Low-intensity pulsed ultrasound stimulates matrix metabolism of human annulus fibrosus cells mediated by transforming growth factor<b>β</b>1 and extracellular signal-regulated kinase pathway

Chen, Mei-Hsiu; Sun, Jui Sheng; Liao, Shao Yu; Tai, Po An; Li, Tin Chou; Chen, Ming Hong

doi:10.3109/03008207.2015.1016609

Cited by 17 publications

(7 citation statements)

References 46 publications

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“…Type 1 diabetes mellitus (T1DM) causes skeletal muscle atrophy [ 2 , 10 , 30 ]. LIPUS can increase the differentiation of muscular lineage cells and favor tissue regeneration [ 13 , 31 , 32 ]. Therefore, we investigated whether LIPUS could improve T1DM-induced skeletal muscle atrophy.…”

Section: Discussionmentioning

confidence: 99%

Low-intensity pulsed ultrasound prevents muscle atrophy induced by type 1 diabetes in rats

Tang

Jian

et al. 2017

Skeletal Muscle

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BackgroundType 1 diabetes mellitus (T1DM) induces serious skeletal muscle atrophy. Low-intensity pulsed ultrasound (LIPUS) is a common treatment for skeletal muscle injury and is effective in accelerating the rate of muscle growth. However, to the best of our knowledge, whether LIPUS can improve skeletal muscle atrophy in type 1 diabetic rats has not been investigated.MethodsThe rats were randomly divided into four groups: the normal control group (NC); the sham-treated diabetic control group (DC); the diabetic, insulin-treated group (DI) as a positive control; and the diabetic LIPUS therapy group (DL). The DL rats were treated with LIPUS (1 MHz, 30 mW/cm2) on the gastrocnemius for 20 min/day.ResultsAfter 6 weeks, the rats in the DC group showed severe muscle atrophy. However, LIPUS significantly improved type 1 diabetes-induced muscle atrophy, as evidenced by significantly enhanced muscle cross-sectional area, muscle mass, and strength. Moreover, compared with the DC group, LIPUS significantly activated Akt and upregulated the expression of mTOR, and LIPUS downregulated the expression of MSTN, its receptor ActRIIB, and FoxO1.ConclusionsThese results indicate that LIPUS improved muscle atrophy induced by type 1 diabetes, and the MSTN/Akt/mTOR&FoxO1 signaling pathway may play a role in this improvement.

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Section: Discussionmentioning

confidence: 99%

Low-intensity pulsed ultrasound prevents muscle atrophy induced by type 1 diabetes in rats

Tang

Jian

et al. 2017

Skeletal Muscle

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“…They also observed an increase in glucose consumption and the initiation of an energy-consuming activity. Chen et al (2015) [62], instead, proved that LIPUS could effectively stimulate matrix metabolism of a certain cell line through the up-regulation of specific pathways.…”

Section: Discussionmentioning

confidence: 99%

Low-intensity pulsed ultrasound increases neurotrophic factors secretion and suppresses inflammation in in vitro models of peripheral neuropathies

et al. 2023

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Objective: In this study, we aimed to verify the beneficial effects of low-intensity pulsed ultrasound (LIPUS) stimulation on two cell types: H2O2-treated RSC96 Schwann cells and THP-1 macrophages, used to model neuropathic inflammation. Approach: Using a set-up guaranteeing a fine control of the ultrasound dose at the target, different frequencies (38 kHz, 1 MHz, 5 MHz) and different intensities (20, 100, 500 mW/cm2) were screened to find the most effective experimental conditions for triggering beneficial effects on metabolic activity and release of neurotrophic cytokines (-NGF, BDNF, GDNF) of RSC96 cells. The combination of parameters resulting the optimal one was applied to evaluate anti-inflammatory effects in terms of ROS and TNF- production, also investigating a possible anti-oxidant activity and mechanotransduction pathway for the anti-inflammatory process. The same optimal combination of parameters was then applied to THP-1 cells, differentiated into M1 and M2 phenotypes, to assess the effect on the expression and release of pro-inflammatory markers (TNF-, IL-1, IL-6, IL-8) and anti-inflammatory ones (IL-10 and CD206). Main results: 5 MHz and 500 mW/cm2 were found as the optimal stimulation parameters on RSC96 cells Such parameters were also found to suppress ROS and TNF- in the same cell line, thus highlighting a possible anti-inflammatory effect, involving the NF-kB pathway An anti-oxidant effect induced by LIPUS was also observed. Finally, the same LIPUS parameters did not induce any differentiation towards the M1 phenotype of THP-1 cells, whereas they decreased TNF- and IL-8 gene expression, reduced IL-8 cytokine release and increased IL-10 cytokine release in M1-polarized THP-1 cells.Significance: This study represents the first step towards the use of precisely controlled low-intensity pulsed ultrasound for the treatment of peripheral neuropathies. 

