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At least 19 recordsLinked to original sources
PubMed1978

Relationship between glomerular mesangial cell proliferation and amyloid deposition as seen by ultrastructural and morphometric analysis in experimental kala-azar of the hamster.

Light and electron microscopic studies combined with a morphometric analysis of the hamster glomerulus in experimental kala-azar showed progressive hyperplasia of mesangial cells beginning on the 10th day and reaching a peak on the 20th day after infection. Afterward, the number of mesangial cells declined and a progressive rise of amyloid deposits over the mesangial matrix was observed. This system for amyloid production is unique if we consider that probably one cell, the mesangial cell, is involved in glomerular amyloid deposition. Our data support a slight modification in the sequence of events of the biphasic theory of amyloid formation. We observed that the number of mesangial cells declines when amyloid deposition increases and that mesangial cell morphology in this stage is not that of an actively secreting cell. It is therefore hypothesized that amyloid precursor material is secreted into the matrix during the proliferative phase. In the second phase, amyloid deposits occur in the extracellular media close to functionally impaired mesangial cells.

Amyloid↗
PubMed2026

Complement expression profiles in human glomerular mesangial cells, endothelial cells, podocytes and proximal tubular epithelial cells.

BACKGROUND: Local expression of complement components in the kidney has been reported sporadically in both diseased and normal kidneys. This study aimed to comprehensively characterize the expression of complement components in human glomerular mesangial cells (GMCs), glomerular endothelial cells (GECs), podocytes, and proximal tubular epithelial cells (PTECs) in non-diseased renal tissue. METHODS: Complement expression in cultured human renal intrinsic cells was initially evaluated using reverse transcription polymerase chain reaction and immunofluorescence staining. These findings were further examined using publicly available single-cell RNA-sequencing datasets and 10×Genomics single-cell RNA sequencing of non-diseased human kidney tissue. The analyses focused on complement components involved in the initiation of the classical, lectin, and alternative pathways, as well as components shared among these activation pathways, terminal pathway components, complement regulators, and complement receptors. RESULTS: Complement components unique to the initial phase for classical pathway (C1S, C1R, C2, C4), lectin pathway (MBL2, FCN1, MASP1), alternative pathway (CFB, CFD), and the C3 component shared by the three activation pathways were detected in these cells. The components shared by the terminal pathways including C5, C6, C7, C8 and C9 exhibited lower expression, while complement regulators (CFH, CFI, CD55/DAF, CD46/MCP, CD59, C4BPB, PROS1/Protein S) or receptors (CD93/C1QR1, CR1), particularly membrane-bound proteins, such as DAF, MCP and CD59, which inhibit complement activation and the formation of the membrane attack complex, showed relatively high expression. CONCLUSION: These results showed that all four types of intrinsic renal cells expressed multiple complement components associated with the classical, lectin, and alternative pathways. In non-diseased kidney tissue, complement regulatory molecules involved in the control of complement activation showed relatively higher expression, whereas components of the terminal complement pathway were expressed at relatively lower levels, suggesting that renal intrinsic cells maintain a locally poised but tightly regulated complement system.

Humans↗
PubMed1976

Diffuse mesangial cell proliferation in focal sclerosing glomerulonephritis.

Morphometrical and clinical investigations were performed in 34 patients with the so-called hypercellular form of focal glomerulosclerosis (FGS), i.e., a form showing clear diffuse mesangial hypercellularity beside focal sclerosis with the light microscopy. This form was compared with focal glomerulosclerosis without remarkable mesangial hypercellularity, with mild mesangioproliferative glomerulonephritis (gn), as well as with normal kidneys. The results were as follows: 1. Morphometrically both the increase in relative mesangial volume as well as in mesangial cell count is statistically significant in the hypercellular form compared with the nonhypercellular form and with controls. Comparison with mild mesangioproliferative gn shows no difference. 2. Even the so-called nonhypercellular form contains more mesangial matrix and mesangial cells than the controls. 3. The frequency of the hypercellular form is higher in males and in older patients. 4. All of our patients with hypercellular FGS had at the time of biopsy manifested nephrotic syndrome. The frequency of additional clinical symptoms (hematuria, hypertension, renal insufficiency) corresponds with the nonhypercellular form, but is different in mild mesangioproliferative gn. 5. Therapeutic response and prognosis is worse in the hypercellular form. The hypercellular form of FGS has to be separated from the nonhypercellular form as a defined entity.

