Platelet lysate activates quiescent cell proliferation and reprogramming in human articular cartilage: Involvement of hypoxia inducible factor 1

2017 ◽  
Vol 12 (3) ◽  
Author(s):  
Van Thi Nguyen ◽  
Ranieri Cancedda ◽  
Fiorella Descalzi
Keyword(s):  
Cell Proliferation ◽  
Articular Cartilage ◽  
Hypoxia Inducible Factor ◽  
Platelet Lysate ◽  
Quiescent Cell ◽  
Human Articular Cartilage ◽  
Hypoxia Inducible Factor 1

scholarly journals Progenitor Cells Activated by Platelet Lysate in Human Articular Cartilage as a Tool for Future Cartilage Engineering and Reparative Strategies

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1052 ◽  
Author(s):  
Simonetta Carluccio ◽  
Daniela Martinelli ◽  
Maria Elisabetta Federica Palamà ◽  
Rui Cruz Pereira ◽  
Roberto Benelli ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Progenitor Cells ◽  
Articular Chondrocytes ◽  
Ex Vivo ◽  
Primary Cultures ◽  
Platelet Lysate ◽  
Cartilage Explants ◽  
Cartilage Tissue ◽  
Human Articular Cartilage

Regenerative strategies for human articular cartilage are still challenging despite the presence of resident progenitor cell population. Today, many efforts in the field of regenerative medicine focus on the use of platelet derivatives due to their ability to reactivate endogenous mechanisms supporting tissue repair. While their use in orthopedics continues, mechanisms of action and efficacy need further characterization. We describe that the platelet lysate (PL) is able to activate chondro-progenitor cells in a terminally differentiated cartilage tissue. Primary cultures of human articular chondrocytes (ACs) and cartilage explants were set up from donor hip joint biopsies and were treated in vitro with PL. PL recruited a chondro-progenitors (CPCs)-enriched population from ex vivo cartilage culture, that showed high proliferation rate, clonogenicity and nestin expression. CPCs were positive for in vitro tri-lineage differentiation and formed hyaline cartilage-like tissue in vivo without hypertrophic fate. Moreover, the secretory profile of CPCs was analyzed, together with their migratory capabilities. Some CPC-features were also induced in PL-treated ACs compared to fetal bovine serum (FBS)-control ACs. PL treatment of human articular cartilage activates a stem cell niche responsive to injury. These facts can improve the PL therapeutic efficacy in cartilage applications.

Hypoxia Inducible Factor-1 Alpha Promotes Mesangial Cell Proliferation in Lupus Nephritis

2014 ◽  
Vol 40 (6) ◽  
pp. 507-515 ◽  
Author(s):  
Wei Deng ◽  
Yile Ren ◽  
Xuebing Feng ◽  
Genhong Yao ◽  
Weiwei Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lupus Nephritis ◽  
Mesangial Cell ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Mesangial Cell Proliferation

scholarly journals Transcriptional Coactivator Cited2 Induces Bmi1 and Mel18 and Controls Fibroblast Proliferation via Ink4a/ARF

2003 ◽  
Vol 23 (21) ◽  
pp. 7658-7666 ◽  
Author(s):  
Kamil R. Kranc ◽  
Simon D. Bamforth ◽  
José Bragança ◽  
Chris Norbury ◽  
Maarten van Lohuizen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hypoxia Inducible Factor ◽  
Polycomb Group ◽  
Growth Fraction ◽  
Fibroblast Proliferation ◽  
Transcriptional Coactivator ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Hypoxia Inducible Factor 1 ◽  
Polycomb Group Genes

ABSTRACT Cited2 (CBP/p300 interacting transactivator with ED-rich tail 2) is required for embryonic development, coactivation of transcription factor AP-2, and inhibition of hypoxia-inducible factor 1 transactivation. Cited2 is induced by multiple growth factors and cytokines and oncogenically transforms cells. Here, we show that the proliferation of Cited2 −/− mouse embryonic fibroblasts ceases prematurely. This is associated with a reduction in growth fraction, senescent cellular morphology, and increased expression of the cell proliferation inhibitors p16INK4a, p19ARF, and p15INK4b. Deletion of INK4a/ARF (encoding p16INK4a and p19ARF) completely rescued the defective proliferation of Cited2−/− fibroblasts. However, the deletion of INK4a/ARF did not rescue the embryonic malformations observed in Cited2 −/− mice, indicating that INK4a/ARF-independent pathways are likely to be involved here. We found that Cited2 −/− fibroblasts had reduced expression of the polycomb-group genes Bmi1 and Mel18, which function as INK4a/ARF and Hox repressors. Complementation with CITED2-expressing retrovirus enhanced proliferation, induced Bmi1/Mel18 expression, and decreased INK4a/ARF expression. Bmi1- and Mel18-expressing retroviruses enhanced the proliferation of Cited2 −/− fibroblasts, indicating that they function downstream of Cited2. Our results provide genetic evidence that Cited2 controls the expression of INK4a/ARF and fibroblast proliferation, at least in part via the polycomb-group genes Bmi1 and Mel18.

scholarly journals Hypoxia-inducible factor-1 alpha maintains mouse articular cartilage through suppression of NF-κB signaling

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Keita Okada ◽  
Daisuke Mori ◽  
Yuma Makii ◽  
Hideki Nakamoto ◽  
Yasutaka Murahashi ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1

Dual Effect of Platelet Lysate on Human Articular Cartilage: A Maintenance of Chondrogenic Potential and a Transient Proinflammatory Activity Followed by an Inflammation Resolution

2013 ◽  
Vol 19 (11-12) ◽  
pp. 1476-1488 ◽  
Author(s):  
Rui Cruz Pereira ◽  
Monica Scaranari ◽  
Roberto Benelli ◽  
Paolo Strada ◽  
Rui L. Reis ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Platelet Lysate ◽  
Human Articular Cartilage ◽  
Dual Effect ◽  
Chondrogenic Potential ◽  
Proinflammatory Activity ◽  
Inflammation Resolution
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