Clinical Value of lncRNA CASC19 in Myocardial Infarction and its Role in Myocardial Infarction-Induced Cardiomyocyte Apoptosis.

To explore the effect of long non-coding RNA cancer susceptibility 19 (lncRNA CASC19) on the activity, apoptosis, and oxidative stress response of cardiomyocytes, so as to assess the clinical relevance and molecular mechanism of CASC19 in myocardial infarction (MI). CASC19 level was determined by using real-time quantitative polymerase chain reaction (RT-qPCR). MI model was constructed using hypoxia induction, and rat cardiomyocytes H9c2 were divided into control group, MI group, MI small interference negative control (MI-si-NC) group, MI-si-CASC19 group, MI-si-CASC19+microRNA-NC (miR-NC) group, and MI-si-CASC19+miR-218-5p inhibitor group.

Metformin alleviates junctional epithelium senescence via the AMPK/SIRT1/autophagy pathway in periodontitis induced by hyperglycemia.

The junctional epithelium (JE) serves a crucial protective role in the periodontium. High glucose-related aging results in accelerated barrier dysfunction of the gingival epithelium, which may be associated with diabetic periodontitis. Metformin, an oral hypoglycemic therapeutic, has been proposed as a anti-aging agent.

Use of Network Pharmacology and Experiment Validation to Uncover the Mechanism of Jianshen Lishui Prescription in the Treatment of Intracerebral Hemorrhage.

Background: As a Chinese medicinal formula, the Jianshen Lishui prescription has been clinically proven to be effective in treating intracerebral hemorrhage (ICH). Yet, the mechanisms involved are unknown.

Methods: (1) Network pharmacology analysis: It involved the screening of active components in the Jianshen Lishui prescription, identification of potential targets for these components, and the screening of ICH-related targets.

TGF-β1/Smad3 Signaling Is Required to Alleviate Fluoride-Induced Enamel Hypomineralization.

Excessive fluoride intake during enamel development can affect enamel mineralization, leading to dental fluorosis. However, its potential mechanisms remain largely unexplored. In the present study, we aimed to investigate the impact of fluoride on the expressions of RUNX2 and ALPL during mineralization and the effect of TGF-β1 administration on fluoride treatment.

Analysis of antiplatelet therapy adherence in patients with ischemic cerebral stroke.

Background: The related factors affecting the adherence of ischemic cerebral stroke (ICS) patients to antiplatelet therapy have attracted much attention.

Methods: Patients with ICS (confirmed by CT or MRI) were enrolled from January 2020 to July 2021. The demographic data were retrospectively investigated and analyzed.

Shenfu Injection Protects Brain Injury in Rats with Cardiac Arrest through Nogo/NgR Pathway.

The effect of Shenfu injection on brain injury after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) along with the underlying mechanism of axonal regeneration was explored. CA/CPR model in rats was established for subsequent experiments. A total of 160 rats were randomly divided into sham group, model group, conventional western medicine (CWM) group, Shenfu group, and antagonist group ( = 32 per group).

Odontogenesis-Associated Phosphoprotein (ODAPH) Overexpression in Ameloblasts Disrupts Enamel Formation via Inducing Abnormal Mineralization of Enamel in Secretory Stage.

Odontogenesis-associated phosphoprotein (ODAPH) is a recently discovered enamel matrix protein. Our previous study demonstrated that knockouting out Odaph in mice resulted in enamel hypomineralization. To further investigate the effect of Odaph on enamel mineralization, we constructed an Odaph overexpression mouse model, controlled by an amelogenin promoter.

The synergistic effects of TGF-β1 and RUNX2 on enamel mineralization through regulating ODAPH expression during the maturation stage.

Transforming growth factor β1 (TGF-β1) and Runt-related transcription factor 2 (RUNX2) are critical factors promoting enamel development and maturation. Our previous studies reported that absence of TGF-β1 or RUNX2 resulted in abnormal secretion and absorption of enamel matrix proteins. However, the mechanism remained enigmatic.

Expression and localization of amelotin, laminin γ2 and odontogenesis-associated phosphoprotein (ODAPH) on the basal lamina and junctional epithelium.

