566:Membranes / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D009392:Nephrectomy; D051381:Rats
D000205:Actomyosin; D009218:Myosins