scholarly journals Preparation of Foam Dressings Based on Gelatin, Hyaluronic Acid, and Carboxymethyl Chitosan Containing Fibroblast Growth Factor-7 for Dermal Regeneration

Polymers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 3279
Author(s):  
Longhao Jin ◽  
Sun-Jung Yoon ◽  
Dae Hoon Lee ◽  
Yun Chang Pyun ◽  
Woo Youp Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Hyaluronic Acid ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Wound Dressing ◽  
Transmission Rate ◽  
Carboxymethyl Chitosan ◽  
Amide Bond ◽  
Fibroblast Growth

Wound recovery close to the function of the native skin is the goal of wound healing. In this study, we prepared foam dressings (FDs; 2-GHC-FD-1–9, 5-GHC-FD-1–9, and 10-GHC-FD-1–9) composed of various concentrations of gelatin, hyaluronic acid, and carboxymethyl chitosan, which are chemically interconnected through amide bond formation, for evaluating wound healing. Tensile and cell proliferation tests showed that 2-GHC-FD-1–9 are suitable for wound dressing. For further evaluation, three types of FDs, 2-GHC-FD-1, 2-GHC-FD-4, and 2-GHC-FD-8 were chosen. The results of animal intradermal reactivity, water vapor transmission rate, and absorption rate of the three FDs indicated that 2-GHC-FD-8 is the most appropriate scaffold for wound healing. For wound healing acceleration, various concentrations of fibroblast growth factor-7 (FGF-7) was soaked in 2-GHC-FD-8 (2-GHC-FD-8/F1-6) and evaluated by using scanning electron microscopy, cell proliferation, release behavior, and in vivo animal tests. The FDs showed interconnected porous structures, increased cell proliferation until 8.0 × 10−11 M, controlled release with initial burst within 1 h, and sustained release for 48 h. The results of the animal test showed an appropriate concentration of FGF-7 for wound healing. In addition, 2-GHC-FD-8 is a suitable scaffold for wound healing. Therefore, we suggest that 2-GHC-FD-8/F3 is a useful wound dressing for accelerating wound healing.

scholarly journals The Fibroblast Growth Factor 9 (Fgf9) Participates in Palatogenesis by Promoting Palatal Growth and Elevation

2021 ◽  
Vol 12 ◽  
Author(s):  
Ruomei Li ◽  
Yidan Sun ◽  
Zhengxi Chen ◽  
Mengting Zheng ◽  
Yuhua Shan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hyaluronic Acid ◽  
Growth Factor ◽  
Cleft Palate ◽  
Fibroblast Growth Factor ◽  
Cleft Lip ◽  
Cleft Lip And Palate ◽  
Fibroblast Growth ◽  
Exon 2 ◽  
Acid Accumulation

Cleft palate, a common global congenital malformation, occurs due to disturbances in palatal growth, elevation, contact, and fusion during palatogenesis. The Fibroblast growth factor 9 (FGF9) mutation has been discovered in humans with cleft lip and palate. Fgf9 is expressed in both the epithelium and mesenchyme, with temporospatial diversity during palatogenesis. However, the specific role of Fgf9 in palatogenesis has not been extensively discussed. Herein, we used Ddx4-Cre mice to generate an Fgf9–/– mouse model (with an Fgf9 exon 2 deletion) that exhibited a craniofacial syndrome involving a cleft palate and deficient mandibular size with 100% penetrance. A smaller palatal shelf size, delayed palatal elevation, and contact failure were investigated to be the intrinsic causes for cleft palate. Hyaluronic acid accumulation in the extracellular matrix (ECM) sharply decreased, while the cell density correspondingly increased in Fgf9–/– mice. Additionally, significant decreases in cell proliferation were discovered in not only the palatal epithelium and mesenchyme but also among cells in Meckel’s cartilage and around the mandibular bone in Fgf9–/– mice. Serial sections of embryonic heads dissected at embryonic day 14.5 (E14.5) were subjected to craniofacial morphometric measurement. This highlighted the reduced oral volume owing to abnormal tongue size and descent, and insufficient mandibular size, which disturbed palatal elevation in Fgf9–/– mice. These results indicate that Fgf9 facilitates palatal growth and timely elevation by regulating cell proliferation and hyaluronic acid accumulation. Moreover, Fgf9 ensures that the palatal elevation process has adequate space by influencing tongue descent, tongue morphology, and mandibular growth.

Bio-orthogonal Immobilization of Fibroblast Growth Factor 2 for Spatial Controlled Cell Proliferation

2015 ◽  
Vol 1 (9) ◽  
pp. 740-746 ◽  
Author(s):  
Tessa Lühmann ◽  
Gabriel Jones ◽  
Marcus Gutmann ◽  
Jens-Christoph Rybak ◽  
Joachim Nickel ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals The Antimicrobial Peptide Human β-Defensin-3 Accelerates Wound Healing by Promoting Angiogenesis, Cell Migration, and Proliferation Through the FGFR/JAK2/STAT3 Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Miho Takahashi ◽  
Yoshie Umehara ◽  
Hainan Yue ◽  
Juan Valentin Trujillo-Paez ◽  
Ge Peng ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Growth Factors ◽  
Growth Factor ◽  
Antimicrobial Peptide ◽  
Fibroblast Growth Factor ◽  
Human Fibroblasts ◽  
Janus Kinase ◽  
Fibroblast Growth ◽  
Angiogenic Growth Factors

In addition to its antimicrobial activity, the skin-derived antimicrobial peptide human β-defensin-3 (hBD-3) promotes keratinocyte proliferation and migration to initiate the wound healing process; however, its effects on fibroblasts, which are the major cell type responsible for wound healing, remain unclear. We investigated the role of hBD-3 in cell migration, proliferation and production of angiogenic growth factors in human fibroblasts and evaluated the in vivo effect of hBD-3 on promoting wound healing and angiogenesis. Following hBD-3 treatment, the mouse wounds healed faster and showed accumulation of neutrophils and macrophages in the early phase of wound healing and reduction of these phagocytes 4 days later. hBD-3-treated wounds also displayed an increased number of fibroblasts and newly formed vessels compared to those of the control mice. Furthermore, the expression of various angiogenic growth factors was increased in the hBD-3-treated wounds. Additionally, in vitro studies demonstrated that hBD-3 enhanced the secretion of angiogenic growth factors such as fibroblast growth factor, platelet-derived growth factor and vascular endothelial growth factor and induced the migration and proliferation of human fibroblasts. The hBD-3-mediated activation of fibroblasts involves the fibroblast growth factor receptor 1 (FGFR1)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathways, as evidenced by the inhibitory effects of pathway-specific inhibitors. We indeed confirmed that hBD-3 enhanced the phosphorylation of FGFR1, JAK2 and STAT3. Collectively, the current study provides novel evidence that hBD-3 might be a potential candidate for the treatment of wounds through its ability to promote wound healing, angiogenesis and fibroblast activation.

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