At maturation stage of enamel development, a specialized basal lamina (sBL) was built between ameloblasts and enamel. After the teeth eruption, the ameloblasts transform into the inner cell layer of junctional epithelium. The inner cell layer forms the internal basal lamina of junctional epithelium.

The absence of muscle segment homeobox 2 leads to the pyroptosis of ameloblasts by inducing squamous epithelial hyperplasia in the enamel organ.

Muscle segment homeobox 2 (MSX2) has been confirmed to be involved in the regulation of early tooth development. However, the role of MSX2 has not been fully elucidated in enamel development. To research the functions of MSX2 in enamel formation, we used a Msx2 (KO) mouse model with no full Msx2 gene.

Maturation stage enamel defects in Odontogenesis-associated phosphoprotein (Odaph) deficient mice.

Background: Mutation in Odontogenesis-associated phosphoprotein (ODAPH) has been reported to cause recessive hypomineralized amelogenesis imperfecta (AI) in human. However, the exact role of ODAPH in amelogenesis is still unknown.

Results: ODAPH was identified as a novel constituent of the atypical basal lamina located at the interface between maturation ameloblasts and the enamel by dual immunofluorescence staining of ODAPH and LAMC2.

Runx2 deficiency in junctional epithelium of mouse molars decreases the expressions of E-cadherin and junctional adhesion molecule 1.

Junctional epithelium (JE) attaching to the enamel surface seals gaps around the teeth, functioning as the first line of gingival defense. Runt-related transcription factor 2 (Runx2) plays a role in epithelial cell fate, and the deficiency of Runx2 in JE causes periodontal destruction, while its effect on the barrier function of JE remains largely unexplored. In the present study, hematoxylin-eosin (H&E) staining revealed the morphological differences of JE between wild-type (WT) and Runx2 conditional knockout (cKO) mice.

Calcium mitigates fluoride-induced kallikrein 4 inhibition via PERK/eIF2α/ATF4/CHOP endoplasmic reticulum stress pathway in ameloblast-lineage cells.

Objectives: The present study aimed to investigated the effect and mechanism of Ca treatment on fluoride in ameloblast-lineage cells (ALCs).

Materials And Methods: The effects of fluoride and different Ca levels treatment on the proliferative activity, cell apoptosis, cell cycle, intracellular free Ca, were firstly determined. Kallikrein 4 (KLK4), glucose-responsive protein 78 (GRP78), Protein kinase R -like endoplasmic reticulum kinase (PERK), the α subunit of eukaryotic initiation factor 2 (eIF2α), activating transcription factor 4 (ATF4), CCAAT enhancer-binding protein homologous protein (CHOP), were investigated in ALCs.

Epithelium-Specific Runx2 knockout mice display junctional epithelium and alveolar bone defects.

Objective: The aim of this investigation was to study the effects of Runt-related transcription factor 2 (Runx2) on the junctional epithelium and alveolar bone.

Methods: The attachment level of the junctional epithelium and the resorption of alveolar bone were analyzed by histology and scanning electron microscopy. The expression of amelotin was determined by immunohistochemistry, Western blot, and real-time PCR.

RUNX2 contributes to TGF-β1-induced expression of Wdr72 in ameloblasts during enamel mineralization.

The elaborate modulation of the transforming growth factor β (TGF-β) superfamily signaling network plays an essential role in tooth morphogenesis and differentiation. In our previous studies, we have demonstrated that TGF-β1 promotes enamel mineralization and maturation using TGF-β1 gene conditional knockout (TGF-β1-cKO) mice. However, the specific regulatory mechanisms of TGF-β1 during enamel development remain unclear.

Loss of transforming growth factor-β1 in epithelium cells affects enamel formation in mice.

Objectives: In order to understand the specific in vivo function of transforming growth factor-beta1 (TGF-β1), we successfully established aTGF-β1 deficient mouse model using a conditional knockout method. In the present study, we aimed to further understand the potential role of TGF-β1 in enamel formation.

Design: Transgenic mice withoutTGF-β1 in epithelial cells were generated.

Constitutive activation of β-catenin in ameloblasts leads to incisor enamel hypomineralization.

