Genetic variants of microRNA processing genes and risk of non‐syndromic orofacial clefts

Xu, Min; Ma, Lan; Lou, Shu; Du, Yifei; Xu, Yin; Zhang, C; Fan, Liwen; Wang, H; Wang, Z; Zhang, W; Wang, Lei; Pan, Yuqin

doi:10.1111/odi.12741

Cited by 13 publications

(7 citation statements)

References 36 publications

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“…A number of microRNAs (miRs), which are small non-coding RNAs (21–25 nucleotides) that regulate the expression of target genes at the post-transcriptional level ( Hudder and Novak, 2008 ; Hou et al, 2011 ), play important roles in a wide array of cellular functions during the development of various tissues, including the upper lip and the palate ( Shin et al, 2012 ; Seelan et al, 2014 ; Warner et al, 2014 ; Mukhopadhyay et al, 2019 ). For instance, loss of a miR-processing enzyme, such as DROSHA and DICER, results in craniofacial developmental defects in mice ( Zehir et al, 2010 ; Nie et al, 2011 ; Schoen et al, 2017 ), and polymorphisms in DROSHA are associated with risk of CL/P in humans ( Xu et al, 2018 ). In addition, mice with a deletion of miR-17-92 cluster, which is located on chromosome 14 in mice and chromosome 13 in humans, exhibit either bilateral or unilateral CLP and delayed endochondral ossification, hypoplastic lung, and cardiac ventricular septal defect ( Ventura et al, 2008 ; de Pontual et al, 2011 ; Wang et al, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-124-3p Plays a Crucial Role in Cleft Palate Induced by Retinoic Acid

Yoshioka

Mikami

Ramakrishnan

et al. 2021

Front. Cell Dev. Biol.

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Cleft lip with/without cleft palate (CL/P) is one of the most common congenital birth defects, showing the complexity of both genetic and environmental contributions [e.g., maternal exposure to alcohol, cigarette, and retinoic acid (RA)] in humans. Recent studies suggest that epigenetic factors, including microRNAs (miRs), are altered by various environmental factors. In this study, to investigate whether and how miRs are involved in cleft palate (CP) induced by excessive intake of all-trans RA (atRA), we evaluated top 10 candidate miRs, which were selected through our bioinformatic analyses, in mouse embryonic palatal mesenchymal (MEPM) cells as well as in mouse embryos treated with atRA. Among them, overexpression of miR-27a-3p, miR-27b-3p, and miR-124-3p resulted in the significant reduction of cell proliferation in MEPM cells through the downregulation of CP-associated genes. Notably, we found that excessive atRA upregulated the expression of miR-124-3p, but not of miR-27a-3p and miR-27b-3p, in both in vivo and in vitro. Importantly, treatment with a specific inhibitor for miR-124-3p restored decreased cell proliferation through the normalization of target gene expression in atRA-treated MEPM cells and atRA-exposed mouse embryos, resulting in the rescue of CP in mice. Taken together, our results indicate that atRA causes CP through the induction of miR-124-3p in mice.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-124-3p Plays a Crucial Role in Cleft Palate Induced by Retinoic Acid

Yoshioka

Mikami

Ramakrishnan

et al. 2021

Front. Cell Dev. Biol.

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“…[ 25 – 27 ] In addition, SNPs in the miRNA-binding sites or miRNA processing genes were announced to be linked to nonsyndromic orofacial clefts susceptibility. [ 28 , 29 ] In mammals, it is possible for miRNAs to control 30% of the protein-coding genes by means of posttranscriptional silencing; therefore, the dysregulation of miRNAs in CLO, and it is possible for CPO or CLP patients have a far-reaching impact on a wide range of roles in biology. Based on our miRNA microarray data, we found the intersection of differentially expressed miRNAs in CLO, CPO, and CLP.…”

Section: Discussionmentioning

confidence: 99%

Integrated assessment of differentially expressed plasma microRNAs in subtypes of nonsyndromic orofacial clefts

Yan²,

Han³

et al. 2018

Medicine

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“…Many different microRNAs have been identified to temporally and spatially regulate morphogens and transcription factors during palatogenesis (Eberhart et al, 2008;Seelan et al, 2014;Ding et al, 2016;Reiss and Bhakdi, 2017;Schoen et al, 2017). Not surprisingly, microRNAs have been suggested as be new targets for investigating in CL/P studies (Li et al, 2010;Wang et al, 2013Wang et al, , 2017Ma et al, 2014;Gao et al, 2015;Li D. et al, 2016;Li J. et al, 2016;Schoen et al, 2017Schoen et al, , 2018Chen et al, 2018;Grassia et al, 2018;Pan et al, 2018;Suzuki et al, 2018;Wu N. et al, 2018;Xu M. et al, 2018).…”

Section: Ecm Structural Molecules and Soluble Factorsmentioning

confidence: 99%

Extracellular Matrix Composition and Remodeling: Current Perspectives on Secondary Palate Formation, Cleft Lip/Palate, and Palatal Reconstruction

Paiva

Maas

Santos

et al. 2019

Front. Cell Dev. Biol.

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Craniofacial development comprises a complex process in humans in which failures or disturbances frequently lead to congenital anomalies. Cleft lip with/without palate (CL/P) is a common congenital anomaly that occurs due to variations in craniofacial development genes, and may occur as part of a syndrome, or more commonly in isolated forms (non-syndromic). The etiology of CL/P is multifactorial with genes, environmental factors, and their potential interactions contributing to the condition. Rehabilitation of CL/P patients requires a multidisciplinary team to perform the multiple surgical, dental, and psychological interventions required throughout the patient's life. Despite progress, lip/palatal reconstruction is still a major treatment challenge. Genetic mutations and polymorphisms in several genes, including extracellular matrix (ECM) genes, soluble factors, and enzymes responsible for ECM remodeling (e.g., metalloproteinases), have been suggested to play a role in the etiology of CL/P; hence, these may be considered likely targets for the development of new preventive and/or therapeutic strategies. In this context, investigations are being conducted on new therapeutic approaches based on tissue bioengineering, associating stem cells with biomaterials, signaling molecules, and innovative technologies. In this review, we discuss the role of genes involved in ECM composition and remodeling during secondary palate formation and pathogenesis and genetic etiology of CL/P. We also discuss potential therapeutic approaches using bioactive molecules and principles of tissue bioengineering for state-of-the-art CL/P repair and palatal reconstruction.

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Genetic variants of microRNA processing genes and risk of non‐syndromic orofacial clefts

Cited by 13 publications

References 36 publications

MicroRNA-124-3p Plays a Crucial Role in Cleft Palate Induced by Retinoic Acid

MicroRNA-124-3p Plays a Crucial Role in Cleft Palate Induced by Retinoic Acid

Integrated assessment of differentially expressed plasma microRNAs in subtypes of nonsyndromic orofacial clefts

Extracellular Matrix Composition and Remodeling: Current Perspectives on Secondary Palate Formation, Cleft Lip/Palate, and Palatal Reconstruction

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