Calcium signaling is required for ultrasound‐stimulated aggrecan synthesis by rat chondrocytes

Parvızı, Javad; Parpura, Vladimir; Bolander, Mark E.

doi:10.1016/s0736-0266(01)00069-9

Cited by 142 publications

(94 citation statements)

References 42 publications

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“…30 Such change in ion, protein transport, or cation concentration could consequently modify intracellular signals for gene expression. 28,31 Furthermore, the mechanical force transmitted by ultrasound to cytoskeleton could affect cell metabolism and gene expression. 32 Increased activation of TGF-b has also been demonstrated for fibroblasts subjected to strain.…”

Section: Discussionmentioning

confidence: 99%

Ultrasound stimulation of types I and III collagen expression of tendon cell and upregulation of transforming growth factor β

Tsai

Pang

Hsu

et al. 2006

Journal Orthopaedic Research

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Traumatic tendon injuries are commonly treated with ultrasound. However, previous research has not examined the molecular mechanism of this therapeutic effect on collagen synthesis of tendon cells. This study was designed to determine the effect of ultrasound on the expression of type I and type III collagen of tendon cells intrinsic to rat Achilles tendon. Whether a correlation exits between this effect and the expression of transforming growth factor b (TGF-b), which enhances collagen synthesis, was also investigated. Tendon cells after ultrasound treatment and protein expression of types I and III collagen were determined by immunocytochemistry. The mRNA expressions of a1(I) procollagen, a1(III) procollagen, and TGF-b were determined by reverse transcription-polymerase chain reaction (RT-PCR). Furthermore, the concentration of TGF-b in conditioned medium was evaluated by enzyme-linked immunosorbent assay (ELISA). Immunocytochemical staining revealed that ultrasound-treated tendon cells were stained more strongly for types I and III collagen than were control cells. Upregulation of procollagen a1(I) gene, procollagen a1(III) gene, and TGF-b at the mRNA level was confirmed by RT-PCR. A dose-dependent increase in the concentration of TGF-b in conditioned medium obtained from cells treated with ultrasound was demonstrated by ELISA assay (p ¼ 0.043). In conclusion, ultrasound stimulates the expression of type I and type III collagen in a process that is likely mediated by the upregulation of TGF-b. ß

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Section: Discussionmentioning

confidence: 99%

Ultrasound stimulation of types I and III collagen expression of tendon cell and upregulation of transforming growth factor β

Tsai

Pang

Hsu

et al. 2006

Journal Orthopaedic Research

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“…LIPUS not only stimulates bone formation in vitro as well as in vivo [5,10,11,14,15,18], but it also exerts anabolic effects on cartilage formation [2, 13,16,17,[20][21][22]. The stimulatory effect of LIPUS on chondrocytes and cartilage matrix production in fractured bone results in stimulation of the healing process and improves the repair of chondral tissue [2, 12,16,17,20].…”

Section: Introductionmentioning

confidence: 99%

“…The stimulatory effect of LIPUS on chondrocytes and cartilage matrix production in fractured bone results in stimulation of the healing process and improves the repair of chondral tissue [2, 12,16,17,20]. LIPUS has been reported to stimulate rat chondrocyte proliferation and matrix production in vitro, suggesting an overall anabolic effect on cartilage formation [16,17,20]. LIPUS also stimulated the healing of osteochondral defects in rabbit knees in vivo [2].…”

