scholarly journals Expression of smooth muscle cell phenotype by rat mesangial cells in immune complex nephritis. Alpha-smooth muscle actin is a marker of mesangial cell proliferation.

1991 ◽  
Vol 87 (3) ◽  
pp. 847-858 ◽  
Author(s):  
R J Johnson ◽  
H Iida ◽  
C E Alpers ◽  
M W Majesky ◽  
S M Schwartz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Smooth Muscle Actin ◽  
Cell Phenotype ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Mesangial Cell Proliferation ◽  
Smooth Muscle Cell Phenotype

Differentiated phenotype of glomerular mesangial cells in nodular culture

1996 ◽  
Vol 270 (4) ◽  
pp. F614-F622 ◽  
Author(s):  
M. Kitamura ◽  
T. Mitarai ◽  
R. Nagasawa ◽  
N. Maruyama
Keyword(s):  
Smooth Muscle ◽  
Northern Blot ◽  
Blot Analysis ◽  
Northern Blot Analysis ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Smooth Muscle Actin ◽  
Glomerular Mesangial Cells ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin

Prolonged culture of glomerular mesangial cells forms nodular structures composed of cells and surrounding extracellular matrix (ECM), which may mimic the situation in the glomerular mesangium of the kidney. The aim of this study was to investigate whether nodule-associated cells (NAC) exhibit a different phenotype to nodule-unassociated cells (NUC) in vitro. As phenotypic markers for rat mesangial cells, we examined mitogenic activity, expression of alpha-smooth muscle actin, and production of ECM constituents. Autoradiographic and immunohistochemical analyses revealed that NAC showed far less mitogenesis that NUC, like mesangial cells in the normal glomerulus. Immunofluorescence study and Northern blot analysis showed that alpha-smooth muscle actin, a marker of mesangial cell activation/dedifferentiation, was strongly expressed in NUC but faint in NAC. When nodules were dissolved by trypsinization, the dispersed NAC regained both active mitogenesis and alpha-smooth muscle actin expression, suggesting that the altered phenotype was reversible. Northern blot analysis revealed that the ratio of type IV collagen versus type I collagen expression, a marker of mesangial cell differentiation, was elevated in NAC compared with NUC. This phenotypic shift toward differentiation was associated with upregulation of transforming growth factor-beta 1. These findings demonstrate that mesangial cells in nodules exhibit a phenotype which is distinct from that of cells in two-dimensional cultures. We hypothesize that, as a differentiated feature, cultured mesangial cells have the ability to create an appropriate three-dimensional cyto-architecture that resembles the glomerular mesangium.

scholarly journals Smooth-Muscle Calponin in Mesangial Cells: Regulation of Expression and a Role in Suppressing Glomerulonephritis

2002 ◽  
Vol 13 (2) ◽  
pp. 322-331 ◽  
Author(s):  
Youichi Sugenoya ◽  
Ashio Yoshimura ◽  
Hisako Yamamura ◽  
Kiyoko Inui ◽  
Hiroyuki Morita ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Actin Binding ◽  
Luciferase Reporter ◽  
Tnf Α ◽  
Mesangial Cell Proliferation ◽  
Tgf Β1

ABSTRACT. The basic or h1 calponin gene, which encodes an actin-binding protein involved in the regulation of smooth-muscle shortening velocity, is known to be a smooth-muscle differentiation-specific gene. It was found that basic calponin was expressed by cultured mesangial cells and localized along the actin filaments. Among the growth factors involved in the mesangial cell pathophysiology, including platelet-derived growth factor-BB (PDGF-BB), tumor necrosis factor–α (TNF-α), and transforming growth factor–β1 (TGF-β1), TNF-α potently downregulates basic calponin expression in both the mRNA and protein levels, whereas TGF-β1 upregulates the calponin expression. PDGF-BB also reduced its mRNA expression. The half-life of basic calponin mRNA was determined to be similar between TNF-α–treated and –untreated mesangial cells, whereas cell transfection assays that used a luciferase reporter gene construct containing the functional basic calponin promoter showed that TNF-α and PDGF-BB reduced the transcriptional activity. Because stimulation with TNF-α and PDGF-BB was associated with mesangial cell proliferation, basic calponin may play a role in the suppression of mesangial cell proliferation. Treatment with anti–glomerular basement membrane antibody in calponin knockout mice induced more severe nephritis than in wild type mice, as judged from an increase in the urinary protein excretion, glomerular cellularity, and number of proliferating cell nuclear antigen–positive cells in glomerulus. These results suggest that basic calponin expression may serve as one of the intrinsic regulators of glomerular nephritis. Elucidation of the molecular mechanisms for regulation of the basic calponin expression in mesangial cells may improve the understanding of the molecular basis and pathogenesis of the glomerular response to injury.

scholarly journals The activated mesangial cell: a glomerular "myofibroblast"?

