PGC1A is required for chondrocyte metabolism and cartilage homeostasis

Activins are proinflammatory cytokines which belong to the TGFβsuperfamily. Follistatin is an extracellular decoy receptor for activins. Since both activins and follistatin are expressed in articular cartilage, we hypothesized that activin-follistatin signaling participates in the process of joint inflammation and cartilage degeneration. To test this hypothesis, we examined the effects of follistatin in a carrageenan-induced mouse arthritis model. Synovitis induced by intra-articular injection of carrageenan was significantly alleviated by preinjection with follistatin. Macrophage infiltration into the synovial membrane was significantly reduced in the presence of follistatin. In addition, follistatin inhibited proteoglycan erosion induced by carrageenan in articular cartilage. These data indicate that activin-follistatin signaling is involved in joint inflammation and cartilage homeostasis. Our data suggest that follistatin can be a new therapeutic target for inflammation-induced articular cartilage degeneration.

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YAP/TAZ in Bone and Cartilage Biology

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.788773 ◽

2022 ◽

Vol 9 ◽

Author(s):

Mylène Zarka ◽

Eric Haÿ ◽

Martine Cohen-Solal

Keyword(s):

Cell Fate ◽

Bone Biology ◽

Organ Growth ◽

Cellular Models ◽

Cartilage Homeostasis ◽

Cartilage Biology ◽

Cartilage Cells ◽

And Function ◽

And Cartilage

YAP and TAZ were initially described as the main regulators of organ growth during development and more recently implicated in bone biology. YAP and TAZ are regulated by mechanical and cytoskeletal cues that lead to the control of cell fate in response to the cellular microenvironment. The mechanical component represents a major signal for bone tissue adaptation and remodelling, so YAP/TAZ contributes significantly in bone and cartilage homeostasis. Recently, mice and cellular models have been developed to investigate the precise roles of YAP/TAZ in bone and cartilage cells, and which appear to be crucial. This review provides an overview of YAP/TAZ regulation and function, notably providing new insights into the role of YAP/TAZ in bone biology.

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Adipokine Contribution to the Pathogenesis of Osteoarthritis

Mediators of Inflammation ◽

10.1155/2017/5468023 ◽

2017 ◽

Vol 2017 ◽

pp. 1-26 ◽

Cited By ~ 58

Author(s):

Daniel Azamar-Llamas ◽

Gabriela Hernández-Molina ◽

Bárbara Ramos-Ávalos ◽

Janette Furuzawa-Carballeda

Keyword(s):

Adipose Tissue ◽

Risk Factor ◽

Weight Bearing ◽

Epidemiological Studies ◽

Overweight And Obesity ◽

Cartilage Explants ◽

Metabolic Factors ◽

Physiological Mechanisms ◽

Cartilage Homeostasis ◽

And Cartilage

Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

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MicroRNAs’ Involvement in Osteoarthritis and the Prospects for Treatments

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/236179 ◽

2015 ◽

Vol 2015 ◽

pp. 1-13 ◽

Cited By ~ 23

Author(s):

Xiao-Ming Yu ◽

Hao-Ye Meng ◽

Xue-Ling Yuan ◽

Yu Wang ◽

Quan-Yi Guo ◽

...

Keyword(s):

Molecular Mechanisms ◽

Target Genes ◽

Noncoding Rnas ◽

Genetic Changes ◽

Future Studies ◽

Small Noncoding Rnas ◽

Cartilage Homeostasis ◽

Target Binding ◽

And Cartilage

Osteoarthritis (OA) is a chronic disease and its etiology is complex. With increasing OA incidence, more and more people are facing heavy financial and social burdens from the disease. Genetics-related aspects of OA pathogenesis are not well understood. Recent reports have examined the molecular mechanisms and genes related to OA. It has been realized that genetic changes in articular cartilage and bone may contribute to OA’s development. Osteoclasts, osteoblasts, osteocytes, and chondrocytes in joints must express appropriate genes to achieve tissue homeostasis, and errors in this can cause OA. MicroRNAs (miRNAs) are small noncoding RNAs that have been discovered to be overarching regulators of gene expression. Their ability to repress many target genes and their target-binding specificity indicate a complex network of interactions, which is still being defined. Many studies have focused on the role of miRNAs in bone and cartilage and have identified numbers of miRNAs that play important roles in regulating bone and cartilage homeostasis. Those miRNAs may also be involved in the pathology of OA, which is the focus of this review. Future studies on the role of miRNAs in OA will provide important clues leading to a better understanding of the mechanism(s) of OA and, more particularly, to the development of therapeutic targets for OA.

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