Jiliang Wen

Second Hospital of Shandong University

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Xiulin Zhang

Second Hospital of Shandong University

Mengmeng Zhao

Renmin Hospital of Wuhan University

Jiaxin Liu

Capital Medical University

Shulu Zu

Second Hospital of Shandong University

Hanwen Liu

Huazhong University of Science and Technology

Nan Ge

China Medical University

Ning Ding

Eastern Hepatobiliary Surgery Hospital

Jieke Yan

Second Hospital of Shandong University

Zhenghao Chen

Capital Medical University

Shaoyong Wang

Second Hospital of Shandong University

Cooperative Institutions

Second Hospital of Shandong University

Shandong University

Shandong Provincial Hospital

Shandong First Medical University

Chinese Academy of Medical Sciences & Peking Union Medical College

Qilu Hospital of Shandong University

Chinese Academy of Sciences

Affiliated Hospital of Shandong University of Traditional Chinese Medicine

Peking University

Huazhong University of Science and Technology

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EFFECT OF ALTITUDE HYPOXIA ON CAROTID BODY ULTRASTRUCTURE IN MARMOTA HIMALAYANA,OCHOTON A CURZONIAE AND HILLTOP SPRAGUE DAWLEY RAT

Acta Theriologica Sinica (1989)

Q. Chen Y. Ye Jiliang Wen

This investigation reveals with the ultrastructural effects of hypoxia in native plateau species Marmota himalayana (3300m above sea level), Ochotona curzoniae (3300m) and plateau-migrated rats (the fourth filial generation of the Wistar rats imported to Xining and migrated to 3300m),and the Hilltop Sprague Dawley rats divided into 2 groups: (l)quickly brought to altitude (3300m), (2)remained in Shanghai(control). Their left and right carotid bodies were investigated with transmission electron micro-scope and scanning electron microscope. There were an increase in the number of type I cells,decrease in the number of de-nse-cored vesicles, degenerated mitochondria, an increase in number and size of the vacuoles,decrease in the synaptic vesicle of the nerve endings and reduced microtriches in the surface of type I cell in the Sprague Dawley altitude-brought rats. However, no change had been observed in these indexes mentioned above in native O.curzoniae and M.himalayana at the same experimental conditions. The light damage of hypoxia of carotid bodies was observed in plateau-migrated Wistar rats.

Hypoxia

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Kidney Injury Molecule-1 Level is Associated with the Severity of Renal Interstitial Injury and Prognosis in Adult Henoch–Schönlein Purpura Nephritis

Archives of Medical Research (2017)

Yuanyuan Zhang LI Aiju Jiliang Wen Junhui Zhen Qiufa Hao

Blood urea nitrogen

Nephritis

10.1016/j.arcmed.2017.10.005

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Citations (14)

Decreased urinary excretion of urodilatin in patients with essential hypertension

Journal of the American College of Cardiology (1998)

Young Sung Hwang Y.-J. Lee Jiliang Wen S.J. Shin J.-H. Taai

Essential hypertension

10.1016/s0735-1097(98)80278-7

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Brain Research (2021)

Jiliang Wen Zhenghao Chen Si Wang Mengmeng Zhao Shaoyong Wang

Rheobase

Tonic (physiology)

Dorsal root ganglion

Stimulus (psychology)

10.1016/j.brainres.2020.147251

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Citations (2)

Upregulation of transient receptor potential cation channel subfamily M member-3 in bladder afferents is involved in chronic pain in cyclophosphamide-induced cystitis

Pain (2022)