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“…Kwon et al ( 28 ) also illustrated that both Smad2/3 and Smad1/5/8 were upregulated in degenerative bovine NPCs, and activated Smad1/5/8 could inhibit Smad2/3 expression, leading to further IDD. Accumulating evidence has indicated that TGF-β can stimulate ECM production via Smad2/3 overexpression ( 29 , 30 ). TIMP-3 has a specific protective effect on cartilage, and the TGF-β/Smad2/3 pathway can enhance the expression of TIMP-3( 31 ), thereby explaining the protective effect on the ECM.…”

Section: Discussionmentioning

confidence: 99%

High‑dose TGF‑β1 degrades human nucleus pulposus cells via ALK1‑Smad1/5/8 activation

Zhang

Chen

et al. 2020

Exp Ther Med

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Transforming growth factor β1 (TGF-β1) can promote the proliferation and differentiation of intervertebral disc cells and participates in its repair process. However, whether TGF-β1 engages in the process of disc degeneration has not yet been fully elucidated. The present study aimed to investigate the function of high-dose TGF-β1 on the metabolism of nucleus pulposus cells (NPCs). TGF-β1 levels in human degenerative intervertebral disc tissues and tumor necrosis factor (TNF)-α-induced degenerative NPCs were analyzed. Furthermore, NPCs were treated with TGF-β1 and inhibitors of TGF-β1 receptors [ALK tyrosine kinase receptor (ALK) 1 and ALK5] to determine the effect of the receptors in the mediation of NPC degeneration. The NPC state was determined by the components of secretory collagen I/II, tissue inhibitor of metalloproteinase-3 (TIMP-3) and matrix metalloproteinase (MMP)-13. The mRNA expression of Smad1/2/3/5/8, the downstream gene of TGF-β1 mediated by ALK, was also measured. Results showed that TGF-β1 and ALK1 were positively associated with the degree of degeneration of NP or NPCs in vitro, but negatively associated with ALK5. Furthermore, high-doses of TGF-β1 suppressed collagen II, but enhanced collagen I, TIMP-3, MMP-13, ALK1/5 and Smad1/2/3/5/8 expression. ALK5 inhibition induced the suppression of Smad2/3 and aggravated high-dose TGF-β1-induced NPC degeneration, as shown by the reduction in collagen II and increase in collagen I, TIMP-3 and MMP-13. By contrast, ALK1 inhibition resulted in Smad1/5/8 suppression and alleviated high-dose TGF-β1-induced NPC degeneration. Taken together, it was concluded that high-doses of TGF-β1 contributed to the degeneration of NPCs via the upregulation of ALK1 and Smad1/5/8.

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Low-intensity pulsed ultrasound stimulates matrix metabolism of human annulus fibrosus cells mediated by transforming growth factorβ1 and extracellular signal-regulated kinase pathway

Abstract: The findings suggested that LIPUS could be useful as a physical stimulation of cell metabolism for the repair of the AF.

Cited by 17 publications

References 46 publications

Low-intensity pulsed ultrasound prevents muscle atrophy induced by type 1 diabetes in rats

Low-intensity pulsed ultrasound prevents muscle atrophy induced by type 1 diabetes in rats

Low-intensity pulsed ultrasound increases neurotrophic factors secretion and suppresses inflammation in in vitro models of peripheral neuropathies

High‑dose TGF‑β1 degrades human nucleus pulposus cells via ALK1‑Smad1/5/8 activation

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