scholarly journals Expression of types I, II, and III TGF-beta receptors in human glomerulonephritis.

1998 ◽  
Vol 9 (12) ◽  
pp. 2253-2261
Author(s):  
T Yamamoto ◽  
T Watanabe ◽  
N Ikegaya ◽  
Y Fujigaki ◽  
K Matsui ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lupus Nephritis ◽  
Iga Nephropathy ◽  
Membranoproliferative Glomerulonephritis ◽  
Type I ◽  
Tgf Beta ◽  
Matrix Deposition ◽  
Peritubular Capillaries ◽  
Tubulointerstitial Lesions ◽  
Beta Receptors

Protein and mRNA expression of transforming growth factor-beta (TGF-beta) receptor type I (TbetaRI), type II (TbetaRII), and type III (TbetaRIII) were studied in serial sections of kidney samples obtained from patients with glomerulonephritis. In minimal change disease, weak expression of TbetaRI and TbetaRII was observed mainly in glomerular endothelial cells, peritubular capillaries, and interstitial arteriolar endothelial cells, whereas TbetaRIII expression was found mainly in the interstitium. Expression of all three TGF-beta receptors (TbetaR) was increased remarkably in glomerular and Bowman's capsular cells comprising the tuft adhesions to Bowman's capsules in glomerulonephritis with increased matrix accumulation, including IgA nephropathy, lupus nephritis, focal and segmental glomerulosclerosis, myeloperoxidase-antineutrophil cytoplasmic antibody-associated crescentic glomerulonephritis, and membranoproliferative glomerulonephritis. Increased expression of the three TbetaR was also seen in glomerular epithelial cells in the vicinity of glomerulosclerotic lesions, in crescent cells, and in some tubules and infiltrative mononuclear cells found in the periglomerular and tubulointerstitial lesions with increased matrix deposition. In contrast, no remarkable TbetaRII expression was noted in mesangial proliferative lesions in IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis. These data suggest that distinctive modulation of TbetaR expression may be involved in the development of adhesive, sclerotic, and proliferative renal lesions in human glomerulonephritis.

Interstitial Inflammatory and Chronic Tubulointerstitial Lesions in Lupus Nephritis: Comparison with those in IgA Nephropathy

Lupus ◽  
1993 ◽  
Vol 2 (1_suppl) ◽  
pp. 261-268 ◽  
Author(s):  
Tatsuo Yamamoto ◽  
Mitsumasa Nagase ◽  
Akira Hishida ◽  
Nishio Honda
Keyword(s):  
Lupus Nephritis ◽  
Iga Nephropathy ◽  
Immune Complexes ◽  
Prognostic Significance ◽  
Underlying Disease ◽  
Inflammatory Lesions ◽  
Tubulointerstitial Lesions ◽  
Glomerular Lesions ◽  
Renal Prognosis

The significance of interstitial inflammatory and chronic tubulointerstitial lesions was studied in relation to the severity of glomerular lesions in 62 patients with lupus nephritis and 88 with IgA nephropathy. Severe interstitial inflammatory and chronic tubulointerstitial lesions were found in patients with severe glomerular lesions in both lupus nephritis and IgA nephropathy. In such cases, the serum creatinine levels at biopsy were high and the renal prognosis was poor regardless of the underlying disease (lupus nephritis or IgA nephropathy). No IgA nephropathy patients with nil or mild glomerular lesions had moderate or severe interstitial inflammatory and/or chronic tubulointerstitial lesions. In contrast, predominantly severe interstitial inflammatory lesions were found in 36% of lupus nephritis patients with nil or mild glomerular lesions. The prevalence of interstitial immune complexes deposition was markedly high in those with predominant interstitial inflammatory lesions. However, the severity of chronic tubulointerstitial lesions was mild and renal function did not deteriorate in the mean follow-up periods of 68.6 months. It is suggested that, besides the tubulointerstitial lesions attributable to the severe concomitant glomerular damage, the interstitial deposition of immune complexes per se plays a pathogenic role in the interstitial inflammatory lesions in lupus nephritis. Its prognostic significance, however, was considered to be minor.

scholarly journals Constitutive Atg5 overexpression in mouse bone marrow endothelial progenitor cells improves experimental acute kidney injury

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Daniel Patschan ◽  
Katrin Schwarze ◽  
Björn Tampe ◽  
Jan Ulrich Becker ◽  
Samy Hakroush ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Kidney Injury ◽  
Mouse Bone Marrow ◽  
Protective Effects ◽  
Endothelial Progenitor ◽  
Matrix Deposition ◽  
Peritubular Capillaries ◽  
Clinical Consequences

Abstract Background Endothelial Progenitor Cells have been shown as effective tool in experimental AKI. Several pharmacological strategies for improving EPC-mediated AKI protection were identified in recent years. Aim of the current study was to analyze consequences of constitutive Atg5 activation in murine EPCs, utilized for AKI therapy. Methods Ischemic AKI was induced in male C57/Bl6N mice. Cultured murine EPCs were systemically injected post-ischemia, either natively or after Atg5 transfection (Adenovirus-based approach). Mice were analyzed 48 h and 6 weeks later. Results Both, native and transfected EPCs (EPCsAtg5) improved persisting kidney dysfunction at week 6, such effects were more pronounced after injecting EPCsAtg5. While matrix deposition and mesenchymal transdifferentiation of endothelial cells remained unaffected by cell therapy, EPCs, particularly EPCsAtg5 completely prevented the post-ischemic loss of peritubular capillaries. The cells finally augmented the augophagocytic flux in endothelial cells. Conclusions Constitutive Atg5 activation augments AKI-protective effects of murine EPCs. The exact clinical consequences need to be determined.

