Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Tytuł pozycji:

The regulatory mechanism of p38/MAPK in the chondrogenic differentiation from bone marrow mesenchymal stem cells.

Tytuł:
The regulatory mechanism of p38/MAPK in the chondrogenic differentiation from bone marrow mesenchymal stem cells.
Autorzy:
Ma N; Department of Orthopedics, Zhejiang Taizhou Central Hospital (Affiliated Hospital of Taizhou University), No. 999 Donghai Avenue, Jiaojiang District, Taizhou, 318000, Zhejiang, China.
Teng X; Department of Orthopedics, Zhejiang Taizhou Central Hospital (Affiliated Hospital of Taizhou University), No. 999 Donghai Avenue, Jiaojiang District, Taizhou, 318000, Zhejiang, China.
Zheng Q; Department of Orthopedics, Zhejiang Taizhou Central Hospital (Affiliated Hospital of Taizhou University), No. 999 Donghai Avenue, Jiaojiang District, Taizhou, 318000, Zhejiang, China.
Chen P; Department of Orthopedics, Yan Cheng Third People's Hospital (Affiliated Yancheng Hospital of Southeast University Medical College), No.2 Xindu West Road, Yancheng, 224001, Jiangsu, China. .
Źródło:
Journal of orthopaedic surgery and research [J Orthop Surg Res] 2019 Dec 12; Vol. 14 (1), pp. 434. Date of Electronic Publication: 2019 Dec 12.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: London : BioMed Central, 2006-
MeSH Terms:
Chondrogenesis/*physiology
Mesenchymal Stem Cells/*cytology
p38 Mitogen-Activated Protein Kinases/*physiology
Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cells, Cultured ; Chondrogenesis/drug effects ; Chondrogenesis/genetics ; Down-Regulation/physiology ; Enzyme Activation/physiology ; Gene Expression Regulation/physiology ; Humans ; MAP Kinase Signaling System/physiology ; Mesenchymal Stem Cells/drug effects ; Mesenchymal Stem Cells/enzymology ; Transforming Growth Factor beta1/pharmacology ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors ; p38 Mitogen-Activated Protein Kinases/metabolism
References:
Cancer Sci. 2019 Feb;110(2):481-488. (PMID: 30589983)
J Bone Miner Res. 1999 May;14(5):757-63. (PMID: 10320524)
Contrib Nephrol. 2011;170:75-82. (PMID: 21659760)
Proc Nutr Soc. 2014 May;73(2):278-88. (PMID: 24572502)
J Biol Chem. 1998 Jul 24;273(30):19213-9. (PMID: 9668109)
DNA Cell Biol. 2013 Sep;32(9):488-97. (PMID: 23781879)
Curr Stem Cell Res Ther. 2018;13(6):409-422. (PMID: 29714147)
Cells. 2019 Jul 28;8(8):. (PMID: 31357692)
Biomaterials. 2012 Nov;33(33):8395-405. (PMID: 22922021)
Biomater Sci. 2018 May 29;6(6):1556-1568. (PMID: 29696285)
Tissue Eng Part A. 2016 Feb;22(3-4):222-32. (PMID: 26603220)
J Biol Chem. 2003 Oct 17;278(42):41227-36. (PMID: 12893825)
Aging Cell. 2017 Apr;16(2):210-218. (PMID: 28124466)
J Biol Chem. 2006 May 12;281(19):13134-40. (PMID: 16565087)
J Biomed Mater Res A. 2016 Mar;104(3):734-746. (PMID: 26566602)
J Gastroenterol. 2017 Jul;52(7):777-787. (PMID: 28534191)
Osteoarthritis Cartilage. 2015 Mar;23(3):478-86. (PMID: 25529198)
FEBS Lett. 2006 Sep 18;580(21):4984-90. (PMID: 16949582)
Int J Biol Sci. 2012;8(2):272-88. (PMID: 22298955)
Minim Invasive Ther Allied Technol. 2008;17(2):79-90. (PMID: 18465443)
Int J Med Sci. 2012;9(10):862-71. (PMID: 23155360)
Ann Intern Med. 2000 Oct 17;133(8):635-46. (PMID: 11033593)
Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
Bull World Health Organ. 2003;81(9):646-56. (PMID: 14710506)
Mol Med Rep. 2017 Jul;16(1):63-68. (PMID: 28498451)
Arthritis Res Ther. 2016 Jun 23;18:146. (PMID: 27334538)
Biochem Biophys Res Commun. 2008 Apr 18;368(4):990-5. (PMID: 18267113)
Pharmacol Ther. 2019 Aug;200:42-54. (PMID: 30998940)
Cell Prolif. 2010 Aug;43(4):333-43. (PMID: 20590658)
Curr Opin Plant Biol. 2018 Oct;45(Pt A):1-10. (PMID: 29753266)
Autoimmun Rev. 2018 Nov;17(11):1097-1104. (PMID: 30213694)
J Biol Chem. 2000 Feb 25;275(8):5613-9. (PMID: 10681543)
Contributed Indexing:
Keywords: BMSCs; Chondrogenic differentiation; Osteoarthritis; TGF-β1; p38-MAPK
Substance Nomenclature:
0 (Transforming Growth Factor beta1)
EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
Entry Date(s):
Date Created: 20191214 Date Completed: 20200601 Latest Revision: 20200601
Update Code:
20240105
PubMed Central ID:
PMC6909593
DOI:
10.1186/s13018-019-1505-2
PMID:
31831024
Czasopismo naukowe
Background: Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation and joint inflammation, in which growth factors are significantly involved. The extracellular signal-regulated p38 MAPK pathways play important roles in the regulation of osteogenic and chondrogenic differentiation in bone marrow mesenchymal stem cells (BMSCs). However, the exact mechanism remains unclear.
Methods: In this study, the chondrogenic differentiation of human BMSCs was initiated in micromass culture in the presence of TGF-β1 for 14 days. Quantitative RT-PCR and Western blot were performed to detect the transfection effect of shRNA-p38 interfering plasmid in BMSCs. The protein expressions of p/t-p38, SOX9, collagen II, Aggrecan, p/t-Smad1, and p/t-Smad4, as well as the kinase activities of p38/ERK/JNK pathway, were investigated using Western blot analysis. Additionally, the level of chondroitin sulfate and glycosaminoglycans (GAG) expression were measured by Alcian blue staining and GAG assay kit via qualitative and quantitative methods, respectively.
Results: The results demonstrated that p38 pathway was activated in the chondrogenic differentiation of BMSCs induced by TGF-β1. Cartilage-specific genes and chondrogenic regulators, such as SOX9, collagen II, Aggrecan, and GAG, were upregulated by TGF-β1, which could be reversed by predisposed with shRNA-p38 interfering plasmid and p38-MAPK inhibitors (SB203580). Moreover, the activation of p38/ERK/JNK pathways in the presence of TGF-β1 was suppressed by shRNA-p38 and SB203580 treatment.
Conclusion: Collectively, the activation of p38/ERK/JNK/Smad pathways plays a facilitated role in the chondrogenic differentiation induced by TGF-β1. After suppressing the p38 pathway, the chondrogenesis can be inhibited, which can be used to guide the treatment of osteoarthritis.
Zaloguj się, aby uzyskać dostęp do pełnego tekstu.

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies