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Nox2 and Nox4 mediate tumour necrosis factor-α-induced ventricular remodelling in mice.

Moe KT, Yin NO, Naylynn TM, Khairunnisa K, Wutyi MA, Gu Y, Atan MS, Wong MC, Koh TH, Wong P - J. Cell. Mol. Med. (2011)

Bottom Line: ROS was significantly decreased by inhibitors of NADPH oxidase, but not by inhibitors of other ROS production systems.Nox2 and Nox4 siRNA significantly attenuated TNF-α-induced ROS and upregulation of IL-1β and IL-6 in cardiomyocytes.Our study highlights a novel TNF-α-induced chronic ventricular remodelling mechanism mediated by sequential regulation of Nox2 and Nox4 subunits.

View Article: PubMed Central - PubMed

Affiliation: Research and Development Unit, National Heart Centre Singapore, Singapore. moe.kyaw.thu@nhc.com.sg

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Related in: MedlinePlus

TNF-α-induced ventricular hypertrophy. Cryostat sections were prepared and stained with haematoxylin and eosin. Each cardiomyocytes was measured and outline of 30–50 cardiomyocytes was traced in each field. The cross-sectional area was obtained in a blinded fashion with AxioVs40 V4.7 software. Mean values of cardiomyocytes cross-sectional areas of TNF-α-injected mice were normalized with those of controls. Cardiomyocyte cross-sectional area was presented as a percentage of control ± S.D. (A). Heart and body weight ratios were presented in mg/g ± S.D. (B). Total RNA was extracted from the ventricles and ANP mRNA levels were examined using real-time PCR. ANP mRNA level relative to GAPDH was shown (C). Data were expressed as fold ± SD. Ventricular homogenates were examined for ANP protein level by immunoblotting. A representative of ANP proteins was shown (D). C, control; T, TNF-α-injected mice. Densitometric analysis of ANP protein (below) was normalized with GAPDH. *P < 0.05.
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fig04: TNF-α-induced ventricular hypertrophy. Cryostat sections were prepared and stained with haematoxylin and eosin. Each cardiomyocytes was measured and outline of 30–50 cardiomyocytes was traced in each field. The cross-sectional area was obtained in a blinded fashion with AxioVs40 V4.7 software. Mean values of cardiomyocytes cross-sectional areas of TNF-α-injected mice were normalized with those of controls. Cardiomyocyte cross-sectional area was presented as a percentage of control ± S.D. (A). Heart and body weight ratios were presented in mg/g ± S.D. (B). Total RNA was extracted from the ventricles and ANP mRNA levels were examined using real-time PCR. ANP mRNA level relative to GAPDH was shown (C). Data were expressed as fold ± SD. Ventricular homogenates were examined for ANP protein level by immunoblotting. A representative of ANP proteins was shown (D). C, control; T, TNF-α-injected mice. Densitometric analysis of ANP protein (below) was normalized with GAPDH. *P < 0.05.

Mentions: TNF-α injection into the mice resulted in hypertrophy of cardiomyocytes 7 and 28 days post-injection. The myocyte cross-sectional area showed a significant increase in mice injected with TNF-α 7 and 28 days previously compared to controls, while there was no significant change in myocyte area between day-1 treated and control mice (Fig. 4A). The heart and body weight ratio (HW/BW) also increased in mice injected with TNF-α 7 and 28 days previously (Fig. 4B). However, the significant difference was observed only mice 28 days post-injection.


Nox2 and Nox4 mediate tumour necrosis factor-α-induced ventricular remodelling in mice.

Moe KT, Yin NO, Naylynn TM, Khairunnisa K, Wutyi MA, Gu Y, Atan MS, Wong MC, Koh TH, Wong P - J. Cell. Mol. Med. (2011)

TNF-α-induced ventricular hypertrophy. Cryostat sections were prepared and stained with haematoxylin and eosin. Each cardiomyocytes was measured and outline of 30–50 cardiomyocytes was traced in each field. The cross-sectional area was obtained in a blinded fashion with AxioVs40 V4.7 software. Mean values of cardiomyocytes cross-sectional areas of TNF-α-injected mice were normalized with those of controls. Cardiomyocyte cross-sectional area was presented as a percentage of control ± S.D. (A). Heart and body weight ratios were presented in mg/g ± S.D. (B). Total RNA was extracted from the ventricles and ANP mRNA levels were examined using real-time PCR. ANP mRNA level relative to GAPDH was shown (C). Data were expressed as fold ± SD. Ventricular homogenates were examined for ANP protein level by immunoblotting. A representative of ANP proteins was shown (D). C, control; T, TNF-α-injected mice. Densitometric analysis of ANP protein (below) was normalized with GAPDH. *P < 0.05.
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Related In: Results  -  Collection

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fig04: TNF-α-induced ventricular hypertrophy. Cryostat sections were prepared and stained with haematoxylin and eosin. Each cardiomyocytes was measured and outline of 30–50 cardiomyocytes was traced in each field. The cross-sectional area was obtained in a blinded fashion with AxioVs40 V4.7 software. Mean values of cardiomyocytes cross-sectional areas of TNF-α-injected mice were normalized with those of controls. Cardiomyocyte cross-sectional area was presented as a percentage of control ± S.D. (A). Heart and body weight ratios were presented in mg/g ± S.D. (B). Total RNA was extracted from the ventricles and ANP mRNA levels were examined using real-time PCR. ANP mRNA level relative to GAPDH was shown (C). Data were expressed as fold ± SD. Ventricular homogenates were examined for ANP protein level by immunoblotting. A representative of ANP proteins was shown (D). C, control; T, TNF-α-injected mice. Densitometric analysis of ANP protein (below) was normalized with GAPDH. *P < 0.05.
Mentions: TNF-α injection into the mice resulted in hypertrophy of cardiomyocytes 7 and 28 days post-injection. The myocyte cross-sectional area showed a significant increase in mice injected with TNF-α 7 and 28 days previously compared to controls, while there was no significant change in myocyte area between day-1 treated and control mice (Fig. 4A). The heart and body weight ratio (HW/BW) also increased in mice injected with TNF-α 7 and 28 days previously (Fig. 4B). However, the significant difference was observed only mice 28 days post-injection.

Bottom Line: ROS was significantly decreased by inhibitors of NADPH oxidase, but not by inhibitors of other ROS production systems.Nox2 and Nox4 siRNA significantly attenuated TNF-α-induced ROS and upregulation of IL-1β and IL-6 in cardiomyocytes.Our study highlights a novel TNF-α-induced chronic ventricular remodelling mechanism mediated by sequential regulation of Nox2 and Nox4 subunits.

View Article: PubMed Central - PubMed

Affiliation: Research and Development Unit, National Heart Centre Singapore, Singapore. moe.kyaw.thu@nhc.com.sg

Show MeSH
Related in: MedlinePlus