scholarly journals Growth/differentiation Factor-5 Induces Osteogenic Differentiation of Human Ligamentum Flavum Cells through Activation of ERK1/2 and p38 MAPK

2010 ◽  
Vol 26 (2) ◽  
pp. 179-186 ◽  
Author(s):  
Zhao-Ming Zhong ◽  
Jian-Ting Chen ◽  
Yu Zhang ◽  
Ding-Sheng Zha ◽  
Zhuo-Sheng Lin ◽  
...  
Keyword(s):  
Osteogenic Differentiation ◽  
P38 Mapk ◽  
Ligamentum Flavum ◽  
Differentiation Factor ◽  
Growth Differentiation Factor 5

scholarly journals Gold Nanoparticles Combined Human β-Defensin 3 Gene-Modified Human Periodontal Ligament Cells Alleviate Periodontal Destruction via the p38 MAPK Pathway

2021 ◽  
Vol 9 ◽  
Author(s):  
Lingjun Li ◽  
Yangheng Zhang ◽  
Min Wang ◽  
Jing Zhou ◽  
Qian Zhang ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Osteogenic Differentiation ◽  
P38 Mapk ◽  
Periodontal Ligament ◽  
Mapk Pathway ◽  
Periodontal Regeneration ◽  
Periodontal Ligament Cells ◽  
Human Periodontal Ligament Cells ◽  
P38 Mapk Pathway

Periodontitis is a chronic inflammatory disease with plaques as the initiating factor, which will induce the destruction of periodontal tissues. Numerous studies focused on how to obtain periodontal tissue regeneration in inflammatory environments. Previous studies have reported adenovirus-mediated human β-defensin 3 (hBD3) gene transfer could potentially enhance the osteogenic differentiation of human periodontal ligament cells (hPDLCs) and bone repair in periodontitis. Gold nanoparticles (AuNPs), the ideal inorganic nanomaterials in biomedicine applications, were proved to have synergetic effects with gene transfection. To further observe the potential promoting effects, AuNPs were added to the transfected cells. The results showed the positive effects of osteogenic differentiation while applying AuNPs into hPDLCs transfected by adenovirus encoding hBD3 gene. In vivo, after rat periodontal ligament cell (rPDLC) transplantation into SD rats with periodontitis, AuNPs combined hBD3 gene modification could also promote periodontal regeneration. The p38 mitogen-activated protein kinase (MAPK) pathway was demonstrated to potentially regulate both the in vitro and in vivo processes. In conclusion, AuNPs can promote the osteogenic differentiation of hBD3 gene-modified hPDLCs and periodontal regeneration via the p38 MAPK pathway.

Differential effects of growth differentiation factor-5 on porcine dental papilla- and follicle-derived cells

2009 ◽  
Vol 28 (1) ◽  
pp. 56-65 ◽  
Author(s):  
Yoshinori Sumita ◽  
Masaki J. Honda ◽  
Minoru Ueda ◽  
Izumi Asahina ◽  
Hideaki Kagami
Keyword(s):  
Differential Effects ◽  
Dental Papilla ◽  
Differentiation Factor ◽  
Growth Differentiation Factor 5

Abstract 996: Growth Differentiation Factor-5 (GDF-5) Dictates Cardiac Remodelling in a Mouse Model of Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Syed Zaidi ◽  
Ali M Riazi ◽  
Qingling Huang ◽  
Md A Momen ◽  
Mansoor Husain
Keyword(s):  
Myocardial Infarction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Cardiac Remodelling ◽  
Postnatal Life ◽  
Mrna Levels ◽  
Vegf Mrna ◽  
Foetal Development ◽  
Differentiation Factor ◽  
Growth Differentiation Factor 5

Background: Bone Morphogenetic Proteins (BMPs) regulate diverse cellular functions during foetal development and postnatal life. Growth Differentiation Factor 5 (GDF5 a.k.a. BMP-14) is a BMP, which is expressed in a variety of tissues including heart. We previously showed that cardiac GDF5 mRNA levels are elevated after experimental myocardial infarction (MI) caused by permanent left anterior descending coronary artery (LAD) ligation. However, the significance of this finding was not known. Methods & Results: GDF5 knock-out (KO; n = 18 for MI) and wild-type (WT; n = 18 for MI) littermate controls were subjected to chronic LAD ligation in order to investigate the consequences resulting from the loss of GDF5 signalling following MI. At 28 days post-LAD ligation or sham (n = 12 for KO; n = 10 for WT), invasive hemodynamic parameters of cardiac function were examined just prior to sacrifice. Histopathology was assessed by morphometric analyses of perfusion fixed hearts and subsequent immunostaining. At 28 days post-MI, GDF5-KO mice exhibited decreased left ventricular systolic pressure and peak positive- and negative- dP/dt , and increased heart rate as compared to WT littermates ( P < 0.005 for each parameters). GDF5-KO mice also exhibited a significant increase in the area, length and transmural expansion of the infarct, scar thinning and cardiac dilatation ( P < 0.05 for each parameter). In addition, GDF5-KO mice displayed significantly fewer myocardial vessels in the infarct and peri-infarct regions as compared to WT littermates ( P < 0.05) . To explore mechanisms underlying this phenotype, we assessed gene expression levels of relevant potential downstream targets of GDF5. At 7d post-MI, quantitative RT-PCR revealed a significant reduction (35%) in VEGF mRNA levels in hearts of KO (n = 6) as compared to WT mice (n = 5, P = 0.033). Summary & Conclusion: These data suggest that increased GDF5 expression observed in hearts after MI plays an important role in cardiac remodelling. Absence of GDF5 expression in KO mice confers detrimental effects on healing and repair of myocardial and vascular tissues after MI. Regulated levels of GDF5, a BMP family member, play an important role in the repair process following cardiac injury.

scholarly journals Effect of Plastrum Testudinis Extracts on the Proliferation and Osteogenic Differentiation of rBMSCs by Regulating p38 MAPK-Related Genes

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Qi Shang ◽  
Xiang Yu ◽  
Hui Ren ◽  
Gengyang Shen ◽  
Wenhua Zhao ◽  
...  
Keyword(s):  
Protein Expression ◽  
Osteogenic Differentiation ◽  
Mrna Expression ◽  
P38 Mapk ◽  
Bone Diseases ◽  
Treatment Of Osteoporosis ◽  
Osteogenic Induction ◽  
Rat Bone

Extracts from plastrum testudinis (PTE) are active compounds that have been used to treat bone diseases in traditional Chinese medicine for thousands of years. In previous studies, we demonstrated their effects on glucocorticoid-induced osteoporosis both in vivo and in vitro. However, the mechanisms by which PTE regulates the osteogenic differentiation of rat bone marrow-derived mesenchymal stem cells (rBMSCs) in vitro remain poorly understood. In this study, rBMSCs were treated with medium (CON), PTE, osteogenic induction (OI), and a combination of PTE and OI (PTE+OI) over a 21-day period. We found that PTE significantly promoted rBMSCs osteogenic differentiation and mineralisation after 21 days of culturing. Moreover, PTE+OI further enhanced the differentiation and mineralisation process. PTE upregulated STE20, IGF1R, and p38 MAPK mRNA expression and downregulated TRAF6 mRNA expression. The extracts inhibited TRAF6 protein expression and promoted STE20, IGF1R, and phosphorylated p38 MAPK protein expression. Our results imply that PTE promotes the proliferation and osteogenic differentiation of rBMSCs by upregulating p38 MAPK, STE20, and IGF1R and downregulating TRAF6 expression, which may provide experimental evidence of the potential of PTE in the treatment of osteoporosis.

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