Mengmeng Zhao Lei Liu Zhenghao Chen Ning Ding Jiliang Wen

Abstract The transient receptor potential cation channel subfamily M member-3 (TRPM3) channel is a recently recognized noxious heat sensor that is involved in inflammatory thermal hyperalgesia. To examine its involvement in the development of hyperalgesia in interstitial cystitis/painful bladder syndrome (IC/PBS), rats with cyclophosphamide (CYP)-induced chronic cystitis were used as a model of IC/PBS. Mechanical and thermal hyperalgesia in lower abdominal region overlying the bladder in CYP rats were measured using von Frey filaments and radiant heat, respectively. Transient receptor potential cation channel subfamily M member-3 expression at the mRNA, protein, and functional levels in dorsal root ganglion neurons innervating the bladder was detected using RNA in situ hybridization (RNAscope), Western blotting, immunohistochemistry, and Ca 2+ imaging, respectively. Transient receptor potential cation channel subfamily M member-3 channels were expressed on most of the bladder primary afferent nerve terminals containing calcitonin gene–related peptide and their cell bodies in L6-S1 dorsal root ganglion. Activation of TRPM3 in the bladder wall by its specific agonist pregnenolone sulphate or CIM0216 induced spontaneous bladder pain, calcitonin gene–related peptide release, and neurogenic inflammation that was evidenced by edema, plasma extravasation, inflammatory cell accumulation, and mast cell infiltration. In CYP rats, pretreatment with the TRPM3 antagonist primidone (2 mg/kg, i.p.) significantly alleviated the mechanical and thermal hyperalgesia, bladder submucosal edema, mast cell infiltration, and bladder hyperactivity. Cyclophosphamide-induced cystitis was associated with TRPM3 upregulation at the mRNA, protein, and functional levels in bladder afferent neurons. Our results suggest that upregulation of TRPM3 channels is involved in the development of chronic pain in CYP-induced cystitis, and targeting TRPM3 may be a pharmacological strategy for treating bladder pain in IC/PBS.

Neurogenic inflammation

Dorsal root ganglion

10.1097/j.pain.0000000000002616

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Citations (13)

Activation of TRPA1 in Bladder Suburothelial Myofibroblasts Counteracts TGF-β1-Induced Fibrotic Changes

International Journal of Molecular Sciences (2023)

Mengmeng Zhao Ning Ding Haoyu Wang Shulu Zu Hanwen Liu

The activation of the transient receptor potential ankyrin 1 (TRPA1) channel has anti-fibrotic effects in the lung and intestine. Suburothelial myofibroblasts (subu-MyoFBs), a specialized subset of fibroblasts in the bladder, are known to express TRPA1. However, the role of the TRPA1 in the development of bladder fibrosis remains elusive. In this study, we use the transforming growth factor-β1 (TGF-β1) to induce fibrotic changes in subu-MyoFBs and assess the consequences of TRPA1 activation utilizing RT-qPCR, western blotting, and immunocytochemistry. TGF-β1 stimulation increased α-SMA, collagen type I alpha 1 chain(col1A1), collagen type III (col III), and fibronectin expression, while simultaneously suppressing TRPA1 in cultured human subu-MyoFBs. The activation of TRPA1, with its specific agonist allylisothiocyanate (AITC), inhibited TGF-β1-induced fibrotic changes, and part of these inhibition effects could be reversed by the TRPA1 antagonist, HC030031, or by reducing TRPA1 expression via RNA interference. Furthermore, AITC reduced spinal cord injury-induced fibrotic bladder changes in a rat model. The increased expression of TGF-β1, α-SMA, col1A1 and col III, and fibronectin, and the downregulation of TRPA1, were also detected in the mucosa of fibrotic human bladders. These findings suggest that TRPA1 plays a pivotal role in bladder fibrosis, and the negative cross talk between TRPA1 and TGF-β1 signaling may represent one of the mechanisms underlying fibrotic bladder lesions.

Myofibroblast

10.3390/ijms24119501

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Citations (7)

Functional Upregulation of TRPM3 Channels Contributes to Acute Pancreatitis-associated Pain and Inflammation

Inflammation (2024)

Lei Liu Hanwen Liu Mengmeng Zhao Jiliang Wen Jiaxin Liu

10.1007/s10753-024-02138-8

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Piezo2 Channel Upregulation is Involved in Mechanical Allodynia in CYP-Induced Cystitis Rats

Molecular Neurobiology (2023)

Lei Liu Yan Zhao Wenhan An Mengmeng Zhao Ning Ding

Mechanical sensing Piezo2 channel in primary sensory neurons has been shown contribute to mechanical allodynia in somatic chronic pain conditions. Interstitial cystitis (IC)-associated pain is often triggered by bladder filling, a presentation that mimics the mechanical allodynia. In the present study, we aimed to examine the involvement of sensory Piezo2 channel in IC-associated mechanical allodynia using a commonly employed cyclophosphamide (CYP)-induced IC model rat. Piezo2 channels in dorsal root ganglia (DRGs) was knocked down by intrathecal injections of Piezo2 anti-sense oligodeoxynucleotides (ODNs) in CYP-induced cystitis rats, and mechanical stimulation-evoked referred bladder pain was measured in the lower abdomen overlying the bladder using von Frey filaments. Piezo2 expression at the mRNA, protein, and functional levels in DRG neurons innervating the bladder was detected by RNA-fluorescence in situ hybridization, western blotting, immunofluorescence, and Ca2+ imaging, respectively. We found that Piezo2 channels were expressed on most (> 90%) of the bladder primary afferents, including afferents that express CGRP, TRPV1 and stained with isolectin B4. CYP-induced cystitis was associated with Piezo2 upregulation in bladder afferent neurons at the mRNA, protein, and functional levels. Knockdown of Piezo2 expression in DRG neurons significantly suppressed mechanical stimulation-evoked referred bladder pain as well as bladder hyperactivity in CYP rats compared to CYP rats treated with mismatched ODNs. Our results suggest upregulation of Piezo2 channels is involved in the development of bladder mechanical allodynia and bladder hyperactivity in CYP-induced cystitis. Targeting Piezo2 might be an attractive therapeutic approach for IC-related bladder pain.

