MiRNA-470-5p suppresses epithelial-mesenchymal transition of embryonic palatal shelf epithelial cells by targeting during palatogenesis.

MicroRNAs (miRNAs) have been identified as crucial modulators of gene expression and to play a role in palatogenesis. The aim of this study was to explore the potential role and regulatory mechanisms of miRNAs during palatogenesis. RNA-sequencing was performed to compare the RNA expression profiles of mouse embryonic palatal shelf (MEPS) tissue between an all-trans retinoic acid (ATRA)-induced group and control group, followed by reverse transcription-quantitative polymerase chain reaction for validation, demonstrating upregulated expression of miRNA-470-5p and downregulated expression of in the ATRA-induced group.

LncRNA-NONMMUT100923.1 regulates mouse embryonic palatal shelf adhesion by sponging miR-200a-3p to modulate medial epithelial cell desmosome junction during palatogenesis.

Cleft palate (CP) is a common neonatal craniofacial defect caused by the adhesion and fusion dysfunction of bilateral embryonic palatal shelf structures. Long non-coding RNA (lncRNA) is involved in CP formation with regulatory mechanism unknown. In this study, all-trans retinoic acid (ATRA) was used to induced cleft palate in embryonic mice as model group.

A Subpopulation of Schwann Cell-Like Cells With Nerve Regeneration Signatures Is Identified Through Single-Cell RNA Sequencing.

Schwann cell-like cells (SCLCs) derived from human amniotic mesenchymal stem cells (hAMSCs) have been shown to promote peripheral nerve regeneration, but the underlying molecular mechanism was still poorly understood. In order to investigate the heterogeneity and potential molecular mechanism of SCLCs in the treatment of peripheral nerve regeneration at a single cell level, single-cell RNA sequencing was applied to profile single cell populations of hAMSCs and SCLCs. We profiled 6,008 and 5,140 single cells from hAMSCs and SCLCs, respectively.

Integrated analysis identifying long non-coding RNAs (lncRNAs) for competing endogenous RNAs (ceRNAs) network-regulated palatal shelf fusion in the development of mouse cleft palate.

Background: Cleft palate results from the defective palatal fusion of the medial-edge epithelium after cells undergo epithelial-mesenchymal transition, a process that involves regulation by microRNAs (miRNAs). However, in palatal shelf fusion, miRNA regulation by long non-coding RNAs (lncRNAs) when acting as competing endogenous RNAs (ceRNAs) or miRNA sponges, remains unclear.

Methods: We systematically analyzed the correlation between lncRNAs, miRNAs, and mRNAs from RNA sequencing profiling in embryonic gestation day 14.

DNA hypermethylation of Fgf16 and Tbx22 associated with cleft palate during palatal fusion.

Objective: Cleft palate (CP) is a congenital birth defect caused by the failure of palatal fusion. Little is known about the potential role of DNA methylation in the pathogenesis of CP. This study aimed to explore the potential role of DNA methylation in the mechanism of CP.

Position-dependent correlation between TBX22 exon 5 methylation and palatal shelf fusion in the development of cleft palate.

DNA methylation is essential for spatiotemporally-regulated gene expression in embryonic development. TBX22 (Chr X: 107667964-107688978) functioning as a transcriptional repressor affects DNA binding, sumoylation, and transcriptional repression associated with X-linked cleft palate. This study aimed to explore the relationship and potential mechanism between TBX22 exon 5 methylation and palatal shelf fusion induced by all-trans retinoic acid (ATRA).

-mediated autophagy and apoptosis associated with an epithelial-mesenchymal transition in the development of cleft palate induced by all-trans retinoic acid.

Background: Autophagy and apoptosis are involved in embryogenesis. However, little is known about the regulatory mechanism of -mediated autophagy and apoptosis associated with epithelial-mesenchymal transition (EMT) in the development of cleft palate (CP). This study is aimed to elucidate a novel regulatory mechanism by which regulates autophagy and apoptosis associated with EMT during palatal fusion.

Identification of circular RNA-associated competing endogenous RNA network in the development of cleft palate.

Circular RNAs (circRNAs) serve as competing endogenous RNAs (ceRNAs) and indirectly regulate gene expression through shared microRNAs (miRNAs). However, the regulatory mechanisms of circRNA as ceRNA associated with the fusion of palatal shelves in palatogenesis are yet unclear. This study aimed to explore the potential mechanism underlying the role of circRNA as ceRNA in cleft palate (CP).

