The synovial lining cell: Biology and pathobiology

Henderson, Brian E.; Pettipher, E. R.

doi:10.1016/0049-0172(85)90007-1

Cited by 120 publications

(57 citation statements)

References 174 publications

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“…An increase in synovial membrane vascularity is a hallmark of active synovitis and improvement in this parameter could be beneficial. 6,32,33 Articular cartilage sections obtained from OA joints of untreated horses had significantly less SOFG staining as compared to all other evaluated sections. This finding suggests that IL-1Ra had a protective effect on proteoglycan loss and is consistent with SOFG data observed by others.…”

Section: Photographs Of the Intercarpal Joint Highlighting Third Carpmentioning

confidence: 99%

Treatment of experimental equine osteoarthritis by in vivo delivery of the equine interleukin-1 receptor antagonist gene

et al. 2002

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Section: Photographs Of the Intercarpal Joint Highlighting Third Carpmentioning

confidence: 99%

Treatment of experimental equine osteoarthritis by in vivo delivery of the equine interleukin-1 receptor antagonist gene

et al. 2002

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“…The two main functions normally ascribed to synovial lining cells are phagocytosis (type A cells) and synthesis of HA (type B cells). Synovial lining cells also synthesize the extracellular matrix of the synovium (Henderson and Pettipher 1985). The subchondral bone is in most cases characterised by a relatively thin subchondral plate.…”

Section: Gross Anatomy and Histologymentioning

confidence: 99%

Physiology and pathology of the equine joint

Weeren¹,

Brama²

2001

PHK

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SummaryDiseases of the locomotor system are the most commonly encountered disorders in equine practice. Among them, joint-related ailments are most frequent. In this paper a synopsis is given of structure and function of the equine joint with the emphasis on molecular biochemistry. As examples of different pathologic aberrations osteoarthritis (OA) and osteochondrosis (OC) are dealt with. The paper concludes with a short overview of the current trends in equine synovial joint research and a suggestion of what the future might bring. Keywords:Horse, joint, extracellular matrix, collagen, proteoglycans, osteoarthritis, osteochondrosis

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“…The proinflammatory cytokines IL-1␤ and TNF␣ promote cartilage reabsorption, inhibit synthesis of proteoglycans, and cause inflammation, all of which are major symptoms of RA (13)(14)(15)(16). Macrophages are the major immune cell present within the synovial tissues and are recruited in high numbers in RA, suggesting that a majority of IL-1 and TNF␣ release within the joint is from this cell type (17). Subsequent to and building upon these studies, the nuclear receptor estrogen receptor ␤ (ER␤) was detected in macrophages, revealing a mechanism by which estrogen can act to effect molecular signals within the cells (18,19).…”

Section: Conclusion Estrogen Can Modulate Proinflammatory Cytokine Rmentioning

confidence: 99%

17β‐estradiol regulates cytokine release through modulation of CD16 expression in monocytes and monocyte‐derived macrophages

Kramer¹,

Krämer²,

Guan³

2004

Arthritis & Rheumatism

174

127

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Objective. Macrophages release cytokines, such as tumor necrosis factor ␣ (TNF␣), interleukin-1 (IL-1), and IL-6, which modulate the symptoms of rheumatoid arthritis (RA). Macrophage release of these cytokines can be modulated by estrogen. Fc␥ receptor type IIIA (CD16a) is a receptor expressed on macrophages that selectively binds IgG molecules, an important rheumatoid factor in RA. Binding of CD16 by anti-CD16 monoclonal antibodies stimulates macrophage cytokine release. We undertook this study to test the hypothesis that decreased concentrations of estrogen (17␤-estradiol) directly cause an increase in CD16 expression, resulting in increased release of proinflammatory cytokines from monocytes and/or macrophages upon receptor binding.Methods. THP-1 cells and female human primary monocytes and monocyte-derived macrophages were treated with no 17␤-estradiol, physiologic levels (1 ؋ 10 ؊8 M) of 17␤-estradiol, or 1 ؋ 10 ؊8 M 17␤-estradiol followed by withdrawal of 17␤-estradiol. Surface expression of CD16 and CD16 messenger RNA was measured using fluorescence-activated cell sorting (FACS) and semiquantitative reverse transcription-polymerase chain reaction, respectively. Cytokine release from 17␤-estradiol-treated or untreated monocytes was then quantitated by enzyme-linked immunosorbent assay and FACS after crosslinking the receptor with anti-CD16 antibodies.Results. CD16 transcript significantly increased in macrophage-like THP-1 cells and in primary, peripheral blood macrophages in the absence of 17␤-estradiol, and the observed increase in message was dependent on transcription. CD16 receptor levels on CD14؉, transforming growth factor ␤-treated primary monocytes also increased in cells deprived of 17␤-estradiol. Analysis of the cytokines released showed that CD16 crosslinking stimulated significant increases in TNF␣, IL-1␤, and IL-6 due to the absence of estrogen.Conclusion. Estrogen can modulate proinflammatory cytokine release from activated monocytes and/or macrophages, in part through modulation of CD16 expression.

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The synovial lining cell: Biology and pathobiology

Cited by 120 publications

References 174 publications

Treatment of experimental equine osteoarthritis by in vivo delivery of the equine interleukin-1 receptor antagonist gene

Treatment of experimental equine osteoarthritis by in vivo delivery of the equine interleukin-1 receptor antagonist gene

Physiology and pathology of the equine joint

17β‐estradiol regulates cytokine release through modulation of CD16 expression in monocytes and monocyte‐derived macrophages

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