Allodynia

10.1007/s12035-023-03386-9

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Citations (5)

Anti-Cancer Effects of Paris Polyphylla Ethanol Extract by Inducing Cancer Cell Apoptosis and Cycle Arrest in Prostate Cancer Cells

Current Urology (2018)

Denglu Zhang Kailin Li Chao Sun Guangshang Cao Yuanfu Qi

To evaluate the potential anti-prostate cancer effects of Paris polyphylla ethanol extract (PPEE) and its underlying mechanisms.The anti-proliferation activity of PPEE was tested on PC3 and DU145 cells using Cell Counting Kit-8 assay. The pro-apoptotic and cell cycle arrest effects of PPEE were confirmed by flow cytometry. Apoptosis of prostate cancer cells was induced by PPEE through endogenous and exogenous pathways. A mouse xenograft model was used to examine its anti-prostate cancer effects in vivo.We found that the IC50 of PPEE on PC3 cells was 3.98 µg/ml and the IC50 of PPEE on DU145 cells was 8 µg/ml. PPEE induced prostate cancer cell apoptosis in a concentration dependent manner, through endogenous and exogenous pathways. PPEE induced PC3 cell cycle arrest in G0/G1 and G2/M phases, while in DU145cell it induced cell arrest in the G0/G1 phase. PPEE inhibited the growth of prostate cancer cells in vivo.PPEE could inhibit prostate cancer growth in vitro and in vivo, induce apoptosis of prostate cancer cells, and cause cell cycle arrest, which laid the foundation for further research on the anti-tumor mechanism of PPEE.

DU145

10.1159/000447209

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Citations (19)

Significance of piezo‐type mechanosensitive ion channel component 2 in premature ejaculation: An animal study

Andrology (2020)

Zhenghao Chen Mingzhen Yuan Zhen Ma Jiliang Wen Xuesheng Wang

Penile hypersensitivity is one of the main pathological mechanisms of premature ejaculation. However, little is known about the neurophysiological mechanism of penile peripheral nerve sensitization. Piezo Type Mechanosensitive Ion Channel Component 2 (PIEZO2), was recently identified as a mechanically sensitive channel.This study explored the possible neural mechanisms of PIEZO2 action in the mechanisms of premature ejaculation using molecular biology and electrophysiology approaches.One hundred seventy male rats and 85 female rats were recruited. The females were induced estrus by injection of estradiol benzoate and progesterone followed by surgically castrated. Subsequently, the copulatory behaviors were record by a video camera six times, once a week. The last three mating processes of 134 male rats were successfully recorded. The males were divided into three groups according to ejaculation frequency value. Immunocytochemical and molecular methods as well as whole-cell patch clamp recording were used to show the difference between premature ejaculation rats and control rats. To further clarify the involvement of PIEZO2 in premature ejaculation, we constructed a PIEZO2 knockdown model in rats by intrathecal injection of PIEZO2 antisense oligodeoxynucleotides.We showed that PIEZO2 in the penis head and in the dorsal root ganglia(DRG) were significantly increased in premature ejaculation rats. Whole-cell patch clamp recording demonstrated that mechanical stimulation evoked a higher inward current density in premature ejaculation rats compared with control rats, which could be inhibited by the PIEZO2-specific antagonist, FM1-43. PIEZO2 knockdown experiments revealed that the inward current density induced by mechanical stimulation was significantly decreased in PIEZO2 knockdown rats, and that the mount frequency and ejaculation latency and frequency were significantly improved in PIEZO2 knockdown rats.Our data demonstrate PIEZO2 involvement in peripheral nerve sensitization, indicating that pharmacological antagonism of PIEZO2 may be a useful strategy for treating premature ejaculation.

Component (thermodynamics)

Ejaculation

Premature ejaculation

10.1111/andr.12779

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Citations (7)