Interstitial Inflammatory and Chronic Tubulointerstitial Lesions in Lupus Nephritis: Comparison with Those in IgA Nephropathy

Lupus ◽  
1993 ◽  
Vol 2 (4) ◽  
pp. 261-268 ◽  
Author(s):  
Tatsuo Yamamoto ◽  
Mitsumasa Nagase ◽  
Akira Hishida ◽  
Nishio Honda
Keyword(s):  
Lupus Nephritis ◽  
Iga Nephropathy ◽  
Tubulointerstitial Lesions

Beta2-glycoprotein I Expression in Lupus Nephritis Patients with Antiphospholipid-associated Nephropathy

2016 ◽  
Vol 43 (11) ◽  
pp. 2026-2032 ◽  
Author(s):  
Ruitong Gao ◽  
Wenqing Yu ◽  
Yubing Wen ◽  
Hang Li
Keyword(s):  
Endothelial Cells ◽  
Lupus Nephritis ◽  
Antiphospholipid Antibodies ◽  
Kidney Tissue ◽  
Clinical Information ◽  
Severe Condition ◽  
Glycoprotein I ◽  
Biopsy Specimens ◽  
Peritubular Capillaries

Objective.Antiphospholipid-associated nephropathy (aPLN) is a severe condition in patients with lupus nephritis (LN). aPLN should be distinguished from other reasons for renal ischemia. The most important cofactor of antiphospholipid antibodies (aPL), β2-glycoprotein I (β2GPI), was shown in vitro to bind endothelial cells and to induce a procoagulant phenotype. The objectives of this study were to investigate whether β2GPI expression was involved in patients with LN with aPLN and to determine its specificity.Methods.We retrospectively investigated β2GPI expression in 231 renal biopsy specimens of patients with LN. Data from biopsy reports and clinical information were collected. Immunohistochemical staining for β2GPI expression was performed.Results.Histological aPLN was detected in 88 patients with LN (38.1%). The LN with aPLN consisted of 43 patients (18.6%). Expression of β2GPI was detected in endothelial cells in 14 (32.6%) in renal arteries or arterioles, 11 (25.6%) in glomerular or peritubular capillaries, and a total of 15 (34.9%) of the 43 patients with LN with aPLN. It was mainly expressed in the endothelial cells in patients with LN with aPLN (p < 0.05). The specificity of β2GPI expression in patients with LN with aPLN was 97.5%.Conclusion.Expression of β2GPI may be involved in the formation of aPLN in patients with LN. This expression in endothelial cells in kidney tissue may be considered a useful marker for aPLN.

Imbalanced expression of the type I TGF-beta receptors ALK-1 and ALK-5 in pulmonary fibrosis

Pneumologie ◽  
2009 ◽  
Vol 63 (02) ◽  
Author(s):  
I Chrobak ◽  
N Banthien ◽  
K Kitowska ◽  
M Königshoff ◽  
W Seeger ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Type I ◽  
Tgf Beta ◽  
Beta Receptors ◽  
Alk 5

Imbalanced expression of the type I TGF-beta receptors ALK-1 and ALK-5 in pulmonary fibrosis

Pneumologie ◽  
2007 ◽  
Vol 61 (12) ◽  
Author(s):  
I Chrobak ◽  
N Banthien ◽  
M Königshoff ◽  
K Kitowska ◽  
O Eickelberg
Keyword(s):  
Pulmonary Fibrosis ◽  
Type I ◽  
Tgf Beta ◽  
Beta Receptors ◽  
Alk 5

scholarly journals Detection of Duffy Antigen in the Plasma Membranes and Caveolae of Vascular Endothelial and Epithelial Cells of Nonerythroid Organs

Blood ◽  
1997 ◽  
Vol 89 (2) ◽  
pp. 701-712 ◽  
Author(s):  
Asok Chaudhuri ◽  
Søren Nielsen ◽  
Marie-Louise Elkjaer ◽  
Valerie Zbrzezna ◽  
Fang Fang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Epithelial Cells ◽  
Plasma Membranes ◽  
Cell Types ◽  
Immunoblot Analysis ◽  
Type I ◽  
Ultrastructural Studies ◽  
Peritubular Capillaries ◽  
Group Protein

Abstract The nonerythroid expression of the Duffy blood group protein (gp-Fy) was confined to certain cell types. Immunocytochemistry studies of the kidney showed gp-Fy in the endothelium of glomeruli, peritubular capillaries, vasa recta, and the principal cells (epithelial) of collecting ducts. Gp-Fy was also produced in the endothelial cells of large venules and epithelial cells (type-I) of pulmonary alveoli. In the thyroid, only the endothelial cells of capillaries produced gp-Fy. In the spleen, the endothelial cells of capillaries, high endothelial venule, and sinusoids produced abundant gp-Fy. Ultrastructural studies showed that apical and basolateral plasma membrane domains, including caveolae, had gp-Fy. Immunoblot analysis showed substantially less gp-Fy in nonerythroid cells than in erythrocytes. Moreover, the analyzed nonerythroid organs of Duffy-negative individuals did not produce more gp-Fy to compensate for the lack of this protein in their erythrocytes. The nucleotide sequence and the size of kidney mRNA from a Duffy-positive individual were the same as that of bone marrow. It is assumed, therefore, that nonerythroid Duffy protein is the product of the same gene as that of bone marrow. This notion is reinforced by the fact that nonerythroid and erythroid gp-Fy have the same antigenic domains.

scholarly journals Expression of TGF-beta receptors type I and II in human glomerulonephritis.

1998 ◽  
Vol 13 (2) ◽  
pp. 279-284 ◽  
Author(s):  
A. Onetti Muda ◽  
S. Feriozzi ◽  
S. Rahimi ◽  
T. Faraggiana
Keyword(s):  
Type I ◽  
Tgf Beta ◽  
Beta Receptors
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