1992 ◽  
Vol 2 (10) ◽  
pp. S190 ◽  
Author(s):  
R J Johnson ◽  
J Floege ◽  
A Yoshimura ◽  
H Iida ◽  
W G Couser ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Mesangial Cell ◽  
De Novo ◽  
Mesangial Cells ◽  
Smooth Muscle Actin ◽  
Mesangial Matrix ◽  
Glomerular Injury ◽  
Alpha Smooth Muscle Actin ◽  
Glomerular Mesangial Cell ◽  
Structural Support

The glomerular mesangial cell may have several important beneficial functions in the normal glomerulus. These include the production of growth factors to allow normal cell turnover, the provision of structural support for the capillaries via the production of mesangial matrix, and the modulation of glomerular hemodynamics via their contractile properties. However, in various types of glomerular injury, the mesangial cell may acquire characteristics of a "myofibroblast", which may in fact be injurious to the glomerulus. These "activated" mesangial cells can be shown to be proliferating by one or more mechanisms that are mediated by platelets and that also involve the local production of platelet-derived growth factor. Like myofibroblasts in other tissues, the mesangial cell acquires smooth muscle cell-like properties, characterized by the de novo expression of alpha-smooth muscle actin, and by the development of fibroblast-like properties, characterized by the production of interstitial collagens in addition to normal mesangial matrix constituents. Identifying therapeutic strategies that prevent this phenotypic modulation of the mesangial cell may provide new ways to treat golmerular diseases.

Regulation of Mesangial Cell Alpha-Smooth Muscle Actin Expression in 3-Dimensional Matrix by High Glucose and Growth Factors

2008 ◽  
Vol 109 (2) ◽  
pp. e46-e56 ◽  
Author(s):  
Catharine Whiteside ◽  
Snezana Munk ◽  
Eric Ispanovic ◽  
Hong Wang ◽  
Howard Goldberg ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
High Glucose ◽  
Mesangial Cell ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
3 Dimensional ◽  
Dimensional Matrix ◽  
Actin Expression

scholarly journals Insulin-like Growth Factor I (IGF-I) Induces Unique Effects in the Cytoskeleton of Cultured Rat Glomerular Mesangial Cells

1997 ◽  
Vol 45 (4) ◽  
pp. 583-593 ◽  
Author(s):  
Anne K. Berfield ◽  
Douglas Spicer ◽  
Christine K. Abrass
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Smooth Muscle Actin ◽  
Ultrastructural Changes ◽  
Insulin Like Growth Factor ◽  
Glomerular Mesangial Cells ◽  
Muscle Actin ◽  
Igf I

Resident glomerular mesangial cells (MCs) have complex cytoskeletal organizations that maintain functional and structural integrity. The ability of cells to replicate, coordinate movement, change shape, and interact with contiguous cells or extracellular matrix depends on cytoskeletal organization. MCs synthesize insulin-like growth factor (IGF-I), express IGF-I receptors, and respond to IGF-I with increased proliferation. We noted that IGF-I treatment of mesangial cells was associated with a change in morphology. Therefore, these studies were undertaken to define specific IGF-I-mediated changes in cytoskeletal protein organization. Rat MCs were propagated from birth in culture without supplemental insulin. Quiescent, subconfluent cultures were treated with IGF-I (100 nM) for 1 hr. Rearrangements in f-actin, α-smooth muscle actin, β-actin, vimentin, and vinculin were seen by fluorescence microscopy. As the cytoskeleton rearranged, α-smooth muscle actin dissociated from the f-actin bundles and β-actin became polymerized under the leading lamellar edge. Ultrastructural changes were consistent with increased membrane turnover and metabolic activity. The normally sessile mesangial cell was induced by IGF-I to express a wound-healing phenotype characterized by movement and increased pinocytosis. These changes are different from those induced by insulin and have important implications for mesangial cell function.

Sign in / Sign up

Export Citation Format

Share Document