Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Hayakawa, Shinobu; Ohashi, Koji; Shibata, Rei; Kataoka, Yasufumi; Miyabe, Megumi; Enomoto, Takashi; Joki, Yusuke; Shimizu, Yasuhiko; Kambara, Takahiro; Uemura, Yoshiko; Yuasa, Daisuke; Ogawa, Hayato; Matsuo, Kazuhiro; Hiramatsu-Ito, Mizuho; Hoff, Maurice J.B. van den; Walsh, Kenneth; Murohara, Toyoaki; Ouchi, Noriyuki

doi:10.1681/asn.2014020210

Cited by 49 publications

(48 citation statements)

References 60 publications

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“…To investigate the effect of chronic kidney failure on host defense, we performed 5/6-nephrectomy in WT mice. This model system has been shown to reliably induce CKD in the murine system (20,21). Ten days after surgery, pneumonia was induced in these mice by intratracheal injection of viable E. coli bacteria (22).…”

Section: Resultsmentioning

confidence: 99%

FGF23 signaling impairs neutrophil recruitment and host defense during CKD

Rossaint¹,

Oehmichen²,

Aken³

et al. 2016

Journal of Clinical Investigation

241

217

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Section: Resultsmentioning

confidence: 99%

FGF23 signaling impairs neutrophil recruitment and host defense during CKD

Rossaint¹,

Oehmichen²,

Aken³

et al. 2016

Journal of Clinical Investigation

241

217

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“…In agreement with this concept, the current study revealed no effect of either SPARC, SPARCL1 or MGE8 alone on (pro)renin synthesis by As4.1 cells. Additionally, ligands that are known to be involved in blood pressure regulation (NPPC, or natriuretic peptide precursor C), diabetic nephropathy (LGALS1 or galectin-1) 26 , nephrogenesis (MDK or midkine) 27 , renal fibrosis (WFDC2, or WAP four-disulfide core domain protein 2) 28 , and renal injury prevention (FSTL1, or follistatin-related protein 1) 29 also did not directly affect (pro)renin synthesis by As4.1 cells.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Analysis of Human Reninomas as an Approach to Understanding Juxtaglomerular Cell Biology

Martini

Lacombe

et al. 2017

Hypertension

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Renin, a key component in the regulation of blood pressure in mammals, is produced by the rare and highly specialized juxtaglomerular (JG) cells of the kidney. Chronic stimulation of renin release results in a recruitment of new JG cells by the apparent conversion of adjacent smooth muscle cells along the afferent arterioles. Because JG cells rapidly de-differentiate when removed from the kidney, their developmental origin and the mechanism that explains their phenotypic plasticity remain unclear. To overcome this limitation we have performed RNA expression analysis on four human renin-producing tumors. The most highly expressed genes that were common between the reninomas were subsequently used for in situ hybridization in kidneys of 5-day old mice, adult mice and mice treated with captopril. From the top 100 genes, 10 encoding for ligands were selected for further analysis. Medium of HEK293 cells transfected with the mouse cDNA encoding these ligands was applied to (pro)renin-synthesizing As4.1 cells. Among the ligands, only platelet-derived growth factor B (PDGFB) reduced the medium and cellular (pro)renin levels, as well as As4.1 renin gene expression. Additionally, PDGFB-exposed As4.1 cells displayed a more elongated and aligned shape with no alteration in viability. This was accompanied by a downregulated expression of α-smooth muscle actin, and an upregulated expression of interleukin-6, suggesting a phenotypic shift from myo-endocrine to inflammatory. Our results add 36 new genes to the list that characterize renin-producing cells and reveal a novel role for PDGFB as a regulator of renin-synthesizing cells.

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“…cDNA from 500 ng of total RNA was synthesized by reverse transcription using ReverTra Ace qPCR RT master mix (Toyobo Life Science, Osaka, Japan) according to the manufacturer's instructions. Quantitative real-time RT-PCR analysis was performed on a CFX-96 system using Thunderbird qPCR mix (Toyobo Life Science) as a double-stranded DNA-specific dye according to the manufacturer's instructions (Bio-Rad, Hercules, CA) (20). Primers were designed as follows: 5=-ACCACCATCAAGGACTC-3= and 5=-TGACCACTCTCCCTTT G-3= for mouse TNF-␣, 5=-TTCCAATGCTCTCCTAACAG-3= and 5=-C TAGGTTTGCCGAGTAGATC-3= for mouse interleukin-6 (IL-6), 5=-AA ACGGTTTGTCTTCAAC-3= and 5=-ATGGTGAAGTCAATTATGTC-3= for mouse IL-1␤, 5=-CCACTCACCTGCTGCTACTCAT-3= and 5=-TGG TGATCCTCTTGTAGCTCTCC-3= for mouse MCP-1, 5=-TCCTTCTTG GGTATGGAATC-3= and 5=-TAGAGGTCTTTACGGATGTC-3= for mouse ␤-actin, 5=-TTGGGTCAGCACTGGCTCTG-3= and 5=-TGGCGG TGTGCAGTGCTATC-3= for mouse gp91 phox , 5=-CTGGCTGAGGCCAT CAGACT-3= and 5=-AGGCCACTGCAGAGTGCTTG-3= for mouse p67 phox , 5=-GATGTTCCCCATTGAGGCCG-3= and 5=-GTTTCAGGTC ATCAGGCCGC-3= for mouse p47 phox , 5=-TGGTGAACGTGGTGCCTA CA-3= and 5=-TGCAGTCACATCCCACCCT-3= for mouse CTRP9, 5=-C CAATCTGTGTCCTTCTAAC-3= and 5=-GTTTCTGAGCATCGTAGTT G-3= for rat TNF-␣, 5=-AAGGTCACTATGAGGTCTAC-3= and 5=-CAT ATTGCCAGTTCTTCGTA-3= for rat IL-6, and 5=-GGTCATCACTATCG GCAATG-3= and 5=-AGGTCTTTACGGATGTCAAC-3= for rat ␤-actin.…”

