Intravenous renal cell transplantation with SAA1-positive cells prevents the progression of chronic renal failure in rats with ischemic-diabetic nephropathy

Kelly, Katherine J.; Zhang, Jizhong; Han, Ling; Wang, Mingsheng; Zhang, Shaobo; Dominguez, Jesus H.

doi:10.1152/ajprenal.00097.2013

Cited by 18 publications

(14 citation statements)

References 33 publications

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“…52 To provide a multifaceted therapy, we have transplanted adult renal tubular cells in experimental AKI and CKD. 16,17,19,20 The advantages of organ-specific cells for repair have been documented. [53][54][55] These studies led to the hypothesis that the relatively small number of donor cells infused 17,20 acted at a distance on endogenous cells.…”

Section: Discussionmentioning

confidence: 99%

“…pcDNA3.1-SAA1 was manufactured and sequenced in our laboratory, and its construction was previously reported. 16,17 This plasmid is used because tubulogenic SAA1 can be used to track transfer to host kidney cells 19 from donor EV (Figure 1). In addition, male determinant gene SRY was used to track donor male EV in recipient female kidneys.…”

Section: Primary Renal Tubular Cells and Evmentioning

confidence: 99%

“…Transfection was performed with lipofectamine 2000 (Life Technologies, Grand Island, NY); efficiencies were .70%. 19 The transfected cells were cultured in S1 medium: Each 2 L contains F-12 HAM, 10.7 g; DMEM, 8.32 g; L-glutamine, 0.29 g; HEPES, 4.78 g; sodium selenite, 1.7 mg; sodium pyruvate, 0.110 g; 3.2 ml phenol red and pH was adjusted to 7.4 with sodium bicarbonate (Sigma). S1 medium was supplemented with hepatocyte growth factor, 200 ng/ml, and EGF, 400 ng/ml (R&D Systems, Minneapolis, MN).…”

Section: Primary Renal Tubular Cells and Evmentioning

confidence: 99%

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Renal Tubular Cell-Derived Extracellular Vesicles Accelerate the Recovery of Established Renal Ischemia Reperfusion Injury

Dominguez

Liu

Gao

et al. 2017

JASN

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Ischemic renal injury is a complex syndrome; multiple cellular abnormalities cause accelerating cycles of inflammation, cellular damage, and sustained local ischemia. There is no single therapy that effectively resolves the renal damage after ischemia. However, infusions of normal adult rat renal cells have been a successful therapy in several rat renal failure models. The sustained broad renal benefit achieved by relatively few donor cells led to the hypothesis that extracellular vesicles (EV, largely exosomes) derived from these cells are the therapeutic effector We now show that EV from adult rat renal tubular cells significantly improved renal function when administered intravenously 24 and 48 hours after renal ischemia in rats. Additionally, EV treatment significantly improved renal tubular damage, 4-hydroxynanoneal adduct formation, neutrophil infiltration, fibrosis, and microvascular pruning. EV therapy also markedly reduced the large renal transcriptome drift observed after ischemia. These data show the potential utility of EV to limit severe renal ischemic injury after the occurrence.

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Section: Discussionmentioning

confidence: 99%

Section: Primary Renal Tubular Cells and Evmentioning

confidence: 99%

Section: Primary Renal Tubular Cells and Evmentioning

confidence: 99%

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Renal Tubular Cell-Derived Extracellular Vesicles Accelerate the Recovery of Established Renal Ischemia Reperfusion Injury

Dominguez

Liu

Gao

et al. 2017

JASN

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“…These rats were terminated at 28 weeks of age, their kidneys removed, immediately frozen in liquid nitrogen, and RNA extracted (below). In addition, renal tubular cells from 12 week-old normal Sprague Dawley male rats (n=4) were isolated as previously described [12]. …”

Section: Methodsmentioning

confidence: 99%

Renal C3 Complement Component: Feed Forward to Diabetic Kidney Disease

Kelly

Liu²,

Zhang

et al. 2015

Am J Nephrol

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Background: Diabetic nephropathy is the main cause of end-stage renal disease and has reached epidemic proportions. Methods: Comprehensive genomic profiling (RNAseq) was employed in the ZS (F₁ hybrids of Zucker and spontaneously hypertensive heart failure) model of diabetic nephropathy. Controls were lean littermates. Results: Diabetic nephropathy in obese, diabetic ZS was accelerated by a single episode of renal ischemia (DI). This rapid renal decline was accompanied by the activation of the renal complement system in DI, and to a lesser extent in sham-operated diabetic rats (DS). In DI there were significant increases in renal mRNA encoding C3, C4, C5, C6, C8, and C9 over sham-operated lean normal controls (LS). Moreover, mRNAs encoding the receptors for the anaphylatoxins C3a and C5a were also significantly increased in DI compared to LS. The classic complement pathway was activated in diabetic kidneys with significant increases of C1qa, C1qb, and C1qc mRNAs in DI over LS. In addition, critical regulators of complement activation were significantly attenuated in DI and DS. These included mRNAs encoding CD55, decay accelerating factor, and CD59, which inhibit the membrane attack complex. C3, C4, and C9 proteins were demonstrated in renal tubules and glomeruli. The complement RNAseq data were incorporated into a gene network showing interactions among C3-generating renal tubular cells and other immune competent migratory cells. Conclusions: We conclude that local activation of the complement system mediates renal injury in diabetic nephropathy.

