Comparison of TGF-β/BMP Pathways Signaled by Demineralized Bone Powder and BMP-2 in Human Dermal Fibroblasts

2004 ◽  
Vol 19 (10) ◽  
pp. 1732-1741 ◽  
Author(s):  
Shuanhu Zhou ◽  
Julie Glowacki ◽  
Karen E Yates
Keyword(s):  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Bone Powder ◽  
Demineralized Bone

scholarly journals Non pharmacological high-intensity ultrasound treatment of human dermal fibroblasts to accelerate wound healing

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jeong Yu Lee ◽  
Dae-Jin Min ◽  
Wanil Kim ◽  
Bum-Ho Bin ◽  
Kyuhan Kim ◽  
...  
Keyword(s):  
Wound Healing ◽  
High Intensity ◽  
Mapk Pathway ◽  
Dermal Fibroblasts ◽  
Ultrasound Treatment ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Short Term ◽  
High Intensity Ultrasound ◽  
Extracellular Matrix Components

AbstractInspired by the effectiveness of low-intensity ultrasound on tissue regeneration, we investigated the potential effect of short-term high-intensity ultrasound treatment for acceleration of wound healing in an in vitro wound model and dermal equivalent, both comprising human dermal fibroblasts. Short-term ultrasound of various amplitudes significantly increased the proliferation and migration of fibroblasts and subsequently increased the production of the extracellular matrix components fibronectin and collagen type I, both of which are important for wound healing and are secreted by fibroblasts. In addition, ultrasound treatment increased the contraction of a fibroblast-embedded three-dimensional collagen matrix, and the effect was synergistically increased in the presence of TGF-β. RNA-sequencing and bioinformatics analyses revealed changes in gene expression and p38 and ERK1/2 MAPK pathway activation in the ultrasound-stimulated fibroblasts. Our findings suggest that ultrasound as a mechanical stimulus can activate human dermal fibroblasts. Therefore, the activation of fibroblasts using ultrasound may improve the healing of various types of wounds and increase skin regeneration.

Deciphering the role of cartilage protein 1 in human dermal fibroblasts: a transcriptomic approach

2021 ◽  
Author(s):  
Sophia Letsiou ◽  
Manuel Manchado ◽  
Mariela Zografaki ◽  
Sofia Marka ◽  
Liliana Anjos ◽  
...  
Keyword(s):  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts

scholarly journals Inhibition of p38 Mitogen-Activated Protein Kinase Impairs Mayaro Virus Replication in Human Dermal Fibroblasts and HeLa Cells

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1156
Author(s):  
Madelaine Sugasti-Salazar ◽  
Yessica Y. Llamas-González ◽  
Dalkiria Campos ◽  
José González-Santamaría
Keyword(s):  
Protein Expression ◽  
Hela Cells ◽  
Plaque Assay ◽  
Dermal Fibroblasts ◽  
Dependent Manner ◽  
Human Dermal Fibroblasts ◽  
Mitogen Activated Protein ◽  
Mayaro Virus ◽  
The Impact ◽  
Dose Dependent

Mayaro virus (MAYV) hijacks the host’s cell machinery to effectively replicate. The mitogen-activated protein kinases (MAPKs) p38, JNK, and ERK1/2 have emerged as crucial cellular factors implicated in different stages of the viral cycle. However, whether MAYV uses these MAPKs to competently replicate has not yet been determined. The aim of this study was to evaluate the impact of MAPK inhibition on MAYV replication using primary human dermal fibroblasts (HDFs) and HeLa cells. Viral yields in supernatants from MAYV-infected cells treated or untreated with inhibitors SB203580, SP600125, U0126, or Losmapimod were quantified using plaque assay. Additionally, viral protein expression was analyzed using immunoblot and immunofluorescence. Knockdown of p38⍺/p38β isoforms was performed in HDFs using the PROTACs molecule NR-7h. Our data demonstrated that HDFs are highly susceptible to MAYV infection. SB203580, a p38 inhibitor, reduced MAYV replication in a dose-dependent manner in both HDFs and HeLa cells. Additionally, SB203580 significantly decreased viral E1 protein expression. Similarly, knockdown or inhibition of p38⍺/p38β isoforms with NR-7h or Losmapimod, respectively, affected MAYV replication in a dose-dependent manner. Collectively, these findings suggest that p38 could play an important role in MAYV replication and could serve as a therapeutic target to control MAYV infection.

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