Sympathetic hyperinnervation in myofascial trigger points

Cao, Lei; Gao, Yanping; Wu, Kai; Li, Yikai; Chen, Chao; Yuan, Shiguo

doi:10.1016/j.mehy.2020.109633

Cited by 15 publications

(11 citation statements)

References 28 publications

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Section: Discussionmentioning

confidence: 99%

“… 24 , 25 In addition, local sympathetic remodeling happens in MTrPs, which will cause sympathetic hyperinnervation and excessive release of local acetylcholine, finally leading to a variety of relevant symptoms. 26 Additionally, pressing on MTrPs can enhance the excitability of parasympathetic neurons while inhibiting the excitability of sympathetic nerves, resulting in decrease of acetylcholine release at the motor endplates, ultimately improving the symptoms. 27 At the central level, current research believed that pressing on MTrPs decreases subjective pain by affecting autonomic nerves system activities via the prefrontal cortex.…”

Section: Discussionmentioning

confidence: 99%

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Pressing Intervention Promotes the Skeletal Muscle Repair of Traumatic Myofascial Trigger Points in Rats

Jiang¹,

Xiang²,

Liú³

et al. 2021

JPR

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Objective: To observe the effect of pressing intervention on the skeletal muscle repair of myofascial trigger points (MTrPs) in rats and explore the mechanism of pressing intervention on the deactivation of trigger points. Methods: Thirty SPF rats were randomly divided into blank group, model group and press group, with 10 rats in each group. The MTrPs models were established by blunt striking plus eccentric exercise, and then evaluated. The press group was given a pressing intervention with a self-made device for 14 days, and the rats in the other two groups were fed normally. Soft tissue tension (STT) D 0.2 and pressure pain threshold (PPT) were measured before and after intervention. The skeletal muscle tissue at MTrPs was extracted and assessed by hematoxylin-eosin (HE) and Masson staining. The expression of collagen I, collagen III, α-smooth muscle actin (α-SMA), myosin heavy chain (MHC) and fibronectin (FN) were detected by Western Blotting. Enzyme linked immunosorbent assay (ELISA) was used to evaluate the expression of substance P (SP), 5-hydroxytryptamine (5-HT), cyclooxygenase 2 (COX-2) and prostaglandin E2 (PGE2). Results: (1) Compared with the blank group, the PPT and D 0.2 reduced (P < 0.05) in the model group; while compared with the model group, the PPT and D 0.2 increased (P < 0.05) in the press group. (2) Compared with the blank group, the model group showed obvious spontaneous potentials with higher amplitude and frequency, which were also much higher than those of the press group (P < 0.05). (3) The HE and Masson staining results showed evident fibrosis in the muscle tissue of the model group, with a larger area of collagen fibers relative to that of the press group (P < 0.05). ( 4) The amount of collagen I, collagen III, FN, α-SMA, SP, 5-HT, COX-2 and PGE2 increased and the content of MHC decreased (P < 0.05) in the model group, as compared to the blank group; while all the substances (P < 0.05), instead of MHC which increased (P < 0.05), in the press group were decreased as compared to the model group. Conclusion:Pressing intervention on the MTrPs in rats can alleviate chronic inflammation, inhibit fibrosis, promote skeletal muscle repair and relieve pain.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Pressing Intervention Promotes the Skeletal Muscle Repair of Traumatic Myofascial Trigger Points in Rats

Jiang¹,

Xiang²,

Liú³

et al. 2021

JPR

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“…34 Five fields of each slide and five slides were randomly selected for analysis. 35 Immunofluorescence and Immunohistochemistry Confocal culture dishes (φ10 mm) or slides were incubated with anti-runt-related transcription factor 2 (RUNX2) (ab76956, Abcam, Cambridge, UK, 1:100) and antiosteocalcin (DF12303, Affinity, Cincinatti, OH, USA, 1:100) at 4 C for $12 h. The samples were incubated with secondary antibodies at 37 C for 40 min (1:200 or 1:400). Immunofluorescence images were obtained using confocal scanning microscopy (FV1200, Olympus, Tokyo, Japan) after sealing with DAPI, and the immunohistochemical slides were incubated with DAB for 1 to 4 min and stained with hematoxylin for 1 min.…”

Section: A B D Cmentioning

confidence: 99%

Bindarit Reduces Bone Loss in Ovariectomized Mice by Inhibiting CCL2 and CCL7 Expression via the NF‐κB Signaling Pathway

