Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

Takao, Masanobu; Okinaga, Toshinori; Ariyoshi, Wataru; Iwanaga, Kenjiro; Nakamichi, Ikuo; Yoshioka, Izumi; Tominaga, Kazuhiro; Nishihara, Tatsuji

doi:10.1007/s00011-011-0346-1

Cited by 16 publications

(11 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is also evidence that mechanical stress may lead to the release of a range of pro‐inflammatory mediators from joint tissues, including interleukin (IL)‐1beta, cyclooxygenase‐2, prostaglandin E 2 , matrix metalloproteinase (MMP)‐2, MMP‐3, IL‐6, MMP‐9, MMP‐13, receptor activator of nuclear factor‐kappaB ligand, fibroblast growth factor‐2 and IL‐8 . Of note, pro‐inflammatory cytokines such as IL‐6 and C‐reactive protein have been shown to predict both the incidence and progression of arthritis.…”

Section: Hypothesesmentioning

confidence: 99%

Osteoarthritis, obesity and weight loss: evidence, hypotheses and horizons – a scoping review

2014

View full text Add to dashboard Cite

Obesity is widely acknowledged as a risk factor for both the incidence and progression of osteoarthritis, and has a negative influence on outcomes. Loss of at least 10& of body weight, coupled with exercise, is recognized as a cornerstone in the management of obese patients with osteoarthritis, and can lead to significant improvement in symptoms, pain relief, physical function and health-related quality of life. However, questions still remain surrounding optimal management. Given the significant health, social and economic burden of osteoarthritis, especially in obese patients, it is imperative to advance our knowledge of osteoarthritis and obesity, and apply this to improving care and outcomes. This paper overviews what is already known about osteoarthritis and obesity, discusses current key challenges and ongoing hypotheses arising from research in these areas, and finally, postulates what the future may hold in terms of new horizons for obese patients with osteoarthritis.

show abstract

Section: Hypothesesmentioning

confidence: 99%

Osteoarthritis, obesity and weight loss: evidence, hypotheses and horizons – a scoping review

2014

View full text Add to dashboard Cite

show abstract

“…Interestingly, chondrocytes embedded in their own ECM show similar increases in pro‐inflammatory mediators with stress, but not that one's embedded in an agarose matrix, which indicates that native ECM interactions can influence this response. Mechanical stretch also enhances the expression of pro‐inflammatory factors in fibroblast‐like synoviocytes (namely cyclooxygenase (COX)‐2, PGE 2 , and IL‐1β), and in osteoblasts (in particular, IL‐6, COX‐2, and IL‐8) . Moreover, inflammatory mediators, such as IL‐1β, IL‐6, and oncostatin M, affected the osteoblast‐chondrocyte crosstalk .…”

mentioning

confidence: 99%

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

Francisco

Pérez

Pino

et al. 2017

Journal Orthopaedic Research

View full text Add to dashboard Cite

Osteoarthritis is a high-incidence painful and debilitating disease characterized by progressive degeneration of articular joints, which indicates a breakdown in joint homeostasis favoring catabolic processes. Biomechanical loading, associated with inflammatory and metabolic imbalances of joint, strongly contributes to the initiation and progression of the disease. Obesity is a primary risk factor for disease onset, and mechanical factors increased the risk for disease progression. Moreover, inflammatory mediators, in particular, adipose tissue-derived cytokines (better known as adipokines) play a critical role linking obesity and osteoarthritis. The present article summarizes the knowledge about the role of adipokines in cartilage and bone function, highlighting their contribution to the imbalance of joint homeostasis and, consequently, pathogenesis of osteoarthritis. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:594-604, 2018.

show abstract

“…Cytokines that mediate inflammation, such as IL-1β and TNF-α, are well known to be involved in mechanical stretch-induced inflammation. For example, in vitro administration of mechanical stress induces both IL-1β and COX-2 in fibroblast-like synoviocyte cells ( 48 ), epithelial cells ( 49 ), chondrocytes ( 50 ), and cardiac muscle cells ( 51 ) in a time- and force-dependent manner. This increased expression of inflammatory markers corresponded to our findings.…”

Section: Discussionmentioning

confidence: 99%

Mechanical Stress Changes the Complex Interplay Between HO-1, Inflammation and Fibrosis, During Excisional Wound Repair

et al. 2015

View full text Add to dashboard Cite

Mechanical stress following surgery or injury can promote pathological wound healing and fibrosis, and lead to functional loss and esthetic problems. Splinted excisional wounds can be used as a model for inducing mechanical stress. The cytoprotective enzyme heme oxygenase-1 (HO-1) is thought to orchestrate the defense against inflammatory and oxidative insults that drive fibrosis. Here, we investigated the activation of the HO-1 system in a splinted and non-splinted full-thickness excisional wound model using HO-1-luc transgenic mice. Effects of splinting on wound closure, HO-1 promoter activity, and markers of inflammation and fibrosis were assessed. After seven days, splinted wounds were more than three times larger than non-splinted wounds, demonstrating a delay in wound closure. HO-1 promoter activity rapidly decreased following removal of the (epi)dermis, but was induced in both splinted and non-splinted wounds during skin repair. Splinting induced more HO-1 gene expression in 7-day wounds; however, HO-1 protein expression remained lower in the epidermis, likely due to lower numbers of keratinocytes in the re-epithelialization tissue. Higher numbers of F4/80-positive macrophages, αSMA-positive myofibroblasts, and increased levels of the inflammatory genes IL-1β, TNF-α, and COX-2 were present in 7-day splinted wounds. Surprisingly, mRNA expression of newly formed collagen (type III) was lower in 7-day wounds after splinting, whereas, VEGF and MMP-9 were increased. In summary, these data demonstrate that splinting delays cutaneous wound closure and HO-1 protein induction. The pro-inflammatory environment following splinting may facilitate higher myofibroblast numbers and increase the risk of fibrosis and scar formation. Therefore, inducing HO-1 activity against mechanical stress-induced inflammation and fibrosis may be an interesting strategy to prevent negative effects of surgery on growth and function in patients with orofacial clefts or in patients with burns.

show abstract

Role of heme oxygenase-1 in inflammatory response induced by mechanical stretch in synovial cells

Abstract: We found that constitutive HO-1 expression in hemin-pretreated HFLS cells suppressed mechanical stretch-induced inflammatory responses, suggesting that HO-1 may play a role as a regulation factor in synovial tissue inflammation.

Cited by 16 publications

References 36 publications

Osteoarthritis, obesity and weight loss: evidence, hypotheses and horizons – a scoping review

Osteoarthritis, obesity and weight loss: evidence, hypotheses and horizons – a scoping review

Biomechanics, obesity, and osteoarthritis. The role of adipokines: When the levee breaks

Mechanical Stress Changes the Complex Interplay Between HO-1, Inflammation and Fibrosis, During Excisional Wound Repair

Contact Info

Product

Resources

About