Capsular Polysaccharide of <i>Mycoplasma ovipneumoniae</i> Induces Sheep Airway Epithelial Cell Apoptosis <i>via</i> ROS‐Dependent JNK/P38 MAPK Pathways

Jiang, Zhongjia; Song, Fuyang; Li, Yanan; Xue, Ding; Zhao, Ning; Zhang, Jiamei; Deng, Guangcun; Li, Min; Liu, Xiaoming; Wang, Yujiong

doi:10.1155/2017/6175841

Cited by 20 publications

(12 citation statements)

References 49 publications

(61 reference statements)

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“…The effects of propofol differ in various cell types due to the activation or inhibition of different signaling pathways (36). However, since ROS-dependent intrinsic apoptosis is generally mediated by MAPK (37), the present study examined the activation of the NF-κB and MAPK/p38/ERK/JNK signaling pathways, which have been reported to be crucial for CoCl 2 -induced apoptosis of BV2 (18) and HK2 cells (38).…”

Section: Discussionmentioning

confidence: 99%

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

et al. 2020

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Propofol is a widely used intravenous anesthetic shown to exert a cardioprotective role against oxidative stress and ischemia/reperfusion injury in rat cardiac H9c2 cells. However, the regulatory mechanisms and functions of propofol in human cardiomyocytes remain unknown. The present study chemically induced hypoxia with cobalt chloride (CoCl 2 ) to mimic cardiomyocyte ischemic injury in human cardiac AC16 and HCM cells. To investigate its underlying mechanisms, propofol was added to the cells before the chemical hypoxia phase. The present results suggested that, in response to hypoxia, mitochondrial membrane potential was lost, and cardiomyocyte viability and superoxide dismutase levels decreased. However, the present results showed that reactive oxygen species and malondialdehyde levels increased. The present results suggested that these effects were significantly reversed following propofol treatment. Additionally, the present results suggested that the protective effect of propofol against CoCl 2 -induced injury may be inhibited by the activation of the JNK signaling pathways. The present results indicated that propofol pre-treatment inhibited CoCl 2 -induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders.

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Section: Discussionmentioning

confidence: 99%

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

et al. 2020

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“…The pathogenesis of M. ovipneumoniae involves a polysaccharide capsule, which could promote adherence of the organisms to the ciliated epithelium, thus promoting bacterial colonization [ 12 , 13 ]. Furthermore, the polysaccharide capsule may have cytotoxic effects on the epithelial cells, inducing apoptosis [ 14 , 15 ], which would also contribute to the pathogenesis of the disease. Mycoplasma spp.…”

Section: Introductionmentioning

confidence: 99%

Bronchopneumonia in Swedish lambs: a study of pathological changes and bacteriological agents

2018

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BackgroundOne of the most common post-mortem inspection finding of sheep and lambs in Sweden, following routine slaughter is pneumonia and its prevalence is increasing. To our knowledge, the aetiology of pneumonia in lambs is not well-known for Swedish conditions. Chronic bronchopneumonia, also known as “atypical” or chronic non-progressive pneumonia, is a common disease worldwide, affecting lambs up to 12 months old. It is therefore of interest to elucidate if this disease complex is also a common cause of pneumonia among Swedish lambs. Chronic bronchopneumonia has a characteristic macroscopic and histopathologic appearance, and Mycoplasma ovipneumoniae is the microbial agent most frequently found. Although this bacterium is important for the pathogenesis, multiple agents are presumed to be involved. The aim of this study was to describe the macroscopic and histopathologic lung lesions in routinely slaughtered lambs with pneumonia, and to determine the bacterial agents involved.ResultsA total of 41 lungs with gross lesions consistent with pneumonia were examined. Of these, 35 lungs displayed the typical gross appearance of chronic bronchopneumonia, with several or all of the characteristic histological features. M. ovipneumoniae was detected in 83% of the 35 lungs and Mannheimia haemolytica was isolated in 71%. Pneumonia associated with M. ovipneumoniae could be correlated to specific gross lesions consistent with the gross description of chronic bronchopneumonia in lambs.ConclusionIn this study, chronic bronchopneumonia was the most common lung disease in routinely slaughtered Swedish lambs. This diagnosis was based on the characteristic macroscopic and histopathologic pulmonary findings and the frequent presence of the bacterium M. ovipneumoniae. The macroscopic appearance of chronic bronchopneumonia could therefore be used during routine investigation of the lamb carcasses at slaughter, to determine the most likely cause of pneumonia.

