Far-infrared ray radiation promotes neurite outgrowth of neuron-like PC12 cells through AKT1 signaling

Wang, Jue‐Long; Lin, Yong-Chong; Young, Tai‐Horng; Chen, Min-Huey

doi:10.1016/j.jfma.2018.08.015

Cited by 22 publications

(10 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mean total neurite length of each group was calculated from at least 100 neurons. The length of each neurite was calculated manually with Image‐Pro Plus 6.0 software (Media Cybernetics, Silver Spring, MD; J. L. Wang, Lin, Young, & Chen, ).…”

Section: Methodsmentioning

confidence: 99%

miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

Wang

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

Spinal cord injury (SCI) is a devastating disease. Strategies that enhance the intrinsic regenerative ability are very important for the recovery of SCI to radically prevent the occurrence of sensory disorders. Epidermal growth factor (EGF) showed a limited effect on the growth of primary sensory neuron neurites due to the degradation of phosphorylated-epidermal growth factor receptor (p-EGFR) in a manner dependent on Casitas B-lineage lymphoma (CBL) (an E3 ubiquitin-protein ligase). MiR-22-3p predicted from four databases could target CBL to inhibit the expression of CBL, increase p-EGFR levels and neurites length via STAT3/GAP43 pathway rather than Erk1/2 axis. EGF, EGFR, and miR-22-3p were downregulated sharply after injury. In vivo miR-22-3p Agomir application could regulate CBL/p-EGFR/p-STAT3/GAP43/p-GAP43 axis, and restore spinal cord sensory conductive function. This study clarified the mechanism of the limited promotion effect of EGF on adult primary sensory neuron neurite and targeting miR-22-3p could be a novel strategy to treat sensory dysfunction after SCI. K E Y W O R D Scasitas b-lineage lymphoma, epidermal growth factor, epidermal growth factor receptor, miR-22-3p, primary sensory neuron, spinal cord injury

show abstract

Section: Methodsmentioning

confidence: 99%

miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

Wang

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…This nding suggests that there might be other mechanisms independent of cervical muscle modulation. In fact, both electrical stimulation and far-infrared irradiation reportedly cause nerve regeneration and repair directly [32,33]. Further studies using objective and quantitative measurements of muscle stiffness like the ultrasound elastography technique [34] may clarify the local therapy target.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Cervical Muscle Lesions and Autonomic Nervous System in Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS)

Matsui¹,

Hara²,

Iwata³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Patients with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) sometimes coincide with stiffness of cervical muscles. This study examined the effect of local modulation of the cervical muscles on ME/CFS and the underlying mechanism.Methods: In total, 1,226 inpatients with ME/CFS who were resistant to outpatient care were enrolled in this study for 11 years. All patients underwent daily physical therapies to the cervical muscles during hospitalization. Self-rated records documenting the presence and absence of ME/CFS and the representative eight disorders that frequently accompany it at admission and discharge were compared. The pupil diameter was also measured to examine involvement of autonomic nervous system function.Results: The recovery rate of ME/CFS after local therapy was 55.5%, and did not differ significantly by sex, age strata, and hospitalization period. The recovery rates of the eight disorders were variable (36.6－86.9%); however, those of ME/CFS in the disorder subpopulations were similar (52.3－55.8%). The recovery rates of all disorders showed strong associations with that of ME/CFS (p<0.001). The pupil diameter was decreased at discharge, and the change was significantly higher in the ME/CFS-recovered patients than ME/CFS-unrecovered patients in the total population and the subpopulations stratified by sex, age, and hospitalization period.Conclusions: Local therapy to the cervical muscles led to recovery in more than half of patients with ME/CFS, at least partly through amelioration of the autonomic nervous system. There may be a causal relationship between recoveries of ME/CFS and these related whole-body disorders.Trial registration ID: UMIN000036634. Registered 1 May 2019 - Retrospectively registered, https://upload.umin.ac.jp/cgi-open-bin/ctr_e/index.cgi

show abstract

“…PC12 cell line was purchased from American Type Culture Collection and stimulated to form a neuron-like phenotype [ 38 , 39 ] with nerve growth factor (Novoprotein, Shanghai, China, Catalogue No. : C060) (50ng/ml) for 3 days.…”

Section: Methodsmentioning

confidence: 99%

Glucagon-like peptide-1 attenuated carboxymethyl lysine induced neuronal apoptosis via peroxisome proliferation activated receptor-γ

Zhang

Song

Zhu

et al. 2021

Aging

View full text Add to dashboard Cite

Backgrounds and aims: The role of peroxisome proliferator activated receptor-γ (PPAR-γ) in neuronal apoptosis remains unclear. We aim to investigate the role of PPAR-γ in glucagon-like peptide-1 (GLP-1) alleviated neuronal apoptosis induced by carboxymethyl-lysine (CML). Materials and Methods: In vitro , PC12 cells were treated by CML/GLP-1. Moreover. the function of PPAR-γ was blocked by GW9662. In vivo , streptozotocin (STZ) was used to induce diabetic rats with neuronal apoptosis. The cognitive function of rats was observed by Morris water maze. Apoptosis was detected by TUNEL assay. Bcl2, Bax, PPAR-γ and receptor of GLP-1 (GLP-1R) were measured by western blotting or immunofluorescence. Results: In vitro experiment, CML triggered apoptosis, down-regulated GLP-1R and PPAR-γ. Moreover, GLP-1 not only alleviated the apoptosis, but also increased levels of PPAR-γ. GW9662 abolished the neuroprotective effect of GLP-1 on PC12 cells from apoptosis. Furthermore, GLP-1R promoter sequences were detected in the PPAR-γ antibody pulled mixture. GPL-1 levels decreased, while CML levels increased in diabetic rats, compared with control rats. Additionally, we observed elevated bax, decreased bcl2, GLP-1R and PPAR-γ in diabetic rats. Conclusions: GLP-1 could attenuate neuronal apoptosis induced by CML. Additionally, PPAR-γ involves in this process.

show abstract

Far-infrared ray radiation promotes neurite outgrowth of neuron-like PC12 cells through AKT1 signaling

Cited by 22 publications

References 36 publications

miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

miR‐22‐3p enhances the intrinsic regenerative abilities of primary sensory neurons via the CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis

Involvement of Cervical Muscle Lesions and Autonomic Nervous System in Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS)

Glucagon-like peptide-1 attenuated carboxymethyl lysine induced neuronal apoptosis via peroxisome proliferation activated receptor-γ

Contact Info

Product

Resources

About