Tingjun Dai

Qilu Hospital of Shandong University

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Chuanzhu Yan

Qilu Hospital of Shandong University

Yuying Zhao

Tianjin Medical University General Hospital

Ying Hou

Qilu Hospital of Shandong University

Pengfei Lin

Shandong University

Kai Shao

Shandong University

Wei Li

First Affiliated Hospital of Zhengzhou University

Fuchen Liu

Qilu Hospital of Shandong University

Dandan Zhao

Qilu Hospital of Shandong University

Wěi Li

Zhongshan Hospital

Kunqian Ji

Qilu Hospital of Shandong University

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Qilu Hospital of Shandong University

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Shandong University

Chinese Academy of Medical Sciences & Peking Union Medical College

Chinese Academy of Sciences

Sichuan University

Central South University

Sun Yat-sen University

Peking University

Huazhong University of Science and Technology

Fudan University

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Hypoxia increases expression of CXC chemokine receptor 4 via activation of PI3K/Akt leading to enhanced migration of endothelial progenitor cells.

PubMed (2017)

Tingjun Dai Yunsheng Hu Haihong Zheng

Recruitment of endothelial progenitor cells (EPCs) to the ischemia has recently been suggested as an important mechanism of neovascularization. Although tissue ischemia can mobilize EPCs from bone marrow, the effects of hypoxia on the migration of EPCs are little known.In this study, migratory function of EPCs was examined by a modified Boyden chamber technique. The expression of CXCR4 was detected by reverse transcription PCR and flow cytometry assay. The protein expressions of ERK1/2 and PI3K/Akt signaling pathways were detected by Western blotting.Migration of EPCs in response to the chemokine Stomal-derived factory-1α (SDF-1α) was much enhanced by hypoxia. The enhanced migration can be blocked by the CXCR4 antagonist AMD3100 and the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002, whereas mitogen-activated protein ERK1/2 kinase inhibitor PD98056 had no significant effect on enhanced migration induced by hypoxia. The expression of CXCR4 markedly increased under hypoxic conditions. A molecular analysis of these events indicated that augmented CXCR4 expression was regulated by the PI3K/Akt signal transduction pathway.These results indicated that exposure of EPCs to hypoxia resulted in a significant up-regulation of CXCR4 expression by PI3K/Akt activation, leading to enhancing chemotaxis behavior.

CXC chemokine receptors

LY294002

Endothelial progenitor cell

Hypoxia

CXCL14

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Citations (23)

Juvenile idiopathic inflammatory myopathies with anti‐3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase antibodies in a Chinese cohort

CNS Neuroscience & Therapeutics (2021)

Ying Hou Kai Shao Bing Zhao Tingjun Dai Qinzhou Wang

Abstract Aims To characterize the clinical and histopathological characteristics and treatment outcomes of juvenile idiopathic inflammatory myopathies (JIIMs) with anti‐3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase (HMGCR) antibodies in a Chinese cohort. Methods We detected anti‐HMGCR antibodies in a series of Chinese JIIM by ELISA and indirect immunofluorescence assay on HEK293 cells, and summarized the clinical findings of these anti‐HMGCR antibody‐positive patients. Results Of 32 JIIM patients, 5 (15.63%) were found to be anti‐HMGCR antibody‐positive. The disease duration was 1.20 ± 0.45 months. Statin exposure was not found. Four patients had skin lesions, while typical pathological features of dermatomyositis such as perifascicular atrophy or myxovirus resistance protein A expression were not found. The mean creatine kinase level was 16771.60 U/L. Among the four patients who received long‐term (10.46 ± 1.42 years) follow‐up, three exhibited favorable outcomes with prednisone and additional immunosuppressants. Conclusions Our study indicates that anti‐HMGCR antibodies may not be rare in Chinese JIIM. These anti‐HMGCR‐positive JIIMs were characterized by acute onset, substantially elevated creatine kinase level, and skin lesions without perifascicular changes in muscle pathology. The treatment outcome is generally favorable with the combination of steroid and immunosuppressant.

