Exploring the mechanisms of renoprotection against progressive glomerulosclerosis

Oite, Takashi

doi:10.2183/pjab.87.81

Cited by 4 publications

(3 citation statements)

References 42 publications

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“…In contrast to the techniques used in previous micropuncture studies, intravital microscopy is considered less invasive because it involves fewer manipulations of the site of interest, such as the placement of the kidney into a Lucite cup and the insertion of micropipettes. The baseline snGFR determined by multiphoton microscopy was within a similar range to that reported previously for MFW rats based on micropuncture experiments 2,4,5,17,28 . Similarly, the infusion of angiotensin II led to a significant decrease in the snGFR in control rats 23,29 .…”

Section: Discussionsupporting

confidence: 86%

“…The baseline snGFR determined by multiphoton microscopy was within a similar range to that reported previously for MFW rats based on micropuncture experiments. 2,4,5,17,28 Similarly, the infusion of angiotensin II led to a significant decrease in the snGFR in control rats. 23,29 It has been suggested that the preferential constriction of the afferent versus the efferent arteriole and a concomitant reduction in the net renal plasma flow account for the effect of angiotensin II on the snGFR.…”

Section: Discussionmentioning

confidence: 88%

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Mesangial cells regulate the single nephron GFR and preserve the integrity of the glomerular filtration barrier: An intravital multiphoton microscopy study

et al. 2021

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Aim The intraglomerular mesangial cells are located between the glomerular capillaries. Here we hypothesized that mesangial cells regulate the single nephron glomerular filtration rate (snGFR) and that mesangial cells support the integrity of the glomerular filtration barrier. Methods We assessed the function of mesangial cells in vivo by multiphoton microscopy. Mesangial cells were depleted in Munich Wistar Froemter rats using the Thy1.1 antibody model. Results The Thy1.1 antibody caused the cell‐specific loss of 82 ± 3% of mesangial cells. After mesangial cell depletion, the baseline snGFR was reduced to 12.0 ± 1.2 vs 32.4 ± 3.2 nL/min in controls. In control rats, the snGFR decreased after angiotensin II infusion by 61 ± 3% (P = .004), whereas it remained unchanged in Thy1.1‐treated rats. The changes in the snGFR after angiotensin II infusion in control rats were accompanied by the marked rotation of the capillary loops within Bowman's space. This phenomenon was absent in anti‐Thy1.1‐treated rats. The glomerular sieving coefficient (GSCA) for albumin, used as a measure of the integrity of the glomerular filtration barrier, was low in control rats (0.00061 ± 0.00004) and increased after angiotensin II infusion (0.00121 ± 0.00015). In Thy1.1‐treated rats, the GSC was elevated (0.0032 ± 0.00059) and did not change in response to angiotensin II. Electron microscopy revealed the increased thickness of the glomerular basement membrane after mesangial cell depletion. Conclusion Our data suggest that mesangial cells actively contribute to the regulation of the snGFR. Furthermore, mesangial cells are crucially involved in maintaining the integrity of the glomerular filtration barrier, in part by modulating the thickness of the glomerular basement membrane.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 88%

Mesangial cells regulate the single nephron GFR and preserve the integrity of the glomerular filtration barrier: An intravital multiphoton microscopy study

et al. 2021

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“…Using apolipoprotein E knockout mice, our previous study demonstrated that RAS activation was involved in dyslipidemia-mediated renal injuries 14. Accordingly, after treatment with a RAS inhibitor or lipid-lowering drugs, the progression of glomerulosclerosis was attenuated 15, 16. These findings suggested the existence of synergistic effects of RAS activation and lipid disorders in renal injuries.…”

Section: Discussionmentioning

confidence: 93%

Interaction of RAS Activation and Lipid Disorders Accelerates the Progression of Glomerulosclerosis

Ma¹,

Ni²,

Changxian³

et al. 2013

Int. J. Med. Sci.

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Background: The activation of the renin-angiotensin system (RAS) and lipid disorders are major risk factors in progressive chronic kidney disease. This study aimed to investigate the potential synergistic mechanisms of RAS activation and lipid disorders that contribute to glomerulosclerosis. Materials and methods: Human renal mesangial cells (HMCs) were treated with 10-7 mol/L angiotensin II (Ang II) or with 30 μg/ml cholesterol and 1 μg/ml 25-hydroxycholesterol (lipid loading) for 24 hours. Lipid accumulation in the cells was evaluated by Oil Red O staining and intracellular cholesterol quantitative assays. The gene and protein expression of molecules in the low-density lipoprotein receptor (LDLr) pathway, the RAS family, and the extracellular matrix were examined by real-time polymerase chain reaction and Western blotting. The translocation of sterol regulatory element-binding protein (SREBP) cleavage activating protein (SCAP), which escorts SREBP-2 from the endoplasmic reticulum (ER) to the Golgi, was examined by immunofluorescent staining. Results: Ang II increased lipid droplet accumulation in HMCs. Further analysis revealed that Ang II increased the mRNA and protein expression of LDLr, SCAP, and SREBP-2. This increase was correlated with an enhanced translocation of the SCAP/SREBP-2 complex from the ER to the Golgi in HMCs that was induced by Ang II, thereby activating LDLr gene transcription. Interestingly, lipid loading increased the mRNA and protein expression of angiotensinogen, Ang II, renin, angiotensin-converting enzyme, angiotensin II type 1 receptor, and type 2 receptor in HMCs with increased mRNA and protein expression of collagen I, α-smooth muscle actin, and fibronectin. Conclusions: This study demonstrates that the interaction of RAS activation and lipid disorders accelerates the progression of glomerulosclerosis.

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Dahuang Fuzi Decoction ameliorates tubular epithelial apoptosis and renal damage via inhibiting TGF-β1-JNK signaling pathway activation in vivo

Sun

Wan

et al. 2014

Journal of Ethnopharmacology

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Exploring the mechanisms of renoprotection against progressive glomerulosclerosis

Cited by 4 publications

References 42 publications

Mesangial cells regulate the single nephron GFR and preserve the integrity of the glomerular filtration barrier: An intravital multiphoton microscopy study

Mesangial cells regulate the single nephron GFR and preserve the integrity of the glomerular filtration barrier: An intravital multiphoton microscopy study

Interaction of RAS Activation and Lipid Disorders Accelerates the Progression of Glomerulosclerosis

Dahuang Fuzi Decoction ameliorates tubular epithelial apoptosis and renal damage via inhibiting TGF-β1-JNK signaling pathway activation in vivo

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