β-Migrating very low density lipoproteins induce foam cell formation in mouse mesangial cells

Nishikawa, Takeshi; Kobori, Shozo; Takeda, Haruo; Higashi, Takayuki; Sato, Yoshihiro; Sasahara, Takayuki; Yano, Toshihiro; Kasho, Masaya; Anami, Yoshichika; Shichiri, Motoaki

doi:10.1016/0021-9150(94)05476-y

Cited by 7 publications

(2 citation statements)

References 21 publications

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“…The experimental protocol was approved by the Human Ethics Review Committee of our institution and a signed consent form was obtained from each patient. Human glomeruli were isolated according to the method of Gröne et al [13], with minor modifications [14,15]. Briefly, the kidneys of patients with ureteral cancer were removed and the cortices of normal sections were cut and pressed through a series of sieves of decreasing pore size (250, 125 and 110 m).…”

Section: Cellsmentioning

confidence: 99%

Serotonin enhances the production of type IV collagen by human mesangial cells

Kasho

Sakai

Sasahara

et al. 1998

Kidney International

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Section: Cellsmentioning

confidence: 99%

Serotonin enhances the production of type IV collagen by human mesangial cells

Kasho

Sakai

Sasahara

et al. 1998

Kidney International

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“…The mRNA levels of megalin in HRPTEC and HRMC was also decreased by βVLDL load ( Figure 2(C) ). It is reported that accumulation of cholesterol in the mesangial region causes glomerular sclerosis due to foam cell formation of mesangial cells and expansion of glomerulus basement membrane [ 34 ]. We found a decrease in megalin expression in HRMC and our finding suggests a possibility that the decrease in megalin affect the expansion of glomerulus basement membrane, leading to glomerular sclerosis.…”

Section: Discussionmentioning

confidence: 99%

The effect of cholesterol overload on mouse kidney and kidney-derived cells

et al. 2018

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Introduction: Dyslipidemia is one of the onset and risk factors of chronic kidney disease and renal function drop is seen in lipoprotein abnormal animal models. However, the detailed molecular mechanism of renal lipotoxicity has not been clarified. Therefore, the present study aimed to investigate the influence of cholesterol overload using mouse kidney tissue and kidney-derived cultured cells.Methods: C57BL/6 mice were fed normal diet (ND) or 1.25% cholesterol-containing high-cholesterol diet (HCD) for 11 weeks, and we used megalin as a proximal tubule marker for immunohistology. We added beta-very low density lipoprotein (βVLDL) to kidney-derived cells and examined the effect of cholesterol overload on megalin protein and mRNA expression level, cell proliferation and cholesterol content in cells.Results: In the kidney of HCD mice, the gap between glomerulus and the surrounding Bowman’s capsule decreased and the expression level of megalin decreased. After βVLDL treatment to the cells, the protein expression and mRNA expression level of megalin decreased and cell proliferation was restrained. We also observed an increase in cholesterol accumulation in the cell and free cholesterol/phospholipid ratios increased.Conclusions: These findings suggest that the increased cholesterol load on kidney contribute to the decrease of megalin and the overloaded cholesterol is taken into the renal tubule epithelial cells, causing suppression on cell proliferation, which may be the cause of kidney damage.

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