Yuan

Wang

et al. 2022

Orthopaedic Surgery

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Objective To investigate the changes in proinflammatory cytokines and chemokines, namely, C‐C motif ligand (CCL) 2 and CCL7, in postmenopausal osteoporosis (PMOP) and to develop a new drug, bindarit (Bnd), for PMOP in an ovariectomized (OVX) mouse model. Methods Bone marrow macrophages (BMMs) from the femurs of five women with PMOP and five premenopausal women without osteoporosis were detected by RNA sequencing. BMMs from mice were differentiated into osteoclasts and treated with a synthetic inhibitor of CCL2 and CCL7, Bnd, or 17 beta estradiol (E2). Mouse BMMs were differentiated into osteoclasts with or without Bnd for 7 days and analyzed by RNA sequencing. Osteoblasts of mice were induced to undergo osteoblastogenesis and treated with Bnd. OVX mice were treated with E2 or Bnd after surgery. The protein and mRNA expression of CCL2 and CCL7 was detected using immunostaining and qPCR, respectively, in OVX and aged mice and in cells cultured in vitro. Osteoclast formation was detected using a tartrate‐resistant acid phosphatase (TRAP) assay in vitro and in vivo. Alkaline phosphatase (ALP), runt‐related transcription factor 2 (Runx2) and osteocalcin (OCN) were detected using immunostaining to evaluate osteogenesis. Microcomputed tomography was conducted to analyze trabecular bone parameters, the structure model index, bone mineral density and other variables. Nuclear factor‐κB (NF‐κB) signaling pathway‐related protein phosphorylation of IKKα/β (p‐IKKα/β) and p‐NFκB p65 was examined using western blotting. Results CCL2, CCL7 and their receptor of C‐C chemokine receptor‐2 (CCR2), and the NF‐κB signaling pathway, were significantly increased in women with PMOP. CCL2 and CCL7 protein and mRNA expression was increased in OVX mice and aged female mice, but the increases were attenuated by E2 and Bnd. E2 and Bnd effectively inhibited osteoclastogenesis and the protein expression of CCL2 and CCL7 both in vitro and in vivo and reduced bone loss in OVX mice. Bnd did not affect the mineralization of osteoblasts directly in vitro but reduced bone turnover in vivo. p‐IKKα/β and p‐NFκB p65 levels were increased in BMMs of mice after differentiation into osteoclasts but were significantly decreased by Bnd. Conclusion The proinflammatory cytokines and chemokines CCL2, CCL7 and CCR2 were correlated with PMOP. Bnd attenuated the increases in CCL2 and CCL7 levels to affect osteoporosis in OVX mice via the NFκB signaling pathway. Thus, Bnd may be useful as a new therapeutic for the prevention of PMOP.

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“…NE is an important catecholamine neurotransmitter released from sympathetic nerves that can regulate the proliferation and differentiation of numerous cell types. Studies have found that sympathetic nerves of aged mice show aging-related changes, such as decreasing numbers of adrenoceptors (ADR) and sympathetic nerve density [ 19 – 21 ].…”

Section: Introductionmentioning

confidence: 99%

Sympathetic activity is correlated with satellite cell aging and myogenesis via β2-adrenoceptor

Yuan

Zheng

et al. 2021

Stem Cell Res Ther

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Background and objective Sympathetic activity plays an important role in the proliferation and differentiation of stem cells, and it changes over time, thereby exerting differential effects on various stem cell types. Aging causes sympathetic hyperactivity in aged tissues and blunts sympathetic nerves regulation, and sympathetic abnormalities play a role in aging-related diseases. Currently, the effect of sympathetic activity on skeletal muscle stem cells, namely satellite cells (SCs), is unclear. This study aimed to investigate the effects of skeletal muscle sympathetic activity on SC aging and skeletal muscle repair. Materials and methods To evaluate skeletal muscle and fibrotic areas, numbers of SCs and myonuclei per muscle fiber, β2-adrenoceptor (β2-ADR) expression, muscle repair, and sympathetic innervation in skeletal muscle, aged mice, young mice that underwent chemical sympathectomy (CS) were utilized. Mice with a tibialis anterior muscle injury were treated by barium chloride (BaCl2) and clenbuterol (CLB) in vivo. SCs or C2C12 cells were differentiated into myotubes and treated with or without CLB. Immunofluorescence, western blot, sirius red, and hematoxylin–eosin were used to evaluate SCs, myogenic repair and differentiation. Results The number of SCs, sympathetic activity, and reparability of muscle injury in aged mice were significantly decreased, compared with those in young mice. The above characteristics of young mice that underwent CS were similar to those of aged mice. While CLB promoted the repair of muscle injury in aged and CS mice and ameliorated the reduction in the SC number and sympathetic activity, the effects of CLB on the SCs and sympathetic nerves in young mice were not significant. CLB inhibited the myogenic differentiation of C2C12 cells in vitro. We further found that NF-κB and ERK1/2 signaling pathways were activated during myogenic differentiation, and this process could be inhibited by CLB. Conclusion Normal sympathetic activity promoted the stemness of SCs to thereby maintain a steady state. It also could maintain total and self-renewing number of SCs and maintain a quiescent state, which was correlated with skeletal SCs via β2-ADR. Normal sympathetic activity was also beneficial for the myogenic repair of injured skeletal muscle.

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Sympathetic hyperinnervation in myofascial trigger points

Cited by 15 publications

References 28 publications

Pressing Intervention Promotes the Skeletal Muscle Repair of Traumatic Myofascial Trigger Points in Rats

Pressing Intervention Promotes the Skeletal Muscle Repair of Traumatic Myofascial Trigger Points in Rats

Bindarit Reduces Bone Loss in Ovariectomized Mice by Inhibiting CCL2 and CCL7 Expression via the NF‐κB Signaling Pathway

Sympathetic activity is correlated with satellite cell aging and myogenesis via β2-adrenoceptor

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