MURC deficiency in smooth muscle attenuates pulmonary hypertension

Nakanishi, Naohiko; Ogata, Toru; Naito, Daisuke; Miyagawa, Kotaro; Taniguchi, Tetsuo; Hamaoka, Toshiyuki; Maruyama, Naoki; Kasahara, Takeru; Nishi, Masahiro; Matoba, Satoaki; Ueyama, Tomomi

doi:10.1038/ncomms12417

Cited by 23 publications

(24 citation statements)

References 62 publications

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“…Other than being involved in the activity of JNK and MMPs, MURC/Cavin-4 regulates the proliferation and migration of VSMCs [26]. MURC/Cavin-4 overexpression increases the proliferation and migration of VSMCs.…”

Section: Discussionmentioning

confidence: 99%

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Loss of MURC/Cavin-4 induces JNK and MMP-9 activity enhancement in vascular smooth muscle cells and exacerbates abdominal aortic aneurysm

Miyagawa

Ogata

Ueyama

et al. 2017

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

“…Rat VSMCs isolated from thoracic aorta of Sprague-Dawley rats by the collagenase digestion method as previously described [26] were maintained in DMEM with 10% FBS. At sub-confluency, cells were starved 24 h before stimulation.…”

Section: Isolation and Culture Of Vsmcsmentioning

confidence: 99%

Loss of MURC/Cavin-4 induces JNK and MMP-9 activity enhancement in vascular smooth muscle cells and exacerbates abdominal aortic aneurysm

Miyagawa

Ogata

Ueyama

et al. 2017

Biochemical and Biophysical Research Communications

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“…In order to evaluate right ventricular hypertrophy (RVH), the Fulton index was calculated as the weight ratio of the right ventricle (RV) to the left ventricle (LV) and septum (S). [26][27][28] Histological analysis: After measuring the RV pressure, the lungs were fixed with 4% paraformaldehyde, embedded in paraffin, and sectioned to 3 μm slices. The pulmonary artery (20-50 μm external diameter) was randomly chosen after Elastica-Masson (EM) staining (60-90 vessels per mouse).…”

Section: Methodsmentioning

confidence: 99%

Senescence Marker Protein 30 Deficiency Exacerbates Pulmonary Hypertension in Hypoxia-Exposed Mice

et al. 2019

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Pulmonary arterial hypertension is a fatal disease caused by pulmonary arterial vasoconstriction and organic stenosis due to the proliferation of pulmonary smooth muscle cells and endothelial cells. Endothelial dysfunction, including impaired nitric oxide (NO) bioavailability, plays a crucial role in the pathogenesis of pulmonary hypertension, and endothelial nitric oxide synthase (eNOS) is an important modulator of pulmonary vasodilatation. Although senescence marker protein (SMP) 30 is known as an anti-aging protein, the role of SMP30 in pulmonary vessels is still unclear. In this study, we examined the role of SMP30 in pulmonary vasculature using SMP30-deficient mice. We used female SMP30-deficient mice and wild-type littermate (WT) mice at the age of 12 to 18 weeks. The WT and SMP30-deficient mice were exposed to normoxia or hypoxia (10% oxygen for 4 weeks). In normoxia, the right ventricular systolic pressure (RVSP) was not different between the WT and SMP30-deficient mice, but in hypoxia, the RVSP was significantly higher in the SMP30-deficient mice compared to the WT mice (P < 0.05). The hypoxia-induced increases in right ventricular hypertrophy and medial smooth muscle area of the pulmonary artery were comparable between the WT and the SMP30-deficient mice. Western blotting showed that eNOS phosphorylation in lung tissue was reduced in the SMP30-deficient mice compared to the WT mice in normoxia. However, in hypoxic conditions, eNOS phosphorylation was reduced in both the WT and SMP30-deficient mice with no differences in Akt phosphorylation. Our study demonstrated that SMP30 is involved in the development of hypoxia-induced pulmonary hypertension by impairment of eNOS activity.

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“…Overexpression of MURC swelled the caveolae but was not crucial to caveolae formation . MURC was found to be expressed in vascular smooth muscle cells, skeletal muscle cells and cardiomyocytes . A study suggested that pressure overload could induce MURC messenger RNA (mRNA) expression in cardiomyocytes .…”

Section: Introductionmentioning

confidence: 99%

“…7 MURC was found to be expressed in vascular smooth muscle cells, skeletal muscle cells and cardiomyocytes. 8 A study suggested that pressure overload could induce MURC messenger RNA (mRNA) expression in cardiomyocytes. 9 Overexpression of MURC in a transgenic mouse model led to atrial fibrillation and chronic heart failure.…”

Section: Introductionmentioning

confidence: 99%

Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch

Cheng¹,

Wang³

et al. 2018

J Cellular Molecular Medi

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MURC (muscle‐restricted coiled‐coil protein) is a hypertrophy‐related gene. Hypertrophy can be induced by mechanical stress. The purpose of this research was to investigate the hypothesis that MURC mediates hypertrophy in cardiomyocytes under mechanical stress. We used the in vivo model of an aortocaval shunt (AV shunt) in adult Wistar rats to induce myocardial hypertrophy. We also used the in vitro model of cyclic stretch in rat neonatal cardiomyocytes to clarify MURC expression and the molecular regulation mechanism. The flexible membrane culture plate seeding with cardiomyocytes Cardiomyocytes seeded on a flexible membrane culture plate were stretched by vacuum pressure to 20% of maximum elongation at 60 cycles/min. AV shunt induction enhanced MURC protein expression in the left ventricular myocardium. Treatment with atorvastatin inhibited the hypertrophy induced by the AV shunt. Cyclic stretch markedly enhanced MURC protein and mRNA expression in cardiomyocytes. Addition of extracellular‐signal‐regulated kinase (ERK) inhibitor PD98059, ERK small interfering RNA (siRNA), angiotensin II (Ang II) antibody and atorvastatin before stretch, abolished the induction of MURC protein. An electrophoretic mobility shift assay showed that stretch enhanced the DNA binding activity of serum response factor. Stretch increased but MURC mutant plasmid, ERK siRNA, Ang II antibody and atorvastatin reversed the transcriptional activity of MURC induced by stretch. Adding Ang II to the cardiomyocytes also induced MURC protein expression. MURC siRNA and atorvastatin inhibited the hypertrophic marker and protein synthesis induced by stretch. Treatment with atorvastatin reversed MURC expression and hypertrophy under volume overload and cyclic stretch.

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MURC deficiency in smooth muscle attenuates pulmonary hypertension

Cited by 23 publications

References 62 publications

Loss of MURC/Cavin-4 induces JNK and MMP-9 activity enhancement in vascular smooth muscle cells and exacerbates abdominal aortic aneurysm

Loss of MURC/Cavin-4 induces JNK and MMP-9 activity enhancement in vascular smooth muscle cells and exacerbates abdominal aortic aneurysm

Senescence Marker Protein 30 Deficiency Exacerbates Pulmonary Hypertension in Hypoxia-Exposed Mice

Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch

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