mentioning

confidence: 99%

C1q/Tumor Necrosis Factor-Related Protein 9 Protects against Acute Myocardial Injury through an Adiponectin Receptor I-AMPK-Dependent Mechanism

Kambara

Shibata

Ohashi

et al. 2015

Molecular and Cellular Biology

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Obesity is a risk factor for cardiovascular disease. C1q/tumor necrosis factor-related protein 9 (CTRP9) is an adipokine that is downregulated by obesity. We investigated the role of CTRP9 in cardiac injury with loss-of-function genetic manipulations and defined the receptor-mediated signaling pathway downstream of this adipokine. CTRP9-knockout (CTRP9-KO) mice at the age of 12 weeks were indistinguishable from wild-type (WT) mice under basal conditions. CTRP9-KO mice had exacerbated contractile left ventricle dysfunction following intraperitoneal injection of lipopolysaccharide (LPS) compared to WT mice. Administration of LPS to CTRP9-KO mice also resulted in increased expression of proinflammatory cytokines and oxidative stress markers in the heart compared to WT mice. Likewise, CTRP9-KO mice showed increased myocardial infarct size and elevated expression of inflammatory mediators in ischemic heart following ischemia and reperfusion compared to WT mice. Treatment of cardiac myocytes with CTRP9 protein led to suppression of LPS-induced expression of proinflammatory genes, which was reversed by blockade of AMPK or ablation of adiponectin receptor I (AdipoR1). Systemic delivery of CTRP9 attenuated LPS-induced cardiac dysfunction in WT mice but not in muscle-specific transgenic mice expressing dominant-negative mutant form of AMPK or in AdipoR1-knockout mice. CTRP9 protects against acute cardiac damage in response to pathological stimuli by suppressing inflammatory reactions through AdipoR1/ AMPK-dependent mechanisms.O besity causes the progression of various cardiovascular disorders, including ischemic heart disease (1, 2). Adipose tissue functions as an endocrine organ by producing various bioactive secreted proteins, also known as adipokines, that can directly affect the nearby or remote tissues (3). Most adipokines promote obese complications with proinflammatory properties. In contrast, a few numbers of adipokines such as adiponectin are downregulated in obese states, and these factors typically exert salutary actions on obesity-linked cardiovascular disorders (3, 4).C1q/tumor necrosis factor-related protein families (CTRPs) are conserved paralogs of adiponectin that contain collagen-like and globular C1q-like domains (5). CTRP9 has the highest amino acid identity to adiponectin among CTRPs (6). Like adiponectin, CTRP9 is abundantly expressed in adipose tissue. Plasma CTRP9 levels are reduced in diet-induced or leptin-deficient obese mice (6). Clinically, CTRP9 levels associate negatively with visceral fat adiposity and positively with favorable glucose or metabolic phenotypes (7).Several experimental studies demonstrated that CTRP9 acts as an adipokine that modulates metabolic and cardiovascular function. Systemic delivery of CTRP9 lowers glucose levels in obese mice (6). Transgenic overexpression of CTRP9 is protective against diet-induced obesity and glucose intolerance (8), whereas CTRP9-deficiency exacerbates insulin resistance and hepatic steatosis (9). These results suggest that CTRP9 plays a physiolo...

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Cardiac Myocyte-Derived Follistatin-Like 1 Prevents Renal Injury in a Subtotal Nephrectomy Model

Cited by 49 publications

References 60 publications

FGF23 signaling impairs neutrophil recruitment and host defense during CKD

FGF23 signaling impairs neutrophil recruitment and host defense during CKD

Transcriptome Analysis of Human Reninomas as an Approach to Understanding Juxtaglomerular Cell Biology

C1q/Tumor Necrosis Factor-Related Protein 9 Protects against Acute Myocardial Injury through an Adiponectin Receptor I-AMPK-Dependent Mechanism

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