Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model

Ikarashi, Nobutomo; Mizukami, Nanaho; Kon, Risako; Kaneko, Miho; Uchino, Ryogo; Fujisawa, Izumi; Fukuda, Natsuko; Sakai, Hiroyasu; Kamei, Junzo

doi:10.3390/ijms20153782

Cited by 19 publications

(26 citation statements)

References 51 publications

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“…It exists in lactose endothelial cells in the center of villi of small intestine and produces chyle when digesting food. On the basis of this, an experimental study of AQP1 deficient mice was carried out to verify the impaired fat absorption ( Ma et al, 2001 ), and application of AQP3 inhibitors showed that the decreased protein led to diarrhea as well ( Ikarashi et al, 2019 ). Therefore, we deduce that the declined AQP1 and AQP3 in the intestinal mucosa with IBS-D may cause mucosal injuries, break the intestinal barrier, enhance the permeability and reduce fat absorption, thus leading to diarrhea and other symptoms.…”

Section: Discussionmentioning

confidence: 99%

LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients

et al. 2021

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ObjectiveThe study aimed to investigate the role of Long non-coding RNA (LncRNA) H19 in the pathogenesis of Diarrhea Irritable Bowel Syndrome (IBS-D), and further to the regulatory effect of LncRNA H19 on AQP1, 3 in the intestinal mucosa of IBS-D patients, so as to seek a new way to elucidate the mechanism of IBS in clinic.MethodsThe levels of LncRNA H19, AQP1, and AQP3 were detected in colonic tissues of IBS-D patients, compared with that in healthy controls. Through RNA gene interference and activation methods, small activating RNA (saRNA) and small interfering (siRNA) were transfered into Caco-2 cells in vitro experiment, and sub-group for two control group, siH19 empty vector group, siH19 interference group, overexpression H19 vector group, and overexpression H19 empty vector group. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot were applied to evaluate the expression levels of LncRNA H19 and the amount of AQP1 and AQP3 protein expression, respectively.ResultsCompared with healthy volunteers, the levels of LncRNA H19, AQP1, and AQP3 in the colonic mucosa of IBS-D patients were significantly decreased (P < 0.05). The results in vitro transfection experiment revealed that the level of LncRNA H19 in the siH19 interference group was significantly declined (P < 0.05), while there was a remarkable increase in the overexpression H19 vector group (P < 0.05), compared with the corresponding control groups. The expression of AQP1 and AQP3 in Caco-2 cells was of positive correlation with the level of LncRNA H19.ConclusionThat the down-regulation of LncRNA H19 resulted in the expression changes of AQP1 and AQP3 may play an important role in the occurrence and development of IBS-D.

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Section: Discussionmentioning

confidence: 99%

LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients

et al. 2021

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“…Hou et al [44] and Olesen et al [45] demonstrated that DACT2 and KCND3 were found to be substantially related to atrial fibrillation. Ge and Concannon [46], Ferjeni et al [47], Anquetil et al [48], Glawe et al [49], Kawabata et al [50], Li et al [51], Buraczynska et al [52], Amini et al [53], Yang et al [54], Du Toit et al [55], Hirose et al [56], Zhang et al [57], Griffin et al [58], Zouidi et al [59], Trombetta et al [60], Alharbi et al [61], Ikarashi et al [62], Dharmadhikari et al [63], Sutton et al [64] and Deng et al [65] reported that UBASH3A, ZAP70, IDO1, ITGAL (integrin subunit alpha L). ITGB7, RASGRP1, CNR1, SLC2A1, SLC11A1, GPR84, SSTR5, KCNB1, GLUL (glutamate-ammonia ligase), BANK1, CACNA1E, LGR5, AQP3, SIGLEC7, SSTR2 and DNER (delta/notch like EGF repeat containing) could be an index for diabetes, but these genes might be responsible for progression of HF.…”

