Filtered By:
Condition: Osteoarthritis
Infectious Disease: Adenoviruses

This page shows you your search results in order of date.

Order by Relevance | Date

Total 6 results found since Jan 2013.

Platelet-rich plasma attenuates interleukin-1 β-induced apoptosis and inflammation in chondrocytes through targeting hypoxia-inducible factor-2α
Tissue Cell. 2021 Sep 8;73:101646. doi: 10.1016/j.tice.2021.101646. Online ahead of print.ABSTRACTOsteoarthritis (OA) is a prevailing chronic disease in Orthopedics that characterized with severely damaged cartilage and subchondral bone, thus leading to profound disorders of synovial joints. Platelet-rich plasma (PRP) has been applied as a popular non-operative treatment option for promoting musculoskeletal healing. Our previous work demonstrated that PRP protected chondrocytes from interleukin-1β (IL-1β)-induced apoptosis in vitro. However, the underlying mechanism behind the treatment remains unclear. The current study...
Source: Tissue and Cell - September 18, 2021 Category: Cytology Authors: Jinjiang Yang Ai Guo Qiang Li Jie Wu Source Type: research

Zinc finger protein A20 regulates the development and progression of osteoarthritis by affecting the activity of NF- κB p65
CONCLUSION: A20 was reduced in OA cartilage samples, and its overexpression, by suppressing the activity of NF-κB p65, could improve IL-1β-induced chondrocyte degradation and apoptosis in vitro, as well as mitigate the inflammation in OA mice.PMID:34463587 | DOI:10.1080/08923973.2021.1970764
Source: Immunopharmacology and Immunotoxicology - August 31, 2021 Category: Allergy & Immunology Authors: Shu-Bei Cui Tao-Xia Wang Zhen-Wu Liu Ji-Ying Yan Kai Zhang Source Type: research

MiR-145 targeting BNIP3 reduces apoptosis of chondrocytes in osteoarthritis through Notch signaling pathway.
CONCLUSIONS: MiR-145 can reduce OA-induced chondrocyte apoptosis through targeted inhibition on BNIP3 and regulation on Notch signaling pathway. PMID: 32894532 [PubMed - as supplied by publisher]
Source: European Review for Medical and Pharmacological Sciences - September 8, 2020 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Elevated expression of periostin in human osteoarthritic cartilage and its potential role in matrix degradation via matrix metalloproteinase-13 Research Communication
We examined periostin expression by immunohistochemical analysis of lesional and nonlesional cartilage from human and rodent OA knee cartilage. In addition, we used small interfering (si)RNA and adenovirus transduction of chondrocytes to knock down and up-regulate periostin levels, respectively, and analyzed its effect on matrix metalloproteinase (MMP)-13, a disintegrin and MMP with thrombospondin motifs (ADAMTS)-4, and type II collagen expression. We found high periostin levels in human and rodent OA cartilage. Periostin increased MMP-13 expression dose [1–10 µg/ml (EC50 0.5–1 μg/ml)] and time (24&nda...
Source: FASEB Journal - October 1, 2015 Category: Biology Authors: Attur, M., Yang, Q., Shimada, K., Tachida, Y., Nagase, H., Mignatti, P., Statman, L., Palmer, G., Kirsch, T., Beier, F., Abramson, S. B. Tags: Research Communication Source Type: research

Rac1 Is Required for Matrix Metalloproteinase 13 Production by Chondrocytes in Response to Fibronectin Fragments
ConclusionRac1 is required for FN fragment–induced signaling that results in increased MMP‐13 production. EGF receptor ligands, which activate Rac, can promote this effect. The presence of active Rac in OA cartilage and the ability of Rac to stimulate MMP‐13 production suggest that it could play a role in the cartilage matrix destruction seen in OA.
Source: Arthritis and Rheumatism - May 30, 2013 Category: Rheumatology Authors: David L. Long, Jeffrey S. Willey, Richard F. Loeser Tags: Chondrocyte Biology Source Type: research

Rac1 is required for matrix metalloproteinase‐13 production by chondrocytes in response to fibronectin fragments
Conclusion.Rac1 is required for Fnf induced signaling that results in increased MMP‐13 production. EGF receptor ligands, which activate Rac, can promote this effect. The presence of active Rac in OA cartilage and the ability of Rac to stimulate MMP‐13 production suggests that it could play a role in the cartilage matrix destruction seen in OA. © 2013 American College of Rheumatology.
Source: Arthritis and Rheumatism - March 4, 2013 Category: Rheumatology Authors: David L. Long, Jeffrey S. Willey, Richard F. Loeser Tags: Full Length Source Type: research