scholarly journals EP 1 receptor antagonism mitigates early and late stage renal fibrosis

2022 ◽  
Author(s):  
Jean‐Claude Kresse ◽  
Henricus A.M. Mutsaers ◽  
Michael Schou Jensen ◽  
Stine Julie Tingskov ◽  
Mia Gebauer Madsen ◽  
...  
Keyword(s):  
Late Stage ◽  
Renal Fibrosis ◽  
Receptor Antagonism

scholarly journals Immunophenotypical Characterization of M1/M2 Macrophages and Lymphocytes in Cisplatin-Induced Rat Progressive Renal Fibrosis

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 257
Author(s):  
Minto Nakagawa ◽  
Mohammad Rabiul Karim ◽  
Takeshi Izawa ◽  
Mitsuru Kuwamura ◽  
Jyoji Yamate
Keyword(s):  
T Cells ◽  
Late Stage ◽  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Kidney Diseases ◽  
Tubular Damage ◽  
M2 Macrophages ◽  
Renal Interstitial Fibrosis ◽  
M1 Macrophages ◽  
Renal Lesions

Renal fibrosis is regarded as the common final pathway leading to chronic kidney diseases; macrophages and myofibroblasts play important roles in the development of fibrosis. F344 rats were injected once with cisplatin (CDDP; 6 mg/kg BW) for renal lesions. Here, immunophenotypical characteristics of macrophages and lymphocytes in CDDP-induced rat renal lesions were investigated histopathologically; the CDDP-induced renal lesions consisted of tissue damage at the early-stage, worsen the damage and commencement of interstitial fibrosis at the mid-stage, and progressive fibrosis at the late stage; the KIM-1 expression and α-SMA+ myofibroblast area reflected renal tubular damage/abnormal regeneration and renal interstitial fibrosis, respectively. CD68+ M1 macrophages began to increase at the mid-stage, with increased mRNA expressions of M1-related cytokines (INF-γ, TNF-α and IL-6), and then slightly decreased at the late-stage. CD163+ M2 macrophages showed a gradually increased number at the mid- and late-stages, accompanied by increased TGF-β1 mRNA expression (a fibrogenic factor). Double immunofluorescence using fibrotic samples at the late-stage revealed that 62.0–78.0% of CD68+ M1 macrophages co-expressed CD163, indicating that M1/M2 macrophages may contribute to progressive renal fibrosis in cooperation; further, MHC class II-expressing macrophages had a tendency towards M1 polarization, whereas CD204-expressing macrophages towards M2 polarization. In addition, CD4+ and CD8+ T cells were increased at the late-stage. Collectively, progressive renal interstitial fibrosis may be developed by complicated mechanisms that arose via interaction of M1/M2 macrophages (inflammatory for M1 and anti-inflammatory for M2) and T cells reacting to CD4 (for helper) and CD8 (for cytotoxicity). This study would provide some information on the pathogenesis of renal fibrosis based on inflammatory cells.

scholarly journals Renal fibrosis due to multiple cisplatin treatment is exacerbated by kinin B1 receptor antagonism

2021 ◽  
Vol 54 (12) ◽  
Author(s):  
A. Budu ◽  
L.C. Freitas-Lima ◽  
A.C. de Arruda ◽  
M.S. Perilhão ◽  
J. Barrera-Chimal ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Receptor Antagonism ◽  
B1 Receptor ◽  
Kinin B1 Receptor

EP 1 Receptor Antagonism as a Therapeutic Intervention Strategy in Renal Fibrosis

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Jean-Claude Kresse ◽  
Stine Julie Tingskov ◽  
Michael Schou Jensen ◽  
Henricus A. M. Mutsaers ◽  
Helle Praetorius ◽  
...  
Keyword(s):  
Therapeutic Intervention ◽  
Renal Fibrosis ◽  
Intervention Strategy ◽  
Receptor Antagonism
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