Altered Expression of Differential Genes in Thoracic Spinal Cord Involved in Experimental Cholestatic Itch Mouse Model

Chen, Ming; Li, Zhixiao; Wang, Qian; Xiang, Hong‐Bing

doi:10.1007/s11596-018-1930-1

Cited by 7 publications

(7 citation statements)

References 29 publications

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“…Rapid advancements in high-throughput technologies and computational frameworks offer an excellent opportunity to quantify spinal nociception using neuronal activation induced by noxious stimuli. The author's previous study showed that transcriptomics and metabolomics enable the examination of spinal biological systems in unprecedented detail (32)(33)(34)(35)(36). More recently, different patterns were revealed in the metabolic and transcriptional levels of the thoracic spinal cord under myocardial ischemia-reperfusion injury (37)(38)(39).…”

Section: Quantitative Proteomics Reveal the Alterations In The Spinalmentioning

confidence: 99%

Quantitative proteomics reveal the alterations in the spinal�cord after myocardial ischemia‑reperfusion injury in rats

et al. 2019

Int J Mol Med

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There is now substantial evidence that myocardial ischemia-reperfusion (IR) injury affects the spinal cord and brain, and that interactions may exist between these two systems. In the present study, the spinal cord proteomes were systematically analyzed after myocardial IR injury, in an attempt to identify the proteins involved in the processes. The myocardial IR injury rat model was first established by cross clamping the left anterior descending coronary artery for 30-min ischemia, followed by reperfusion for 2 h, which resulted in a significant histopathological and functional myocardial injury. Then using the stable isotope dimethyl labeling quantitative proteomics strategy, a total of 2,362 shared proteins with a good distribution and correlation were successfully quantified. Among these proteins, 33 were identified which were upregulated and 57 were downregulated in the spinal cord after myocardial IR injury, which were involved in various biological processes, molecular function and cellular components. Based on these proteins, the spinal cord protein interaction network regulated by IR injury, including apop-tosis, microtubule dynamics, stress-activated signaling and cellular metabolism was established. These heart-spinal cord interactions help explain the apparent randomness of cardiac events and provide new insights into future novel therapies to prevent myocardial I/R injury.

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Section: Quantitative Proteomics Reveal the Alterations In The Spinalmentioning

confidence: 99%

Quantitative proteomics reveal the alterations in the spinal�cord after myocardial ischemia‑reperfusion injury in rats

et al. 2019

Int J Mol Med

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“…It has been revealed that long non-coding (lnc)RNAs serve a key role in the processing of gene expression signals via the regulation of cell cycle distribution, stem cell differentiation and transcriptional and post-transcriptional control (19,20). Moreover, there are aberrant expression levels of spinal lncRNAs in peripheral diseases, such as pruritus (21,22), acute kidney injury (23), neuropathic pain and inflammation-related pain (24).…”

Section: Introductionmentioning

confidence: 99%

Characterization of novel lncRNAs in upper thoracic spinal cords of rats with myocardial ischemia‑reperfusion injuries

Wang

et al. 2021

Exp Ther Med

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Myocardial ischemia-reperfusion injury (MIRI) is a significant problem in clinical cardiology, and refers to a more serious myocardial injury caused by blood recanalization after a period of myocardial ischemia, as compared with injury caused by vascular occlusion. The spinal cord, as the primary afferent and efferent center of cardiac sensory and sympathetic nerve fibres, has received increased attention in recent years with regards to the regulation of MIRIs. Previous studies have revealed that MIRI has a strong correlation with the abnormal expression of long non-coding (lnc)RNAs in the myocardium; however, there are limited reports on the effects of the altered expression of lncRNAs in the spinal cord following MIRI. To investigate the expression patterns of lncRNAs in the spinal cord after MIRI and their potential role in the early stage of reperfusion, a MIRI model was established in rats. After 30 min of myocardial ischemia and 2 h of reperfusion, the upper thoracic spinal cord tissues were immediately dissected and isolated. lncRNAs and mRNAs in spinal cord tissues were screened using transcriptome sequencing technology, and the expression of several highly deregulated mRNAs, including Frs3, Zfp52, Dnajc6, Nedd4l, Tep1, Myef2, Tgfbr1, Fgf12, Mef2c, Tfdp1 and lncRNA, including ENSRNOT00000080713, ENSRNOT00000090564, ENSRNOT00000082588, ENSRNOT00000091080, ENSRNOT00000091570, ENSRNOT00000087777, ENSRNOT00000082061, ENSRNOT00000091108, ENSRNOT00000087028, ENSRNOT00000086475, were further validated via reverse transcription-quantitative PCR. The number of altered expressed lncRNAs was 126, among which there were 41 upregulated probe sets and 85 downregulated sets. A total of 470 mRNAs were differentially expressed, in which 231 probe sets were upregulated and 239 were downregulated. Gene Ontology analysis indicated that dysregulated transcripts related to biological processes were mainly associated with ‘cell-cell signaling’. Moreover, pathway analysis demonstrated significant changes in the ‘PI3K/Akt signaling pathway’ and the ‘p53 signaling pathway’. Thus, the altered expression of lncRNAs in the spinal cord may be of considerable importance in the process of MIRI. The present results could provide an insight into the potential roles and mechanism of lncRNAs during the early stage of reperfusion.

