miR-21 and cardiac fibrosis: another brick in the wall?: Figure 1

Condorelli, Gianluigi

doi:10.1093/eurheartj/ehv184

Cited by 37 publications

(26 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One in particular was miR-21. In our model of combined volume and pressure overload, miR-21 upregulation was associated with the induction of matrix protein synthesis via TGF-β/ SMAD7 and growth factor secretion via SPRY1 but did not inhibit PTEN and PCDC4, suggesting that fibroblast and cardiomyocyte survival and ECM turnover were unaffected (20,(36)(37)(38)(39). The role of miR-21 in the heart has been controversial.…”

Section: Discussionmentioning

confidence: 83%

“…Early reports in TAC have shown that miR-21 originates from fibroblasts alone, thereby playing a role in fibrosis and the progression to LV failure (40). Others report miR-21 release from cardiomyocytes and endothelial cells, albeit to a lesser extent than from fibroblasts, which thereby induces cell hypertrophy, apoptosis, endothelial-to-mesenchymal transition, and arterial remodeling (36). In contrast, knocking out miR-21 does not prevent fibrosis and leads to early heart failure and death, suggesting that miR-21 may have both deleterious and protective effects (37).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

miR-21 is associated with fibrosis and right ventricular failure

Reddy

Zhao

et al. 2017

JCI Insight

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

miR-21 is associated with fibrosis and right ventricular failure

Reddy

Zhao

et al. 2017

JCI Insight

View full text Add to dashboard Cite

“…Since microRNAs have been described to play a role in cardiac pathological fibrosis3536373839,cardiomyocyte proliferation, progenitors commitment and differentiation40414243, TGF-β-mediated epithelial-to-mesenchymal transition44, and to correlate with CDCs therapeutic potential4546, we selected a panel of miRNA genes to be analyzed in BB and NBB-CDCs20. Preference was given to those miRNAs showing altered expression due to β-blocking agents observed in other systems6747484950.…”

Section: Resultsmentioning

confidence: 99%

Β-blockers treatment of cardiac surgery patients enhances isolation and improves phenotype of cardiosphere-derived cells

Chimenti

Pagano

Angelini

et al. 2016

Sci Rep

Self Cite

View full text Add to dashboard Cite

Β-blockers (BB) are a primary treatment for chronic heart disease (CHD), resulting in prognostic and symptomatic benefits. Cardiac cell therapy represents a promising regenerative treatment and, for autologous cell therapy, the patients clinical history may correlate with the biology of resident progenitors and the quality of the final cell product. This study aimed at uncovering correlations between clinical records of biopsy-donor CHD patients undergoing cardiac surgery and the corresponding yield and phenotype of cardiospheres (CSs) and CS-derived cells (CDCs), which are a clinically relevant population for cell therapy, containing progenitors. We describe a statistically significant association between BB therapy and improved CSs yield and CDCs phenotype. We show that BB-CDCs have a reduced fibrotic-like CD90 + subpopulation, with reduced expression of collagen-I and increased expression of cardiac genes, compared to CDCs from non-BB donors. Moreover BB-CDCs had a distinctive microRNA expression profile, consistent with reduced fibrotic features (miR-21, miR-29a/b/c downregulation), and enhanced regenerative potential (miR-1, miR-133, miR-101 upregulation) compared to non-BB. In vitro adrenergic pharmacological treatments confirmed cytoprotective and anti-fibrotic effects of β1-blocker on CDCs. This study shows anti-fibrotic and pro-commitment effects of BB treatment on endogenous cardiac reparative cells, and suggests adjuvant roles of β-blockers in cell therapy applications.

show abstract

“…Yin et al found that low ambient temperature could cause enlarged heart, ultrastructure damage of myocardium and weakened functions, and Resveratrol treatment could inhibit the increase of miR-328 and effectively suppress these changes at least partially via inhibiting cardiomyocyte apoptosis [16]. MiR-21 is another master regulator of cardiac fibrosis [17][18][19]. Thum et al found that miR-21 induces cardiac fibrosis by targeting sprouty homologue 1 (Spry1), and silencing of miR-21 inhibits pressure-overload-induced interstitial fibrosis and attenuates cardiac dysfunction in mouse [20].…”

Section: Discussionmentioning

confidence: 99%

MiR-22 may Suppress Fibrogenesis by Targeting TGFβR I in Cardiac Fibroblasts

Hong

Cao²,

Wang³

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the development of heart failure, but the mechanisms undelying cardiac fibrosis remained unknown. microRNAs (miRNAs) are novel mechanisms leading to fibrotic diseases, including cardiac fibrosis. Previous studies revealed that miR-22 might be a potential target. However, the roles and mechanisms of miR-22 in cardiac fibrosis remained ill defined. The present study thus addressed the impact of miR-22 in cardiac fibrosis. Methods: After seven days following coronary artery occlusion in mice, tissues used for histology were collected and processed for Masson's Trichrome staining. In addition, cardiac fibroblasts were transfected with mimics and inhibitors of miR-22 using Lipofectamin 2000, and luciferase activity was measured in cell lysates using a luciferase assay kit. Western blotting was used to detect the expression of collagen1, α-SMA and TGFβRI proteins levels, and real time-PCR was employed to measure the Col1α1, Col3α1, miR-22 and TGFβRI mRNA levels. Results: In this study, we found that miR-22 was dynamically downregulated following MI induced by permanent ligation of the left anterior descending coronary artery for 7 days, an effect paralleled by significant collagen deposition. Inhibition of miR-22 with AMO-22 resulted in increased expression of Col1α1, Col3α1 and fibrogenesis in cultured cardiac fibroblasts. Conversely, overexpression of miR-22 in cultured cardiac fibroblasts significantly abrogated angiotensin II-induced collagen formation and fibrogenesis. Furthermore, we found that TGFβRI is a direct target for miR-22, and downregulation of TGFβR may have mediated the antifibrotic effect of miR-22. Conclusion: Our data clearly demonstrate that miR-22 acts as a novel negative regulator of angiotensin II-induced cardiac fibrosis by suppressing the expression of TGFβRI in the heart and may represent a new potential therapeutic target for treating cardiac fibrosis.

show abstract

miR-21 and cardiac fibrosis: another brick in the wall?: Figure 1

Cited by 37 publications

References 19 publications

miR-21 is associated with fibrosis and right ventricular failure

miR-21 is associated with fibrosis and right ventricular failure

Β-blockers treatment of cardiac surgery patients enhances isolation and improves phenotype of cardiosphere-derived cells

MiR-22 may Suppress Fibrogenesis by Targeting TGFβR I in Cardiac Fibroblasts

Contact Info

Product

Resources

About