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“…The attenuation of ERK1/2 phosphorylation accompanied by the activation of JNK was detected in D. bulbifera ethyl acetate fraction (DBEAF)-induced activation of death receptor, Fas and HCT116 cell apoptosis [79]. The capsular polysaccharide induced extrinsic cell apoptosis by upregulating FAS/FASL signaling proteins and cleaved-caspase-8 and promoted a ROS-dependent intrinsic cell apoptosis by activating a JNK and p38 signaling but not ERK1/2 signaling of mitogen-activated protein kinases (MAPK) pathways [80]. The JNK inhibition was validated to block irradiation-induced FasL expression, which was critical in determining non-irradiated hepatocyte injury [81].Short hairpin RNA (shRNA)-mediated knockdown of JNK con rmed its key role in the regulation of sensitivity to this combination as cells with suppressed JNK expression exhibited signi cantly reduced TRAIL/sunitinibmediatedcolon cancer apoptosis [82].…”

Section: Discussionmentioning

confidence: 99%

V-ATPase Deficiency Aggravates Hypoxia-induced Spermatogenesis Reduction by Promoting Spermatocyte Apoptosis via the JNK/c-Jun Pathway in Mice

Yin

Han

et al. 2021

Preprint

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Spermatocyte apoptosis is the primary cause of poor outcome after hypoxia-triggered spermatogenesis reduction (HSR). The vacuolar H+-ATPase (V-ATPase) has been found to be involved in the regulation of hypoxia-induced GC-2 cells apoptosis. However, the mechanism of V-ATPase regulating spermatocyte apoptosis after HSR hasnot been well elucidated. In this study, HSRmodel was established by hypoxia exposure in vivo in V-ATPase-knockout (V-ATPase-/-) and wild-type (WT) mice to investigate theeffectof V-ATPase deficiency on spermatocyte apoptosis. GC-2, amouse pachytene spermatocyte-derived cell line, was introduced in vitro experiments. The sperm count and spermatogenic apoptosis were recorded after 60 d of hypoxia exposure in HSR model. The apoptosis of GC-2 cells was detected by flow cytometry and TUNEL staining. The expression of JNK/c-Jun was evaluated by RNA-seq or western blot. The expression of DR5 and caspase-8 was evaluated by RT-qPCR and western blot. The expression of V-ATPase was determined by western blot in the presence and absence ofLenti-transcription factor EB (TFEB).C-Jun interference was used for evaluating the role of JNK in regulating the apoptosis of GC-2 cells byTUNEL and flow cytometry. The in vivo results suggested that hypoxia induced spermatogenesis reduction and downregulation of V-ATPase. Moreover, V-ATPase deficiency resulted in moresevere spermatogenesis reduction after hypoxia exposure. The spermatogenesis reduction was associated with exacerbation of spermatocyte apoptosis. Hypoxia down-regulated the transcription of V-ATPase through inhibiting TFEB and its nuclear translocation. The mRNA and protein expressions of V-ATPaseincreased after TFEB overexpression in GC-2 cells. Moreover, V-ATPase deficiency enhanced JNK/c-Jun activation and related DR-apoptotic pathwayin GC-2 cells.However,inhibition of c-Jun attenuated V-ATPase deficiency-induced GC-2 cells apoptosis in vitro and HSR in vivo. In conclusion, JNK/c-Jun was involved in the enhancement of V-ATPase-mediated HSR in V-ATPase -/- mice. V-ATPase deficiency aggravates spermatocyte apoptosis, which may account forthe poor spermatogenesis outcomes of V-ATPase-/- mice. The discoveredfunction of V-ATPase modulating spermatocyte apoptosis indicates its potential therapeutic effect against HSR.

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Capsular Polysaccharide of Mycoplasma ovipneumoniae Induces Sheep Airway Epithelial Cell Apoptosis via ROS‐Dependent JNK/P38 MAPK Pathways

Cited by 20 publications

References 49 publications

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

Propofol protects human cardiac cells against chemical hypoxiainduced injury by regulating the JNK signaling pathways

Bronchopneumonia in Swedish lambs: a study of pathological changes and bacteriological agents

V-ATPase Deficiency Aggravates Hypoxia-induced Spermatogenesis Reduction by Promoting Spermatocyte Apoptosis via the JNK/c-Jun Pathway in Mice

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