Endothelial cell-selective adhesion molecule regulates albuminuria in diabetic nephropathy

Hara, Tetsuya; Ishida, Tatsuro; Cangara, Husni; Hirata, Ken‐ichi

doi:10.1016/j.mvr.2009.01.002

Cited by 35 publications

(45 citation statements)

References 29 publications

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“…[18][19][20][21] The EC surface proteins involved in DN are known as cell adhesion molecules (CAMs), which are distributed at various time courses of activations and expressions. 22,23 The original interactions between polymorphonuclear (PMN) cells and ECs are mediated via CAM expressed on the EC surface. 24 This CAM-mediated interaction leads to the rolling of PMNs along vessel walls and upregulation of intercellular adhesion molecule-1 (ICAM-1) on the PMNs.…”

mentioning

confidence: 99%

Quercetin nanoparticle complex attenuated diabetic nephropathy via regulating the expression level of ICAM-1 on endothelium

Tong¹,

Liu²,

Yan³

et al. 2017

IJN

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The purpose of the study was to reveal the therapeutic effect of quercetin (QUE) nanoparticle complex on diabetic nephropathy (DN) by regulating the expression of intercellular adhesion molecular-1 (ICAM-1) on endothelium as compared to free QUE. QUE 10 mg/kg as a single abdominal subcutaneous injection daily for 8 weeks continuously in diabetic rats and 10 mg/kg QUE nanoparticle complex as a single abdominal subcutaneous injection every 5 days, continuously administered for 8 weeks to diabetic rats. Blood and left kidneys were collected; pathological change of kidney, renal function, oxidative stress level, blood glucose level, serum lipid, urine protein, and albumin/creatinine ratio were measured; and neutrophil adhesion, ICAM-1 expression, and CD11b + cells infiltration were observed. Both QUE and QUE nanoparticle complex preconditioning ameliorated the pathological damage of kidney and improved renal function, alleviated renal oxidative stress injury, restricted inflammatory cells infiltration, and downregulated the ICAM-1 expression as compared to DN group, while QUE nanoparticle complex significantly alleviated this effect.

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mentioning

confidence: 99%

Quercetin nanoparticle complex attenuated diabetic nephropathy via regulating the expression level of ICAM-1 on endothelium

Tong¹,

Liu²,

Yan³

et al. 2017

IJN

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“…Western blotting was performed using anti-VCAM-1 (Santa Cruz Laboratory, Santa Cruz, CA), inducible nitric oxide synthase (iNOS) (BD Transduction Laboratories, Bedford, MA), apolipoprotein (apo)A-1 (Abcam, Cambridge, UK), or anti-␤ -actin antibody (Sigma-Aldrich) as described previously ( 14 ). The relative densities of the acquired bands were determined by using the ImageJ software version 1.38 from the National Institutes of Health (available on the World Wide Web).…”

Section: Immunoblot and Histological Analysesmentioning

confidence: 99%

“…Quantitative real-time PCR was performed as previously reported ( 14 ). PCR primers for mouse TNF-␣ and GAPDH were purchased from Takara-Bio Perfect Real Time Support System (Takara, Shiga, Japan).…”

Section: Real-time Pcrmentioning

confidence: 99%

Targeted deletion of endothelial lipase increases HDL particles with anti-inflammatory properties both in vitro and in vivo

Hara

Ishida

Kojima

et al. 2011

Journal of Lipid Research

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“…ESAM deficiency in endothelial tight junctions disturbs neutrophil extravasation to inflamed tissues by reduction of acti-vated Rho proteins (13). The deficiency also increases vascular permeability of the renal glomeruli, resulting in urinary albumin elevation (14). Additionally, it has been shown that ESAM is also expressed on megakaryocytes and platelets (12), where it is involved in the regulation of thrombus formation (15).…”

mentioning

confidence: 99%

The Endothelial Antigen ESAM Monitors Hematopoietic Stem Cell Status between Quiescence and Self-Renewal

Sudo

Yokota

Oritani

et al. 2012

The Journal of Immunology

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Whereas most hematopoietic stem cells (HSC) are quiescent in homeostasis, they actively proliferate in response to bone marrow (BM) injury. Signals from the BM microenvironment are thought to promote entry of HSC into the cell cycle. However, it has been cumbersome to assess cycle status of viable HSC and thus explore unique features associated with division. In this study, we show that expression of endothelial cell-selective adhesion molecule (ESAM) can be a powerful indicator of HSC activation. ESAM levels clearly mirrored the shift of HSC between quiescence and activation, and it was prominent in comparison with other HSC-related Ags. ESAMhi HSC were actively dividing, but had surprisingly high long-term reconstituting capacity. Immunohistochemical analyses showed that most ESAMhi HSC were located near vascular endothelium in the BM after 5-fluorouracil treatment. To determine the importance of ESAM in the process of BM recovery, ESAM knockout mice were treated with 5-fluorouracil and their hematopoietic reconstruction was examined. The ESAM deficiency caused severe and prolonged BM suppression, suggesting that ESAM is functionally indispensable for HSC to re-establish homeostatic hematopoiesis. With respect to intracellular regulators, NF-κB and topoisomerase II levels correlated with the ESAM upregulation. Thus, our data demonstrate that the intensity of ESAM expression is useful to trace activated HSC and to understand molecular events involved in stem cell states.

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Endothelial cell-selective adhesion molecule regulates albuminuria in diabetic nephropathy

Cited by 35 publications

References 29 publications

Quercetin nanoparticle complex attenuated diabetic nephropathy via regulating the expression level of ICAM-1 on endothelium

Quercetin nanoparticle complex attenuated diabetic nephropathy via regulating the expression level of ICAM-1 on endothelium

Targeted deletion of endothelial lipase increases HDL particles with anti-inflammatory properties both in vitro and in vivo

The Endothelial Antigen ESAM Monitors Hematopoietic Stem Cell Status between Quiescence and Self-Renewal

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