Genome-Wide mRNA-Seq Profiling Reveals that LEF1 and SMAD3 Regulate Epithelial-Mesenchymal Transition Through the Hippo Signaling Pathway During Palatal Fusion.

Background: Epithelial-mesenchymal transition (EMT) of the medial edge epithelium (MEE) occurs through fusion of the palatal shelves and is a crucial step in palatogenesis. The key genes, however, and the related signaling pathway of EMT are not yet fully understood. Therefore, the aim of this study was to reveal the key genes and the related signaling pathway of EMT during palatal fusion.

A novel lncRNA-mediated trans-regulatory mechanism in the development of cleft palate in mouse.

Background: Increasing evidence indicates that long non-coding RNAs (lncRNAs) play crucial regulatory roles in epithelial-mesenchymal transition (EMT). However, the regulatory mechanisms during EMT of the medial edge epithelium (MEE) remain elusive. The aim of this work is to reveal a novel lncRNA-regulated dysfunction of EMT involved in the development of cleft palate (CP).

Genome-Wide DNA Methylation Profile of Gene cis-Acting Element Methylations in All-trans Retinoic Acid-Induced Mouse Cleft Palate.

DNA methylation epigenetically regulates gene expression. This study is aimed to investigate genome-wide DNA methylations involved in the regulation of palatal fusion in the all-trans retinoic acid-induced mouse cleft palate model. There were 4,718,556 differentially CCGG methylated sites and 367,504 CCWGG methylated sites for 1497 genes between case and control embryonic mouse palatal tissues.

Correlation between HDAC4 enhancer DNA methylation and mRNA expression during palatal fusion induced by all-trans retinoic acid.

Epithelial-mesenchymal transformation of the medial edge epithelium is the most crucial process in embryonic palatal fusion. This study aimed to explore the relationship and potential mechanism between enhancer DNA methylation and mRNA expression of histone deacetylase 4 (HDAC4) during palatal fusion induced by maternal exposure to all-trans retinoic acid (ATRA). Pregnant mice were administered ATRA (70 mg/kg) by gavage at embryonic gestation day 10.

Genome-Wide DNA Methylation Analysis During Palatal Fusion Reveals the Potential Mechanism of Enhancer Methylation Regulating Epithelial Mesenchyme Transformation.

Epithelial mesenchyme transformation (EMT) of the medial edge epithelium (MEE) is the crucial process during palatal fusion. This work is aimed to elucidate the enhancer regulatory mechanism by genome-wide DNA methylation analysis of EMT during palatal fusion. Over 800 million clean reads, 325 million enzyme reads, and 234 million mapping reads were generated.

Efficiency of stem cell based therapy in the treatment of diabetic foot ulcer: a meta-analysis.

Diabetic foot ulcer is a chronic, refractory, frequent complication in diabetic patient. Its treatment often requires multidisciplinary joint efforts, diverse strategies have been adopted to address this annoying issue, including stem cell-based therapy/acellular dermal matrix/negative pressure wound therapy etc. However, consensus has not been reached.

Matrigel basement membrane matrix induces eccrine sweat gland cells to reconstitute sweat gland-like structures in nude mice.

Background: Severe burn results in irreversible damage to eccrine sweat glands, for which no effective treatment is available. Interaction between the extracellular matrix and epithelial cells is critical for proper three-dimensional organization and function of the epithelium.

Methods: Matrigel-embedded eccrine sweat gland cells were subcutaneously implanted into the inguinal regions of nude mice.

Localization of Na(+)-K(+)-ATPase α/β, Na(+)-K(+)-2Cl-cotransporter 1 and aquaporin-5 in human eccrine sweat glands.

In order to evaluate the function of the repaired or regenerated eccrine sweat glands, we must first localize the proteins involved in sweat secretion and absorption in normal human eccrine sweat glands. In our studies, the cellular localization of Na(+)-K(+)-ATPase α/β, Na(+)-K(+)-2Cl-cotransporter 1 (NKCC1) and aquaporin-5 (AQP5) in eccrine sweat glands were detected by immunoperoxidase labeling. The results showed that Na(+)-K(+)-ATPase α was immunolocalized in the cell membrane of the basal layer and suprabasal layer cells of the epidermis, the basolateral membrane of the secretory coils, and the cell membrane of the outer cells and the basolateral membrane of the luminal cells of the ducts.