Creatine kinase

10.1111/cns.13658

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Citations (5)

Gasdermine E-Dependent Mitochondrial Pyroptotic Pathway in Dermatomyositis: A Possible Mechanism of Perifascicular Atrophy

Journal of Neuropathology & Experimental Neurology (2020)

Meirong Liu Ling Li Tingjun Dai Ying Hou Wei Li

Abstract Different mechanisms have been proposed to explain the pathological basis of perifascicular atrophy (PFA), a pathognomonic histologic feature of dermatomyositis (DM); however, the detailed mechanisms remain to be elucidated. There is mitochondrial dysfunction in PFA and expression of mitochondrial apoptosis molecules has been reported in DM. Overexpression of gasdermin E (GSDME) can turn mitochondrial apoptosis to mitochondrial pyroptosis, a newly characterized form of programmed cell death. We determined the expression of proteins involved in the caspase-3- and GSDME-dependent mitochondrial pyroptotic pathway, including BAX, BAK, cytochrome C, caspase-9, caspase-3, GSDME, and IL-1α, in biopsied muscles from DM and control patients. Immunohistochemical analysis showed that those markers were expressed in most fibers in PFA in DM. GSDME-positive and IL-1α-positive staining was mainly localized around punched-out vacuoles or sarcolemma. These markers were significantly upregulated at the protein and mRNA levels in DM versus controls. Our results suggest that caspase-3- and GSDME-dependent mitochondrial pyroptosis are involved in the pathogenetic mechanisms of PFA in DM and that targeting GSDME-dependent mitochondrial pyroptosis may be an effective therapeutic approach for this condition.

Pyroptosis

10.1093/jnen/nlaa023

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Citations (12)

Protein kinase R is highly expressed in dermatomyositis and promotes interferon-beta-induced muscle damage

Annals of the Rheumatic Diseases (2024)

G. Zhang Lining Zhang Dandan Zhao Xiaoyu Liu Wei Li

Objectives Dermatomyositis (DM) has been consistently linked to the type I interferon (IFN-I) pathway. However, the precise pathogenesis remains incompletely elucidated. We aimed to explore potential molecular mechanisms and identify promising therapeutic targets in DM. Methods We employed bioinformatics analysis to investigate molecular signatures, aiming to shed light on the pathogenesis of DM. The expression of protein kinase R (PKR) in DM muscle tissues was determined by real-time quantitative PCR, western blot and immunohistochemistry (IHC) analysis. We then assessed the sensitivity and specificity of sarcoplasmic PKR expression by IHC in a consecutive DM cohort and other diseases in this retrospective study. Furthermore, IFN-β was used to stimulate myoblasts and myotubes, and the relationship between PKR and IFN-β-induced pathogenic molecules was investigated in vitro. Results Bioinformatics analysis indicated two primary pathological processes: viral infection and the IFN-I signalling pathway. We subsequently verified that PKR was notably expressed in the cytoplasm of myofibers in DM patients. The sensitivity and specificity of sarcoplasmic PKR expression in DM were 84.6% and 97.6%, respectively. In vitro studies revealed that IFN-β upregulates the expression of PKR, along with several molecules associated with DM muscle damage. Conversely, inhibiting PKR has been shown to downregulate IFN-β-induced pathogenic molecules in both myoblasts and myotubes. Conclusions We observed that PKR exhibits specific expression in the cytoplasm of DM muscle and inhibiting PKR ameliorates IFN-β-induced muscle damage in vitro. These findings provide insights into the diagnostic and therapeutic roles of PKR in DM.

Protein kinase R

EIF-2 kinase

Pathogenesis

10.1136/ard-2024-226057

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Evaluation of the reliability of pathological classification criteria for adult idiopathic inflammatory myopathies with in depth analysis of muscle biopsies

Journal of the Neurological Sciences (2017)

Chuanzhu Yan Ying Hou Yong Luo Tingjun Dai W. Li

10.1016/j.jns.2017.08.3062

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Severe rhabdomyolysis and respiratory failure occurred after exposure to monensin- a case report and literature review

Research Square (Research Square) (2022)

Lihua Song Bei Jiang Tingjun Dai Yuying Zhao Xiaoyan Xiao

Abstract Background: Cases of human monensin toxicosis are rare. Symptoms such as rhabdomyolysis and severe respiratory failure may occur after exposure to monensin. Case presentation: A 44-year-old male worker in a pharmaceutical factory complained of generalized muscle pain, muscular weakness, and dark brown colored urine. His creatine kinase (CK) value was as high as 69881IU/L. Aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) was significantly increased, suggesting a high possibility of rhabdomyolysis. During the hospitalization, the patient developed severe respiratory failure and was relieved after receiving bilevel positive airway pressure (BiPAP) ventilation and a large amount of fluids, methylprednisolone, sodium bicarbonate, and other treatments. His muscle biopsy showed that enzymatic activities of cytochrome C oxidase (COX) and succinate dehydrogenase（SDH）were partially absent. After treatment with hormones, urine alkalization, nutritional therapy of mitochondria, and fully rehydration, the patient's symptoms were relieved. Conclusions : Early attention and intervention are needed for rhabdomyolysis and severe respiratory failure caused by monensin.

