MicroRNAs: pleiotropic players in congenital heart disease and regeneration

Hoelscher, Sarah C.; Doppler, S.; Dreßen, Martina; Lahm, Harald; Lange, Rüdiger; Krane, Markus

doi:10.21037/jtd.2017.03.149

Cited by 40 publications

(26 citation statements)

References 134 publications

(165 reference statements)

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“…These data suggest that miRNAs are fundamental for normal cardiac development. miRNA expression has been studied in several congenital heart diseases (e.g., hypoplastic heart syndrome, tetralogy of Fallot, ventricular septal defects, and Holt–Oram syndrome; Hoelscher et al., 2017). However, no study has focused on dilated cardiomyopathy type 1A and “Heart‐Hand” syndrome linked to lamins.…”

Section: Mirnas In Hereditary Laminopathiesmentioning

confidence: 99%

MicroRNAs in hereditary and sporadic premature aging syndromes and other laminopathies

et al. 2018

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SummaryHereditary and sporadic laminopathies are caused by mutations in genes encoding lamins, their partners, or the metalloprotease ZMPSTE24/FACE1. Depending on the clinical phenotype, they are classified as tissue‐specific or systemic diseases. The latter mostly manifest with several accelerated aging features, as in Hutchinson–Gilford progeria syndrome (HGPS) and other progeroid syndromes. MicroRNAs are small noncoding RNAs described as powerful regulators of gene expression, mainly by degrading target mRNAs or by inhibiting their translation. In recent years, the role of these small RNAs has become an object of study in laminopathies using in vitro or in vivo murine models as well as cells/tissues of patients. To date, few miRNAs have been reported to exert protective effects in laminopathies, including miR‐9, which prevents progerin accumulation in HGPS neurons. The recent literature has described the potential implication of several other miRNAs in the pathophysiology of laminopathies, mostly by exerting deleterious effects. This review provides an overview of the current knowledge of the functional relevance and molecular insights of miRNAs in laminopathies. Furthermore, we discuss how these discoveries could help to better understand these diseases at the molecular level and could pave the way toward identifying new potential therapeutic targets and strategies based on miRNA modulation.

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Section: Mirnas In Hereditary Laminopathiesmentioning

confidence: 99%

MicroRNAs in hereditary and sporadic premature aging syndromes and other laminopathies

et al. 2018

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“…Abnormal miRNA expression has been observed in both physiological and pathological processes multiple human cancers like proliferation, invasion, apoptosis, and chemotherapy resistance 12. MicroRNA‐130b‐3p (miR‐130b) targets CYLD to suppress growth of cells and induce programmed death in human gastric cancer cells 13, 14.…”

Section: Introductionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are non-coding RNA molecules with around 20 to 25 nucleotides that can lead to a downregulation of target proteins through the degradation of this mRNA or through translational inhibition, which play an important role in various malignancies. 11,12 Abnormal miRNA expression has been observed in both physiological and pathological processes multiple human cancers like proliferation, invasion, apoptosis, and chemotherapy resistance. 12 MicroRNA-130b-3p (miR-130b) targets CYLD to suppress growth of cells and induce programmed death in human gastric cancer cells.…”

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confidence: 99%

“…11,12 Abnormal miRNA expression has been observed in both physiological and pathological processes multiple human cancers like proliferation, invasion, apoptosis, and chemotherapy resistance. 12 MicroRNA-130b-3p (miR-130b) targets CYLD to suppress growth of cells and induce programmed death in human gastric cancer cells. 13,14 Moreover, miR-130b was recorded to be lifted in triple negative breast cancer tissue in comparison with adjacent healthy ones, and miR-130b mediated CCNG2 that could be closely connected with the deteriorating development of the cancer in question.…”

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confidence: 99%

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MicroRNA‐130b targets PTEN to induce resistance to cisplatin in lung cancer cells by activating Wnt/β‐catenin pathway

Zhang

Sun

et al. 2018

Cell Biochemistry & Function

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More and more studies indicate the relevance of miRNAs in inducing certain drug resistance. Our study aimed to investigate whether microRNA‐130b‐3p (miR‐130b) mediates the chemoresistance as well as proliferation of lung cancer (LC) cells. MTS assay and apoptosis analysis were conducted to determine cell proliferation and apoptosis, respectively. Binding sites were identified using a luciferase reporter system, whereas mRNA and protein expression of target genes was determined by RT‐PCR and immunoblot, respectively. Mouse xenograft model was used to evaluate the role of miR‐130b in cisplatin resistance in vivo. The rising level of miR‐130b in cisplatin resistance LC cell lines (A549/CR and H446/CR) versus its parental cell lines, indicated its crucial relevance for LC biology. We identified PTEN as miR‐130b's major target and inversely correlated with miR‐130b expression in LC. Moreover, excessive miR‐130b expression promoted drug resistance and proliferation, decreased apoptosis of A549 cells. Suppression of miR‐130b enhanced drug cytotoxicity and reduced proliferation of A549/CR cells both internally and externally. Particularly, miR‐130b mediated Wnt/β‐catenin signalling pathway activities, chemoresistance and proliferation in LC cell, which was partially blocked following knockdown of PTEN. These findings suggest that miR‐130b targets PTEN to mediate chemoresistance, proliferation, and apoptosis via Wnt/β‐catenin pathway. The rising level of miR‐130b in cisplatin resistance LC cell lines (A549/CR and H446/CR) versus its parental cell lines, indicated its crucial relevance for LC biology. Moreover, excessive miR‐130b expression promoted drug resistance and proliferation, decreased apoptosis of A549 cells. These findings suggest that miR‐130b targets PTEN to mediate chemoresistance, proliferation, and apoptosis via Wnt/β‐catenin pathway.

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“…Hoelscher et al (28) review the role of microRNAs in congenital heart disease and further discuss potential therapeutic strategies for such patients based on microRNAs.…”

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confidence: 99%