Section: Discussionmentioning

confidence: 99%

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Vastrad¹,

Tengli

Vastrad³

2021

Preprint

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Heart failure (HF) is a heterogeneous clinical syndrome and affects millions of people all over the world. HF occurs when the cardiac overload and injury, which is a worldwide complaint. The aim of this study was to screen and verify hub genes involved in developmental HF as well as to explore active drug molecules. The expression profiling by high throughput sequencing of GSE141910 dataset was downloaded from the Gene Expression Omnibus (GEO) database, which contained 366 samples, including 200 heart failure samples and 166 non heart failure samples. The raw data was integrated to find differentially expressed genes (DEGs) and were further analyzed with bioinformatics analysis. Gene ontology (GO) and REACTOME enrichment analyses were performed via ToppGene; protein-protein interaction (PPI) networks of the DEGs was constructed based on data from the HiPPIE interactome database; modules analysis was performed; target gene - miRNA regulatory network and target gene - TF regulatory network were constructed and analyzed; hub genes were validated; molecular docking studies was performed. A total of 881 DEGs, including 442 up regulated genes and 439 down regulated genes were observed. Most of the DEGs were significantly enriched in biological adhesion, extracellular matrix, signaling receptor binding, secretion, intrinsic component of plasma membrane, signaling receptor activity, extracellular matrix organization and neutrophil degranulation. The top hub genes ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 were identified from the PPI network. Module analysis revealed that HF was associated with adaptive immune system and neutrophil degranulation. The target genes, miRNAs and TFs were identified from the target gene - miRNA regulatory network and target gene - TF regulatory network. Furthermore, receiver operating characteristic (ROC) curve analysis and RT-PCR analysis revealed that ESR1, PYHIN1, PPP2R2B, LCK, TP63, PCLAF, CFTR, TK1, ECT2 and FKBP5 might serve as prognostic, diagnostic biomarkers and therapeutic target for HF. The predicted targets of these active molecules were then confirmed. The current investigation identified a series of key genes and pathways that might be involved in the progression of HF, providing a new understanding of the underlying molecular mechanisms of HF.

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“…Decreased dermal water content has been reported in AQP3 knockout mice [26][27][28]. Furthermore, skin AQP3 expression has been shown to be reduced in the presence of psoriasis [29], leukoplakia [30,31], diabetes mellitus [32], and aging [33,34], each of which cause dry skin. In this manner, AQP3 in the skin plays a crucial role in skin moisture retention.…”

Section: Discussionmentioning

confidence: 99%

Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Erlotinib Induces Dry Skin via Decreased in Aquaporin-3 Expression

et al. 2020

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An adverse reaction of dry skin occurs frequently during treatment with anticancer epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). In this study, we conducted basic research to clarify the mechanism of EGFR-TKI-induced dry skin and propose new treatments or preventative measures. Dermal water content was significantly lower in the erlotinib-treated mice than in the control group. An assessment of the expression levels of functional genes in the skin revealed that only the expression of the water channel aquaporin-3 (AQP3) was significantly decreased in the erlotinib-treated group. When erlotinib was added to epidermal keratinocyte HaCaT cells, the expression levels of both AQP3 mRNA and protein decreased. Erlotinib treatment also significantly decreased the expression levels of phospho-EGFR and phospho-extracellular signal-regulated kinase (ERK), both in HaCaT cells and mouse skin. Dry skin due to erlotinib may be caused by the decreased expression of AQP3 in the skin, thereby limiting water transport from the vascular side to the corneum side. The decrease in AQP3 may also be attributable to ERK suppression via inhibition of EGFR activity by erlotinib. Therefore, substances that increase AQP3 expression may be effective for erlotinib-induced dry skin.

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Study of the Mechanism Underlying the Onset of Diabetic Xeroderma Focusing on an Aquaporin-3 in a Streptozotocin-Induced Diabetic Mouse Model

Cited by 19 publications

References 51 publications

LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients

LncRNA H19 as a Competing Endogenous RNA to Regulate AQP Expression in the Intestinal Barrier of IBS-D Patients

Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis

Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Erlotinib Induces Dry Skin via Decreased in Aquaporin-3 Expression

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