The cellular localization of Na(+)/H(+) exchanger 1, cystic fibrosis transmembrane conductance regulator, potassium channel, epithelial sodium channel γ and vacuolar-type H+-ATPase in human eccrine sweat glands.

The secretory portions of human eccrine sweat glands secrete isotonic fluid into the lumen and then the primary fluid is rendered hypotonic during its passage to the skin surface. During the processes of sweat secretion and absorption, many enzymes and proteins play important roles. In the study, the cellular localizations of Na(+)/H(+) exchanger 1 (NHE1), cystic fibrosis transmembrane conductance regulator (CFTR), potassium channel (KC), epithelial sodium channel γ (γENaC) and vacuolar-type H+-ATPase (V-ATPase) in human eccrine sweat glands and epidermis were detected using immunofluorescence labeling.

[Three-dimensional culture and morphological observation of human eccrine sweat gland cells].

Objective: To investigate the three-dimensional (3D) culture and morphology of human eccrine sweat gland cells.

Methods: The human eccrine sweat gland cells were isolated from normal abdominal full thickness skin by digestion of type II collagenase, and cultured in defined-keratinocyte serum free medium supplemented with 5 ng/mL recombinant human epidermal growth factor, 25 mg/mL bovine pituitary extract, 100 U/mL penicillin, and 100 microg/mL streptomycin at 37 degrees C in a humidified atmosphere of 5%CO2/95% air incubator. When the cell fusion reached above 80%, the cells were harvested and the concentration was adjusted to 1 x 10(5) cells/mL.

A case-control study of environmental exposures for nonsyndromic cleft of the lip and/or palate in eastern Guangdong, China.

Objective: To study the relationship between environmental factors and nonsyndromic cleft of the lip and/or palate (NSCLP) in eastern Guangdong for the prevention of NSCLP.

Methods: A 1:1 retrospective case-control study was carried out. Data from 479 children with NSCLP who accepted comprehensive care in our center were recruited as cases from April 2010 to April 2013.

[Association between single nucleotide polymorphisms of v-maf musculoaponeurotic fibrosarcoma oncogene homolog B gene and non-syndromic cleft lip with or without cleft palate].

Objective: To reveal the association between the single nucleotide polymorphism (SNP) of v-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB) gene rs17820943 locus and non-syndromic cleft lip with or without cleft palate (NSCL/P) in the southern Chinese Han population.

Methods: Genotyping of MAFB gene rs17820943 polymorphism was carried out in 300 patients with NSCL/P, 354 normal controls, and an additional 168 case-parent trios with matrix-assisted laser desorption/ionisation time-of-flight (MALDI-TOF) mass spectrometry. Then based on the genotyping results, both a case-control association study and a case-parent trio association study were performed.

Association between single-nucleotide polymorphisms on chromosome 1p22 and 20q12 and nonsyndromic cleft lip with or without cleft palate: new data in Han Chinese and meta-analysis.

Background: Nonsyndromic cleft lip with or without cleft palate (NSCL/P) is a common congenital malformation associated with genetic and environmental risk factors. A recent genome-wide association study identified two novel susceptibility loci on chromosomes 1p22 and 20q12; however, conflicting results, especially for 1p22, have been reported in Han Chinese population. The aims of this study were to replicate this association with risk of NSCL/P in the southern Han Chinese population and to discern the effect of these loci by a meta-analysis.

PVRL1 as a candidate gene for nonsyndromic cleft lip with or without cleft palate: no evidence for the involvement of common or rare variants in southern Han Chinese patients.

The poliovirus receptor related-1 (PVRL1) gene encodes nectin-1, a cell-cell adhesion molecule (OMIM #600644), and is mutated in the cleft lip with or without cleft palate/ectodermal dysplasia-1 syndrome (CLPED1, OMIM #225000). In addition, PVRL1 mutations have been associated with nonsyndromic cleft lip with or without a cleft palate (NSCL/P) in studies of multiethnic samples. To investigate the possible involvement of this gene in southern Han Chinese NSCL/P patients, we performed (i) a case-control association study, and (ii) a resequencing study.

[Study on risk factors of nonsyndromic cleft lip and palate in Chinese Guangdong population].

Objective: To investigate the association between environmental factors and nonsyndromic cleft lip and palate (NSCLP), and to explore the interaction of main risk factors in Chinese Guangdong population.

Methods: A hospital-based case-control study was used. NSCLP children were selected from Cleft Lip & Palate Treatment Centre of Second Affiliated Hospital of Medical College of Shantou University between September 2009 and March 2010 as cases.