Section: Introductionmentioning

confidence: 99%

Low-intensity pulsed ultrasound affects human articular chondrocytes in vitro

Korstjens

Rijt

Albers

et al. 2008

Med Biol Eng Comput

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We investigated whether low-intensity pulsed ultrasound (LIPUS) stimulates chondrocyte proliferation and matrix production in explants of human articular cartilage obtained from donors suffering from unicompartimental osteoarthritis of the knee, as well as in isolated human chondrocytes in vitro. Chondrocytes and explants were exposed to LIPUS (30 mW/cm 2 ; 20 min/day, 6 days). Stimulation of [35 S]-sulphate incorporation into proteoglycans by LIPUS was 1.3-fold higher in degenerative than in collateral monolayers as assessed biochemically and 1.9-fold higher in explants as assessed by autoradiography. LIPUS decreased the number of cell nests containing 1-3 chondrocytes by 1.5 fold in collateral and by 1.6 fold in degenerative explants. LIPUS increased the number of nests containing 4-6 chondrocytes by 4.8 fold in collateral and by 3.9 fold in degenerative explants. This suggests that LIPUS stimulates chondrocyte proliferation and matrix production in chondrocytes of human articular cartilage in vitro. LIPUS might provide a feasible tool for cartilage tissue repair in osteoarthritic patients, since it stimulates chondrocyte proliferation and matrix production.

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“…Related to this point, it is now known that IL-1␤ suppressed GAG biosynthesis by down-regulating GlcAT-I expression and activity (8). A second factor regulating aggrecan synthesis is the intracellular calcium concentration (9,10). In smooth muscle and Sertoli cells, calcium channel blockers have been shown to alter proteoglycan synthesis (11,12).…”

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confidence: 99%

Activation of TonEBP by Calcium Controls β1,3-Glucuronosyltransferase-I Expression, a Key Regulator of Glycosaminoglycan Synthesis in Cells of the Intervertebral Disc

Hiyama

Gajghate

Sakai

et al. 2009

Journal of Biological Chemistry

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The goal of this investigation was to study the expression and regulation of ␤1,3-Glucuronosyltransferase-I (GlcAT-I), a key enzyme regulating GAG synthesis in cells of the intervertebral disc. There was a robust expression of GlcAT-I in the nucleus pulposus in vivo. Treatment with the calcium ionophore ionomycin resulted in increased GlcAT-I expression, whereas GlcAT-I promoter constructs lacking TonE site or a mutant TonE were unresponsive to the ionophore. Experiments using TonEBP and DN-TonEBP constructs showed that TonEBP positively regulated GlcAT-I promoter activity. ChIP analysis confirmed binding of TonEBP to the promoter. We further validated the role of TonEBP in controlling GlcAT-I expression using mouse embryo fibroblasts from TonEBP null mice. GlcAT-I promoter activity in null cells was significantly lower than the wild type cells. In contrast to wild type cells, treatment with ionomycin failed to increase GlcAT-I promoter activity in null cells. We then investigated if calcineurin (Cn)-NFAT signaling played a regulatory role in GlcAT-I expression. Inhibition of Cn following ionomycin treatment did not block GlcAT-I and tauT, a TonEBP-responsive reporter activity. GlcAT-I promoter activity was suppressed by co-expression of Cn, NFAT2, NFAT3, and NFAT4. Moreover, following ionomycin treatment, fibroblasts from CnA␣ and CnA␤ null mice exhibited robust induction in GlcAT-I promoter activity compared with wild type cells. Results of these studies demonstrate that calcium regulates GlcAT-I expression in cells of the nucleus pulposus through a signaling network comprising both activator and suppressor molecules. The results suggest that by controlling both GAG and aggrecan synthesis, disc cells can autoregulate their osmotic environment and accommodate mechanical loading.

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Calcium signaling is required for ultrasound‐stimulated aggrecan synthesis by rat chondrocytes

Cited by 142 publications

References 42 publications

Ultrasound stimulation of types I and III collagen expression of tendon cell and upregulation of transforming growth factor β

Ultrasound stimulation of types I and III collagen expression of tendon cell and upregulation of transforming growth factor β

Low-intensity pulsed ultrasound affects human articular chondrocytes in vitro

Activation of TonEBP by Calcium Controls β1,3-Glucuronosyltransferase-I Expression, a Key Regulator of Glycosaminoglycan Synthesis in Cells of the Intervertebral Disc

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