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“…To investigate the mechanism of pruritus in the presence of cholestasis and thus to evaluate the effectivity of therapeutic drugs, animal models are needed. Several rodent models of cholestasis have been established by drug treatment, 9,10) surgery, 11,12) and genetic manipulation. 13) Among them, mice with surgically-induced cholestasis more closely mimicked the human disease.…”

Section: Introductionmentioning

confidence: 99%

“…9,10,13) Recently, a mouse model of cholestatic pruritus induced by common bile duct ligation (BDL) was reported, 11) although its life time was short. 11,12) Since the severity of cholestatic pruritus is associated with chronic progression of cholestasis, long-term survival of the mouse model is required in order to develop the most effective treatment. Therefore, in this study, we developed a new cholestatic pruritus mouse model induced by BDL and evaluated its treatment with several anti-pruritic drugs.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Characterization of a Novel Mouse Model of Cholestatic Pruritus

Andoh

Suzuki

Konno

et al. 2020

Biological & Pharmaceutical Bulletin

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Patients with cholestatic liver diseases, such as primary biliary cirrhosis, usually suffer from pruritus. However, the pathogenesis of cholestatic pruritus is unclear, and there is no current effective treatment for it. In order to find a treatment for the condition, an appropriate mouse model should be developed. Therefore, here, we established a surgically-induced mouse model of cholestatic pruritus. The bile duct was ligated in order to block bile secretion from the anterior, right, and left lobes, with the exception of the caudate lobe. Serum levels of total bile acid increased after bile duct ligation (BDL). The spontaneous hind paw scratching was also increased in BDL mice. Spontaneous scratching was reduced in BDL mice by naloxone (µ-opioid receptor antagonist), U-50,488H (κ-opioid receptor agonist), and clonidine (α2-adrenoceptor agonist). Azelastine (H 1 receptor antagonist with membrane-stabilizing activity) slightly reduced scratching. However, terfenadine (H 1 receptor antagonist), methysergide (serotonin (5-HT) 2 receptor antagonist), ondansetron (5-HT 3 receptor antagonist), proteinase-activated receptor 2-neutralizing antibody, fluvoxamine (selective serotonin reuptake inhibitor), milnacipran (serotonin-noradrenalin reuptake inhibitor), and cyproheptadine (H 1 and 5-HT 2 receptor antagonist) did not affect scratching. These results suggested that partial obstruction of bile secretion in mice induced anti-histamine-resistant itching and that central opioid system is involved in cholestatic itching.

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Altered Expression of Differential Genes in Thoracic Spinal Cord Involved in Experimental Cholestatic Itch Mouse Model

Cited by 7 publications

References 29 publications

Quantitative proteomics reveal the alterations in the spinal�cord after myocardial ischemia‑reperfusion injury in rats

Quantitative proteomics reveal the alterations in the spinal�cord after myocardial ischemia‑reperfusion injury in rats

Characterization of novel lncRNAs in upper thoracic spinal cords of rats with myocardial ischemia‑reperfusion injuries

Pharmacological Characterization of a Novel Mouse Model of Cholestatic Pruritus

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