Enamel is the hardest tissue with the highest degree of mineralization protecting the dental pulp from injury in vertebrates. The ameloblasts differentiated from ectoderm-derived epithelial cells are a single cell layer and are important for the enamel formation and mineralization. Wnt/β-catenin signaling has been proven to exert an important role in the mineralization of bone, dentin and cementum.

Ablation of Runx2 in Ameloblasts Suppresses Enamel Maturation in Tooth Development.

Runt-related transcription factor 2 (Runx2) is involved in the early stage of tooth development. However, only few studies have reported the role of Runx2 in enamel development, which may be attributed to that Runx2 full knockout mice cannot survive after birth. In the present study, we successfully established a Runx2-deficient mouse model using a conditional knockout (cKO) method.

Combination of Runx2 and Cbfβ upregulates Amelotin gene expression in ameloblasts by directly interacting with cis‑enhancers during amelogenesis.

Amelotin (Amtn) is a recently identified enamel protein secreted by ameloblasts at late stage of enamel development. Runt‑related transcription factor 2 (Runx2) in combination with the coactivator core‑binding factor β (Cbfβ) regulates the early stages of tooth development. The aim of the present study was to investigate the role of Runx2 in the regulation of Amtn gene expression in ameloblasts.

Overexpression of constitutively active MAP3K7 in ameloblasts causes enamel defects of mouse teeth.

Objective: Compelling evidence suggests that mitogen-activated protein kinases (Mapks) play an important role in amelogenesis. However, the role of transforming growth factor (TGF)-β-activating kinase 1 (Tak1, Map3k7), which is a known upstream kinase of Mapks, during amelogenesis remains to be determined. The aim of this study was to investigate the possible involvement of Map3k7 in amelogenesis.

[Exploration of the oral health education experimental teaching for oral health education reform].

Objective: This study aimed to improve students' ability in practical and theoretical courses of oral health education and to promote students' learning interest and initiative.

Methods: Fourth-year students of the oral medical profession from 2006 to 2008 at Weifang Medical University were chosen as research objects for oral health education to explore the experimental teaching reform. The students were divided into test and control groups, with the test group using the "speak out" way of teaching and the control group using the traditional teaching method.

Transforming growth factor-β1 regulates expression of the matrix metalloproteinase 20 (Mmp20) gene through a mechanism involving the transcription factor, myocyte enhancer factor-2C, in ameloblast lineage cells.

Matrix metalloproteinase-20 (Mmp20) plays an essential role in amelogenesis during tooth development and is regulated by transforming growth factor-β1 (TGF-β1) in mouse ameloblast lineage cells (ALCs). The objective of this study was to explore the role of myocyte enhancer factor-2C (MEF2C), a key transcription factor in craniofacial development, in TGF-β1-induced Mmp20 gene expression. We investigated Mmp20 expression in ALCs over-expressing MEF2C and in ALCs with MEF2C knocked down.

Role of the BCA2 ubiquitin E3 ligase in hormone responsive breast cancer.

The BCA2 protein contains a RING H2 finger and a Zn finger near the N-terminus and has E3 ligase activity. RING finger proteins play critical roles in mediating the transfer of ubiquitin and ubiquitin like modifiers to heterologous substrates as well as to the RING finger proteins themselves. Protein modification by ubiquitin and small ubiquitin-related modifier (SUMO) plays a pivotal role in protein homeostasis and is critical to regulating basic cellular processes such as proliferation, differentiation, apoptosis, intracellular signaling, and gene-transcriptional regulation.

Distribution of amelotin in mouse tooth development.

Amelotin is expressed and secreted by ameloblasts in tooth development, but amelotin distribution during enamel development is not clear. In this report, we first investigated amelotin expression in developing teeth by immunohistochemistry. Amelotin was detected in the enamel matrix at the secretion and maturation stages of enamel development.

TGF-beta1 and TGFBR1 are expressed in ameloblasts and promote MMP20 expression.

Transforming growth factor-beta (TGF-beta) signaling exerts a wide spectrum of biological functions. To investigate TGF-beta signaling in amelogenesis, we initially assessed the expression of TGF-beta1 and TGF-beta receptor 1 (TGFBR1) in developing teeth by immunohistochemistry. Both TGF-beta1 and TGFBR1 were strongly expressed in secreting ameloblasts.