FK506 ameliorates spontaneous locomotor activity in collagen-induced arthritis: implication of distinct effect from suppression of inflammation

Sasakawa, Tatsuya; Sasakawa, Yuka; Ohkubo, Y.; Mutoh, Seitaro

doi:10.1016/j.intimp.2004.10.012

Cited by 22 publications

(23 citation statements)

References 26 publications

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“…Therefore a lower bone density and muscle fi ber atrophy would be induced by decreased motor activities. Indeed, previous studies observed that animal models [13][14][15][16] and patients [17] with arthritis showed decreased spontaneous motor activities because of severe chronic pain. Although antigravity muscles, such as the slow soleus muscle, have been used as atrophied muscles in unloaded animal models [7,8], we used the tibialis anterior muscle in this study for the following reasons: (1) The mouse soleus muscle consists of 58% slow-twitch oxidative fi bers and 42% fast-twitch oxidative fibers.…”

Section: Discussionmentioning

confidence: 99%

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Bone Density of the Femur and Fiber Cross-Sectional Area and Oxidative Enzyme Activity of the Tibialis Anterior Muscle in Type II Collagen-Induced Arthritic Mice

Okiura

Nagatomo

et al. 2008

J. Physiol. Sci

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Femur bone densities and tibialis anterior muscle properties of type II collagen-induced arthritic mice were determined. Furthermore, voluntary running activities of arthritic mice were compared with those of controls. Arthritis was induced by an intradermal injection of type II collagen in the adjuvant. Body and muscle weights were lower in arthritic mice than in controls. Cortical and trabecular bone densities and muscle fiber crosssectional areas were decreased by arthritis. After classifying the arthritic severity into slight, intermediate, and severe levels based on the degree of knuckle swelling, cortical and trabecular bone densities, fiber cross-sectional areas, and fiber succinate dehydrogenase activities were lowest when arthritis was most severe. Furthermore, arthritic mice, especially those with intermediate and severe levels, showed lower voluntary running activities. These findings indicate that lower bone density and muscle atrophy of type II collagen-induced arthritic mice are related to arthritic severity and decreased motor activity.Key words : bone density, cross-sectional area, motor activity, mouse, muscle fiber, succinate dehydrogenase activity, type II collagen-induced arthritis.Degeneration in the musculoskeletal system, including muscle atrophy and bone osteoporosis, is widely accepted as being induced by aging [1][2][3][4][5], hind-limb suspension [6][7][8], or exposure to microgravity [9][10][11][12]. These changes are considered to result from decreased motor activity.Previous studies observed that animal models [13-16] and patients [17] with arthritis showed decreased spontaneous motor activities because of severe chronic pain in the joints. Type II collagen-induced arthritis is a model of polyarthritis induced in susceptible rodents by immunization with type II collagen [18,19]. Muscle atrophy and decreased bone density occur in type II collageninduced arthritic rodents because these animals may have lower motor activities as a result of their distal joint pain. Therefore this study investigated cortical and trabecular bone densities of the femur and fiber cross-sectional areas and succinate dehydrogenase (SDH) activities of the tibialis anterior muscle in type II collagen-induced arthritic mice. Furthermore, voluntary running activities of arthritic mice were compared with those of controls. METHODSAll experimental procedures and animal care were conducted in accordance with the Guide for the Care and Use of Laboratory Animals prepared by the Physiological Society of Japan. This study was also approved by the Institutional Animal Care and Use Committee of Kyoto University.Antigens and immunizations. Sixty-day-old DBA/1J male mice were randomly divided into control ( n = 5) and arthritic ( n = 13) groups. All mice were individually housed in cages of the same size. The mice in the arthritic group were immunized from 60 to 81 days after birth. Type II collagen was solubilized from fetal bovine articular cartilage by limited proteolysis with pepsin [20]. Type II collagen was...

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Section: Discussionmentioning

confidence: 99%

“…Previous studies observed that animal models [13][14][15][16] and patients [17] with arthritis showed decreased spontaneous motor activities because of severe chronic pain in the joints. Type II collagen-induced arthritis is a model of polyarthritis induced in susceptible rodents by immunization with type II collagen [18,19].…”

mentioning

confidence: 99%

Bone Density of the Femur and Fiber Cross-Sectional Area and Oxidative Enzyme Activity of the Tibialis Anterior Muscle in Type II Collagen-Induced Arthritic Mice

Okiura

Nagatomo

et al. 2008

J. Physiol. Sci

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“…It is a calcineurin inhibitor that suppresses activation of T cells by inhibiting nuclear localization of NFAT [25]. FK506 suppresses T cell-derived cytokines and antigen presenting cell-derived inflammatory cytokines, TNFa and IL-1h, in the presence of T cell activation [26][27][28]. Clinically, FK506 improves quality of life for RA patients who do not tolerate with methotrexate (MTX) well [29,30].…”

Section: Introductionmentioning

confidence: 99%

FK506 inhibits prostaglandin E2 production from synovial cells by suppressing peripheral blood mononuclear cells

Sasakawa

Ohkubo

et al. 2005

International Immunopharmacology

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“…Oxidative stress-induced transformation of synovial fibroblasts into proliferating cells is thought to be a key event in mechanisms underlying the joint destruction in RA (52,53). Type-II CIA in Lewis rats is a widely used experimental animal model of inflammatory polyarthritis with clinical and pathological features similar to those seen with RA in humans, which is dependent on both humoral and cellular immunity to the immunizing antigen (54,55).…”

Section: Induction Of Collagen-induced Arthritis (Cia) and Culture Ofmentioning

confidence: 99%

Possible Involvement of Glutamatergic Signaling Machineries in Pathophysiology of Rheumatoid Arthritis

Hinoi

Yoneda

2011

J Pharmacol Sci

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Abstract. The prevailing view is that L-glutamate (Glu) functions as an excitatory amino acid neurotransmitter through a number of molecular machineries required for the neurocrine signaling at synapses in the brain. These include Glu receptors for signal input, Glu transporters for signal termination, and vesicular Glu transporters for signal output through exocytotic release. Although relatively little attention has been paid to the functional expression of these molecules required for glutamatergic signaling in peripheral tissues, recent molecular biological analyses including ours give rise to a novel function for Glu as an extracellular signal mediator in the autocrine and/or paracrine system in several peripheral and non-neuronal tissues, including bone and cartilage. In particular, a drastic increase is demonstrated in the endogenous levels of both Glu and aspartate in the synovial fluid with intimate relevance to increased edema and sensitization to thermal hyperalgesia in experimental arthritis models. However, to date, there is only limited information about the physiological and pathological significance of glutamatergic signaling machineries expressed by articular synovial tissues. In this review, we have outlined the role of Glu in synovial fibroblasts in addition to the possible involvement of glutamatergic signaling machineries in the pathogenesis of joint diseases such as rheumatoid arthritis.

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FK506 ameliorates spontaneous locomotor activity in collagen-induced arthritis: implication of distinct effect from suppression of inflammation

Cited by 22 publications

References 26 publications

Bone Density of the Femur and Fiber Cross-Sectional Area and Oxidative Enzyme Activity of the Tibialis Anterior Muscle in Type II Collagen-Induced Arthritic Mice

Bone Density of the Femur and Fiber Cross-Sectional Area and Oxidative Enzyme Activity of the Tibialis Anterior Muscle in Type II Collagen-Induced Arthritic Mice

FK506 inhibits prostaglandin E2 production from synovial cells by suppressing peripheral blood mononuclear cells

Possible Involvement of Glutamatergic Signaling Machineries in Pathophysiology of Rheumatoid Arthritis

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