Involvement of complement 3 in the salt-sensitive hypertension by activation of renal renin-angiotensin system in spontaneously hypertensive rats

We previously showed that complement 3 (C3) is highly expressed in mesenchymal tissues in spontaneously hypertensive rats (SHR). We targeted C3 gene by zinc-finger nuclease (ZFN) gene-editing technology and investigated blood pressure and phenotype in SHR. Blood pressure was measured by tail-cuff an...

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Veröffentlicht in:American journal of physiology. Renal physiology 2018-12, Vol.315 (6), p.F1747-F1758
Hauptverfasser: Negishi, Eriko, Fukuda, Noboru, Otsuki, Tomoyasu, Katakawa, Mayumi, Komatsu, Kazutoshi, Chen, Lan, Tanaka, Sho, Kobayashi, Hiroki, Hatanaka, Yoshinari, Ueno, Takahiro, Endo, Morito, Mashimo, Tomoji, Nishiyama, Akira, Abe, Masanori
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container_end_page F1758
container_issue 6
container_start_page F1747
container_title American journal of physiology. Renal physiology
container_volume 315
creator Negishi, Eriko
Fukuda, Noboru
Otsuki, Tomoyasu
Katakawa, Mayumi
Komatsu, Kazutoshi
Chen, Lan
Tanaka, Sho
Kobayashi, Hiroki
Hatanaka, Yoshinari
Ueno, Takahiro
Endo, Morito
Mashimo, Tomoji
Nishiyama, Akira
Abe, Masanori
description We previously showed that complement 3 (C3) is highly expressed in mesenchymal tissues in spontaneously hypertensive rats (SHR). We targeted C3 gene by zinc-finger nuclease (ZFN) gene-editing technology and investigated blood pressure and phenotype in SHR. Blood pressure was measured by tail-cuff and telemetry methods. Histology and expression of liver X receptor α (LXRα), renin, Krüppel-like factor 5 (KLF5), and E-cadherin were evaluated in kidneys. Mesangial cells (MCs) were removed from glomeruli from three strains, and we evaluated the phenotype in vitro. SHR showed the salt-sensitive hypertension that was abolished in C3 knockout (KO) SHR. Proliferation of MCs from SHR was higher than that from Wistar-Kyoto (WKY) rats and showed a synthetic phenotype. Renal injury scores were higher in SHR than in WKY rats and C3 KO SHR. Expression of E-cadherin was lower, and expression of renin was higher in the nephrotubulus from SHR than WKY rats and C3 KO SHR. Expression of C3 α-chain protein and α-smooth muscle actin protein was significantly higher in renal medulla from SHR than from WKY rats. Expression of angiotensinogen, LXRα, renin, and KLF5 mRNA was increased in kidney from SHR compared with C3 KO SHR. Intrarenal angiotensin II levels were significantly higher in kidney from SHR than WKY rats and C3 KO SHR. Urinary epinephrine and norepinephrine excretions were significantly higher in SHR than in WKY rats and C3 KO SHR. These findings showed that increased C3 induces salt-sensitive hypertension with increases in urinary catecholamine excretion and intrarenal activation of the renin-angiotensin system by the dedifferentiation of mesenchymal tissues in kidney from SHR.
doi_str_mv 10.1152/ajprenal.00370.2018
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Expression of E-cadherin was lower, and expression of renin was higher in the nephrotubulus from SHR than WKY rats and C3 KO SHR. Expression of C3 α-chain protein and α-smooth muscle actin protein was significantly higher in renal medulla from SHR than from WKY rats. Expression of angiotensinogen, LXRα, renin, and KLF5 mRNA was increased in kidney from SHR compared with C3 KO SHR. Intrarenal angiotensin II levels were significantly higher in kidney from SHR than WKY rats and C3 KO SHR. Urinary epinephrine and norepinephrine excretions were significantly higher in SHR than in WKY rats and C3 KO SHR. 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Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>315</volume><issue>6</issue><spage>F1747</spage><epage>F1758</epage><pages>F1747-F1758</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>We previously showed that complement 3 (C3) is highly expressed in mesenchymal tissues in spontaneously hypertensive rats (SHR). We targeted C3 gene by zinc-finger nuclease (ZFN) gene-editing technology and investigated blood pressure and phenotype in SHR. Blood pressure was measured by tail-cuff and telemetry methods. Histology and expression of liver X receptor α (LXRα), renin, Krüppel-like factor 5 (KLF5), and E-cadherin were evaluated in kidneys. Mesangial cells (MCs) were removed from glomeruli from three strains, and we evaluated the phenotype in vitro. SHR showed the salt-sensitive hypertension that was abolished in C3 knockout (KO) SHR. 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title Involvement of complement 3 in the salt-sensitive hypertension by activation of renal renin-angiotensin system in spontaneously hypertensive rats
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