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Related Concept Videos

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Anchoring junctions are multiprotein complexes that help cells connect to other cells and the extracellular matrix. Anchoring junctions are present on the lateral and basal surfaces of cells, providing strong and flexible connections. Focal adhesions are often formed due to cell interactions with the ECM substrata, which initiate signal transduction via kinase cascades and other mechanisms. Together, they provide stability and tissue integrity. There are three types of anchoring junctions:...
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The term desmosome derives from the Greek words "desmo" and "soma" meaning "adhesion bodies." This structure was first observed during the late 1800s and described as small, dense nodules in the epidermis. Desmosomes are button-like structures that help form an interlinked network of intermediate filaments across the cells. These junctions are  essential to hold cells together under mechanical stress and to maintain tissue integrity. Desmosomes are multi-protein...
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Blebs are a type of membrane protrusion formed by the internal hydrostatic pressure of the cytoplasm. Blebs are observed in several cell types, including fibroblasts, immune cells, and single-celled organisms like the amoeba. The primary function of blebs is cell locomotion and apoptosis, but they are also found during necrosis and cell division. The life cycle of a bleb comprises an initiation phase followed by the expansion and retraction phases.
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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
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CREB3L2 Regulates Hemidesmosome Formation during Epithelial Sealing.

Y Li1, J Zhang1, W Cai1

  • 1Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Center of Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Center of Zhejiang University, Hangzhou, China.

Journal of Dental Research
|August 9, 2023
PubMed
Summary
This summary is machine-generated.

Gingival mesenchymal stem cell (MSC) sheets enhance dental implant sealing by promoting hemidesmosome formation via the PI3K/AKT pathway and the transcription factor CREB3L2. This improves soft tissue integration and implant success.

Keywords:
cell adhesiondental implantsgingivamesenchymal stem cell transplantationregenerative medicinesignal transduction pathway

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Area of Science:

  • Biomaterials Science
  • Regenerative Medicine
  • Cell Biology

Background:

  • Dental implant success relies on a strong biological seal between the implant and surrounding soft tissues.
  • Mesenchymal stem cells (MSCs) show potential for improving soft tissue integration around implants, but their precise molecular mechanisms remain unclear.
  • The application of MSC sheets for soft tissue integration is an emerging area of research.

Purpose of the Study:

  • To investigate the molecular mechanisms by which gingival tissue-derived MSC (GMSC) sheets enhance epithelial sealing around dental implants.
  • To elucidate the role of hemidesmosome (HD) formation and the PI3K/AKT pathway in GMSC sheet-mediated soft tissue integration.
  • To identify key regulatory factors, such as transcription factors, involved in this process.

Main Methods:

  • Treatment of gingival epithelial cells (GECs) with GMSC sheets.
  • Analysis of hemidesmosome-related gene and protein expression.
  • High-throughput transcriptome sequencing to identify upregulated pathways.
  • Pharmacological inhibition of the PI3K/AKT pathway.
  • Gene manipulation (overexpression/knockdown) of transcription factor CREB3L2.
  • In vivo study using an early implant placement model in rats.

Main Results:

  • GMSC sheet treatment significantly increased the expression of HD-related genes and proteins in GECs, strengthening epithelial sealing.
  • Transcriptome sequencing revealed significant upregulation of the PI3K/AKT pathway by GMSC sheets.
  • CREB3L2 expression was downregulated by GMSC sheets and upregulated by PI3K inhibition, indicating CREB3L2 is downstream of this pathway.
  • CREB3L2 manipulation affected HD formation, confirming its role in GMSC sheet-regulated epithelial sealing.
  • In vivo, GMSC sheet-implant complexes enhanced HD formation and reduced epithelial penetration.

Conclusions:

  • GMSC sheets promote epithelial sealing around dental implants by upregulating hemidesmosome formation, mediated by the PI3K/AKT pathway and the transcription factor CREB3L2.
  • CREB3L2 acts as a key downstream regulator in the GMSC sheet-induced enhancement of epithelial attachment.
  • These findings provide a mechanistic understanding of MSC sheet application in regenerative medicine for dental implants.