Adolescent↗
PubMed1976

Long-term alloxan diabetes in the rat. Study of mesangial cell morphology by serial biopsies.

Experimental diabetes in the rat was induced by alloxan (40 mg/kg body weight) and resulted in permanent hyperglycaemia (mean glycaemia: 403.0 mg/100 ml). The animals were left untreated for more than 16 months. The mesangial cell of the renal glomerulus was studied by serial biopsies performed each month under light anaesthesia in the diabetic animals and in normal controls of the same age. Large dense bodies appeared in the cytoplasm after 3 months in the diabetics and after 10 months in the controls. With time, a larger number of mesangial cells contained these dense bodies. At the end stage they seem to be mainly lipidic. When NO3Ag is given in the drinking water the dense bodies accumulate particles of silver, suggesting that they contain fragments of the basement membrane. While the acid phosphatase reaction was negative in biopsy specimens from diabetic animals, it remains possible that the large dense bodies belong to the lysosomial system. This point, as well as the pathologic significance of the dense bodies is currently investigated.

Acid Phosphatase↗
PubMed1979

Role of marrow-derived monocytes and mesangial cells in removal of immune complexes from renal glomeruli.

Phagocytosis of intravenously administered immune complexes by cells in the mesangium was investigated. The model used was that of exchange marrow transplantation between Chediak-Higashi (CH) mice and syngeneic partners after X-irradiation. This model was chosen since marrow-derived macrophages could be differentiated from resident mesangial cells by the presence of the characteristic giant lysosomes in phagocytic cells of the CH mice. Injected immune complexes were cleared normally and localized in the glomerular mesangium in CH or C57BL/6J mice receiving either C57BL/6J or CH marrow. C57BL/6J mice with CH marrow injected with immune complexes prepared with reduced and alkylated antibodies accumulated many cells within the mesangium that contained both giant lysosomes and electron dense deposits. Deposits were not found in cells with subplasmalemmal microfilaments and perpheral dense bodies. Conversely, the cells in the mesangium of CH mice with C57BL/6J marrow that contained electron dense deposits were devoid of giant lysosomes. Based on these observations, we concluded that (a) marrow-derived monocytes contribute to mesangial hypercellularity after deposition of immune complexes and (b) phagocytosis of immune complexes localized in the glomerular mesangium was by marrow-derived monocytes rather than by mesangial cells.

Animals↗
PubMed1977

[Reserve production of renin by glomerular mesangial cells following experimental decrease in renal circulation].

The aorta was partially constricted between the origins of the two renal arteries in rats. The renin activity was studied separately in the capillary parts of the isolated glomeruli and in their arterioles. The renin activity was found in the capillary parts of the glomeruli 3 to 4 weeks after the constriction. The rough and smooth endoplasmic reticulum and the Golgi complex of the mesangial cells were activated at this period. The authors consider these results as a confirmation of the hypothesis on the reserve renin production by mesangial cells under prolonged decrease of renal circulation.

Animals↗
PubMed1979

[Dynamics of renin production by the juxtaglomerular and mesangial cells of individual rat kidney glomeruli following adrenalectomy].

Adrenal incompetence developed in rats 6 weeks after adrenalectomy without any salt and hormonal compensation. In individual fragments of the isolated glomeruli containing juxtaglomerular cells (JGC) renin activity increased 1.2 times on the average, and there was revealed renin-like activity (RLA) in the fragments containing mesangial cells (MC). Signs of intensified renin secretion (expressed in reduction of granule count, marked development of granular endoplasmic reticulum, Golgi complex and microtubules) were noted in the JGC. In MC such organoids were well developed, but no granules were revealed. The following occurred in 8 to 12 weeks with the restoration of the 11-OCS and sodium level in the plasma: renin JGC activity became normal, RLA activity in MC disappeared, and the initial ultrastructure of both of these cells was restored. The reserve role of MC as the source of renin-like substances was confirmed.

Adrenal Glands↗
PubMed1979

Nephrotic syndrome with mesangial-cell proliferation in children--a distinct entity?