Monensin

Creatine kinase

10.21203/rs.3.rs-2328307/v1

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Liver anomalies as a phenotype parameter of Bardet–Biedl syndrome

Clinical Genetics (2015)

Leora Branfield Day Claudia Quammie Elise Héon Aparna Bhan Vaishnavi Batmanabane

Sick child

10.1111/cge.12684

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Citations (20)

Clinical and pathological study of Guillain-Barré syndrome with treatment-related fluctuations

Chin J Neurol (2017)

Qinzhou Wang Wěi Li Dong Zhang Yuying Zhao Tingjun Dai

Objective To investigate the clinical and pathological features of Guillain-Barre syndrome with treatment-related fluctuations (GBS-TRF). Methods Clinical data were obtained from medical records of patients with GBS-TRF during the period 1999 to 2014 in our Hospital. Sural nerve specimens were collected and summarized retrospectively (two cases). Results Eight of 868 cases with GBS had at least one TRF including three chronic hepatitis B patients. The onset of disease was ranged in age from six to 63 years, averaging 34 years. It is more common in men than in women in a ratio of seven to one. Triggering infections occurred in three patients. The initial symptom included weakness of the lower limbs (five cases) and upper extremities (three cases). Sensory symptom was presented in six patients. Five patients had associated respiratory paralysis. None of them had cranial nerve palsy or autonomic dysfunction. The examination of cerebrospinal fluid showed protein and cell separation. Five patients had two attacks, one had three attacks and two had six attacks. The interval between attacks ranged between 14 days and 46 days (mean 23 days). The striking pathologic finding was the presence of sectional selective nerve fiber degeneration (SNFD) with evidence of demyelination. Conclusions Patients with GBS-TRF show similar onset age, preceding infection, cerebrospinal fluid findings, and electrophysiologic characteristics comparing to patients with GBS, while there are more male patients than female patients. SNFD found in sural nerve biopsy reveals ischemic neuropathy, which predicts that injury of arterioles might play an important role in the pathogenesis of GBS-TRF. Key words: Guillain-Barre syndrome; Recurrence; Biopsy

Sural nerve

Pathogenesis

10.3760/cma.j.issn.1006-7876.2017.04.010

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Citations (1)

Myofascial edema of gastrocnemius: A prominent MRI characteristic in dermatomyositis patients with anti‐transcriptional intermediate factor 1‐γ antibody

CNS Neuroscience & Therapeutics (2024)

Chao Jie Zhen Bing Zhao Jingzhen He Wei Li Chuanzhu Yan

This study was designed to evaluate the magnetic resonance imaging (MRI) patterns of the lower limb muscles in dermatomyositis (DM) with anti-transcriptional intermediate factor 1-γ (anti-TIF1-γ) antibody.

Gastrocnemius muscle

10.1111/cns.14647

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Citations (1)

The pathological characteristics of plasmacytoid dendritic cells in muscle tissue of dermatomyositis

Chin J Neurol (2011)

Fuchen Liu Wei Li Shuping Liu Tingjun Dai Yuying Zhao

Objective To study the histological features of plasmacytoid dendritic cells (pDC) in muscle tissue affected by dermatomyositis (DM) and to discuss the pathological significations of pDC.Methods Muscle tissues from 30 cases of DM and 25 cases of polymyositis (PM) were collected.HE stain, immunohistochemistry studies were carried out in all muscle samples.Results Pathological features of DM included: perifascicular atrophy (25/30); punched-out fiber (14/30); perivasculitis (17/30),inflammatory infiltration in the endomysium(6/30).Using immunohistochemistry study, 19 cases from DM were infiltrated by macrophages which are CD68 positive and CD303 negative, 20 cases with DM were infiltrated by pDC which are CD303 positive.The location of pDC were: perivascular of interfascicular septae only (15/20); endomysium only (3/20) and both (2/20).Myopathic damage such as necrotic and regenerating fibers and inflammatory infiltration could be seen in PM.There was few pDC infiltration in PM.Conclusions There is few pDC in muscle tissue affected by PM and many pDC in muscle tissue affected by DM with infiltration mainly in the wide interfascicular septae.pDC may be connected to perifascicular atrophy and play a roll in the pathogenesis of DM. Key words: Dermatomyositis; Dendritic cells; Antigens,CD; Immunohistochemistry

CD68

Infiltration (HVAC)

Endomysium

Muscle Atrophy

Muscle tissue

10.3760/cma.j.issn.1006-7876.2011.03.007

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