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“…DN was considered as a major complication of diabetes in global population (Kelly et al., ) and its development, management, and prevention were regulated by nutrition and diet (Selcuk et al., ). Obesity‐ and/or diabetes‐induced hyperglycemia is the main key factor for the development and progression of DN, which activates the various signaling pathways such as polyol, hexosamine, NF‐kB, AGE, PKC, Bax/Bcl‐2, and other pathways via ROS generation and lead to the insulin resistance associated with renal damage (Haq, Banday, & Bashir, ).…”

Section: Discussionmentioning

confidence: 99%

Mangosteen Vinegar Rind from Garcinia mangostana Prevents High‐Fat Diet and Streptozotocin‐Induced Type II Diabetes Nephropathy and Apoptosis

Karim

Chanudom

et al. 2019

Journal of Food Science

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Type II diabetes (T2D) nephropathy, a major cause of end-stage kidney disease, progresses and develops from oxidative stress. Natural polyphenols can protect the kidney from diabetic nephropathy exerting antioxidant activities. The present approach enumerates the reno-protective and anti-apoptotic effects of mangosteen vinegar rind (MVR, a phenolic aqueous extract) against high-fat diet (5 g/day up to five weeks)-/streptozotocin (single ip, dose 30 mg/kgBW)induced T2D nephropathy of albino mice. In vitro total phenolic content, 2,2'-azino-bis(3-ethylbenzothiazoline-6sulphonic acid) (ABTS) activity, 2,2-diphenyl-1-picrylhydrazyl (DPPH) antioxidant capacity, and α-amylase inhibition activity as antidiabetic assay of MVR were performed. In vivo mice body weight, oral glucose, and maltose tolerance test, metabolic parameters (plasma glucose, insulin level, omeostasis model assessment-estimated insulin resistance), biochemical parameters (kidney hypertrophy, blood urea nitrogen, creatinine), oxidative stress parameters (malondialdehyde, superoxide dismutase, catalase) were estimated in an intervention study. Additionally, renal morphology and early apoptosis were observed following the H & E staining and TUNEL assay of the tissue frozen section. We found that the aqueous extract of MVR possesses potent in vitro antioxidative and antidiabetic activities. Animal intervention results showed that MVR 100, 200 mg/kgBW, and Glibenclamide 60 mg/kgBW treatments significantly improved (P < 0.05) the abovementioned parameters compared to the diabetic control group. Furthermore, treatments also significantly restored (P < 0.05) kidney histological alterations and reduced cellular apoptosis compared to the diabetic control group. These findings concluded that MVR treatments significantly modulated the glucose intolerance, metabolic alterations, and oxidative stress-induced pathological alterations and cellular apoptosis of diabetic kidney.Practical Application: Garcinia mangostana, a polyphenol rich natural product, is obtained from the tropical rain forest area of Southeast Asian countries and processes diverse biological activities including antioxidant, anti-proliferative, antiinflammatory, anti-carcinogenic, and so on. This research first time focuses on the nephro-protective and anti-apoptotic effects of mangosteen vinegar rind (MVR) from the mangosteen fruit pericarp. Our study provides the efficient data to prove the beneficial effect of MVR as a dietary supplement for the prevention and management of diabetic nephropathy.

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Intravenous renal cell transplantation with SAA1-positive cells prevents the progression of chronic renal failure in rats with ischemic-diabetic nephropathy

Abstract: Intravenous renal cell transplantation with SAA1-positive cells prevents the progression of chronic renal failure in rats with ischemic-diabetic nephropathy.

Cited by 18 publications

References 33 publications

Renal Tubular Cell-Derived Extracellular Vesicles Accelerate the Recovery of Established Renal Ischemia Reperfusion Injury

Renal Tubular Cell-Derived Extracellular Vesicles Accelerate the Recovery of Established Renal Ischemia Reperfusion Injury

Renal C3 Complement Component: Feed Forward to Diabetic Kidney Disease

Mangosteen Vinegar Rind from Garcinia mangostana Prevents High‐Fat Diet and Streptozotocin‐Induced Type II Diabetes Nephropathy and Apoptosis

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