Various morphologic patterns have been identified in renal biopsies of children with the idiopathic nephrotic syndrome. Children with focal segmental glomerulosclerosis have clinicopathologic features sufficiently distinct to warrant a separate subclassification. "Immunoglobulin M (IgM) nephropathy" and other morphologic patterns are less well defined. The clinicopathologic characteristics of eight patients with the nephrotic syndrome, increased mesangial cellularity on renal biopsy, and hematuria (mesangioproliferative nephropathy) were evaluated. Response to standardized prednisone therapy was poor. Of the seven children followed for 7-29 months, only two were in remission at the time of writing, and each of these had had one prior relapse. The eighth patient was lost to follow-up after one month. Although the number of patients studied was small, there was a strong correlation between degree of mesangial-cell proliferation and failure of primary treatment. As concepts of the pathogenesis of idiopathic nephrotic syndrome in children continue to evolve, the mesangioproliferative lesion should be recognized and marked for further study.

Adolescent↗
PubMed1977

The mesangial cell in glomerulonephritis. I. Mechanisms of hypercellularity in experimental immune complex glomerulonephritis.

One-shot active immune complex glomerulonephritis was induced in rabbits by intravenous bovine serum albumin (250 mg. per kg.) and the mechanism of glomerular hypercellularity investigated. Most of the extra cells were mononuclear with few polymorphonuclear leukocytes. Fibrin was present in severe lesions. Glomerular mitoses were seen in normal kidneys but were more common in hypercellular glomeruli. This is direct evidence of local proliferation. Also, biopsies taken 1 hour after giving tritiated thymidine contained locally labeled cells. The mitotic rate and degree of local labeling both varied in proportion to the degree of hypercellularity. By electron microscopy both mesangial and endothelial cells were identified in mitosis. The majority of the mononuclear cells in the hypercellular glomeruli could not be identified by position or ultrastructure. Infiltration by nonglomerular cells was confirmed by the presence of macrophages, lymphocytes, and plasma cells.

Animals↗
PubMed1976

Human glomerular smooth muscle (mesangial) cells in culture.

Glomerular smooth muscle cells were grown and subcultured from human glomeruli in vitro. These cells, stained with antiserum to smooth muscle actomyosin and examined by immunofluorescence, had brightly stained intracellular fibrils similar to those seen in smooth muscle cells. Actomyosin fibrils were altered by conditions affecting actomyosin in vitro. Glomerular smooth muscle cells lacked the antihemophilic factor and blood group antigens present in endothelial cells, and are, therefore, most likely derived from the smooth muscle cells of the glomerular mesangium. By radio-labeled amino acid analysis, they synthesize a collagen differing from that of fibroblasts, and which probably differs from basement membrane collagen. Other cell types could be grown and subcultured using a different glomerular isolation technique, culture medium and method of subculture.

Actomyosin↗
PubMed1978

Cell characteristics of cultured glomeruli from different animal species.

A modified sieving technique has been developed to isolate pure glomeruli from monkey, sheep, dog, rabbit and rat kidney. Glomeruli from all these species have been grown in tissue culture and the glomerular cell outgrowth studied by light microscopy and time-lapse cinemicroscopy. The pattern of growth was the same for all the species studied. In all species, three cell populations have been identified with the features of epithelial cells, mesangial cells and macrophages, although the latter population is only rarely observed. The morphology and culture characteristics of each cell type in all species were similar, including the relative numbers present and rates of division.

Animals↗
PubMed1979

Cellular aspects of rabbit Masugi nephritis. IV. Cell quantitation of proliferative glomerulonephritis.

Diffuse proliferative glomerulonephritis was induced in the rabbit with injection of goat nephrotoxic serum, and cell dynamics in the glomerulus were quantitatively investigated. The mean total cell number of a normal glomerulus in cross-section was 54.8, consisting of 24.1 endothelial cells, 16.0 podocytes, and 14.3 mesangial cells. In 5 selected nephritic rabbits, the mean total cell number of a glomerulus at the florid stage (7 to 12 experimental days) was 2.4 times as great as the control. It was revealed that the cells consisted of 27.9 endothelial cells, 14.9 podocytes, 21.1 mesangial cells, and 57.8 monocytic cells, indicating that about 76 per cent of the increased cells were of monocytic origin. Mesangial cells showed moderate increase in number (1.5 times) which persisted until 100 days, whereas endothelial cells increased only slightly. The monocytic cells promptly disappeared at 40 days correlating well with resolution of the proliferative change. Although the cellular compositions varied in each case, it was concluded that monocytes were essential in producing proliferative glomerular changes in the reversible type of Masugi nephritis.

Animals↗