The anti-microbial peptide LL-37/CRAMP levels are associated with acute heart failure and can attenuate cardiac dysfunction in multiple preclinical models of heart failure

Zhou, Qing; Pan, Li; Xue, Rui‐De; Ni, Gehui; Duan, Yi; Bai, Yuzheng; Shi, Chao; Ren, Zhengnan; Wu, Chengfei; Li, Guoping; Agerberth, Birgitta; Sluijter, Joost P.G.; Sun, Jia; Xiao, Junjie

doi:10.7150/thno.46225

Cited by 24 publications

(21 citation statements)

References 52 publications

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“…Electroacupuncture pretreatment promoted angiogenesis by increasing serum HIF-1α and VEGF protein expression in myocardial infarction area [ 67 ]. ISO is often used to construct models of heart disease in rats, e.g., heart failure (HF) [ 68 ], cardiac hypertrophy [ 69 ] and chronic myocardial ischemia [ 67 ]. At the same time, ISO injection and left anterior descending (LAD) ligation are commonly used to construct rat models of myocardial fibrosis [ 70 – 72 ].…”

Section: Discussionmentioning

confidence: 99%

Downregulation of lncRNA Miat contributes to the protective effect of electroacupuncture against myocardial fibrosis

Ren

et al. 2022

Chin Med

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Background Myocardial fibrosis changes the structure of myocardium, leads to cardiac dysfunction and induces arrhythmia and cardiac ischemia, threatening patients’ lives. Electroacupuncture at PC6 (Neiguan) was previously found to inhibit myocardial fibrosis. Long non-coding RNAs (lncRNAs) play a variety of regulatory functions in myocardial fibrosis, but whether electroacupuncture can inhibit myocardial fibrosis by regulating lncRNA has rarely been reported. Methods In this study, we constructed myocardial fibrosis rat models using isoproterenol (ISO) and treated rats with electroacupuncture at PC6 point and non-point as control. Hematoxylin–eosin, Masson and Sirius Red staining were performed to assess the pathological changes and collagen deposition. The expression of fibrosis-related markers in rat myocardial tissue were detected by RT-qPCR and Western blot. Miat, an important long non-coding RNA, was selected to study the regulation of myocardial fibrosis by electroacupuncture at the transcriptional and post-transcriptional levels. In post-transcriptional level, we explored the myocardial fibrosis regulation effect of Miat on the sponge effect of miR-133a-3p. At the transcriptional level, we studied the formation of heterodimer PPARG–RXRA complex and promotion of the TGF-β1 transcription. Results Miat was overexpressed by ISO injection in rats. We found that Miat can play a dual regulatory role in myocardial fibrosis. Miat can sponge miR-133a-3p in an Ago2-dependent manner, reduce the binding of miR-133a-3p target to the 3ʹUTR region of CTGF mRNA and improve the protein expression level of CTGF. In addition, it can also directly bind with PPARG protein, inhibit the formation of heterodimer PPARG–RXRA complex and then promote the transcription of TGF-β1. Electroacupuncture at PC6 point, but not at non-points, can reduce the expression of Miat, thus inhibiting the expression of CTGF and TGF-β1 and inhibiting myocardial fibrosis. Conclusion We revealed that electroacupuncture at PC6 point can inhibit the process of myocardial fibrosis by reducing the expression of lncRNA Miat, which is a potential therapeutic method for myocardial fibrosis.

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Section: Discussionmentioning

confidence: 99%

Downregulation of lncRNA Miat contributes to the protective effect of electroacupuncture against myocardial fibrosis

Ren

et al. 2022

Chin Med

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“…The mice cardiac hypertrophy model induced by transverse aortic constriction (TAC) surgery, angiotensin II (Ang II)- and isoproterenol (ISO) infusion were performed as described previously. 9 Mice were randomly divided into different groups. Five mice were fed in each cage.…”

Section: Methodsmentioning

confidence: 99%

Targeting miR-30d reverses pathological cardiac hypertrophy

et al. 2022

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“…The obtained cells were then incubated in Dulbecco's modified Eagle's medium (Gibco, USA) supplemented with 10% fetal bovine serum (Gibco, USA) in a 5% CO 2 humidified atmosphere at 37°C. Cardiomyocyte hypertrophy was induced by Ang-II (1 μ M) or PE (50 μ M) treatment following the previous reports [ 20 ] [ 21 ] with a brief modification.…”

Section: Methodsmentioning

confidence: 99%

RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx

Xue

Shi

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Receptor-interacting protein 3(RIP3), a RIP family member, has been reported as a critical regulator of necroptosis and involves in the pathogenesis of various heart diseases. However, its role in the development of myocardial hypertrophy after pressure overload is unclear. We aimed to investigate the roles of RIP3 in pathological cardiac hypertrophy. A rat model of myocardial hypertrophy induced by the aortic banding method was used in this study. Neonatal rat cardiomyocytes (NRCMs) were stimulated with angiotensin II (Ang-II) or phenylephrine (PE) to induce neurohumoral stress. Our results showed that RIP3 level was significantly elevated in the hypertrophic myocardium tissues from patients, rats subjected to AB surgery, and NRCMs treated with Ang-II or PE. After downregulation of RIP3 expression in NRCMs, the phenotypes of myocardial hypertrophy were obviously alleviated. In mechanism, we demonstrated that RIP3 interacts with mixed lineage kinase domain-like protein (MLKL) and promotes its cell membrane localization to increase the influx of calcium within cells, thereby mediating the development of myocardial hypertrophy. More interestingly, we found the blockage of calcium influx by 2-aminoethoxydiphenyl borate, and lanthanum chloride efficiently reverses RIP3-induced cardiac remodeling in NRCMs. Taken together, our findings indicate a key role of the RIP3-MLKL signaling pathway in myocardial hypertrophy, which may be a novel promising treatment strategy for myocardial hypertrophy.

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The anti-microbial peptide LL-37/CRAMP levels are associated with acute heart failure and can attenuate cardiac dysfunction in multiple preclinical models of heart failure

Cited by 24 publications

References 52 publications

Downregulation of lncRNA Miat contributes to the protective effect of electroacupuncture against myocardial fibrosis

Downregulation of lncRNA Miat contributes to the protective effect of electroacupuncture against myocardial fibrosis

Targeting miR-30d reverses pathological cardiac hypertrophy

RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx

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