Insulin treatment prevents wounding associated changes in tissue and circulating neutrophil MMP-9 and NGAL in diabetic rats

Abdollahi, Maryam; Ng, Taria Shin Yi; Rezaeizadeh, Alireza; Aamidor, Sarah E.; Twigg, Stephen M.; Min, Danqing; McLennan, Susan V.

doi:10.1371/journal.pone.0170951

Cited by 20 publications

(17 citation statements)

References 31 publications

(41 reference statements)

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“…It has been reported that insulin treatment of STZ-induced diabetic mice leads to decreased LCN2 expression in skin excisional wound tissues, which has been proposed as a potential therapeutic target for improving diabetic wound healing (79). Further, HFD-fed mice show insulin resistance and hyperinsulinemia (80).…”

Section: Discussionmentioning

confidence: 99%

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

et al. 2019

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Diabetic encephalopathy is a severe diabetes-related complication in the central nervous system (CNS) that is characterized by degenerative neurochemical and structural changes leading to impaired cognitive function. While the exact pathophysiology of diabetic encephalopathy is not well-understood, it is likely that neuroinflammation is one of the key pathogenic mechanisms that cause this complication. Lipocalin-2 (LCN2) is an acute phase protein known to promote neuroinflammation via the recruitment and activation of immune cells and glia, particularly microglia and astrocytes, thereby inducing proinflammatory mediators in a range of neurological disorders. In this study, we investigated the role of LCN2 in multiple aspects of diabetic encephalopathy in mouse models of diabetes. Here, we show that induction of diabetes increased the expression of both Lcn2 mRNA and protein in the hippocampus. Genetic deficiency of Lcn2 significantly reduced gliosis, recruitment of macrophages, and production of inflammatory cytokines in the diabetic mice. Further, diabetes-induced hippocampal toxicity and cognitive decline were both lower in Lcn2 knockout mice than in the wild-type animals. Taken together, our findings highlight the critical role of LCN2 in the pathogenesis of diabetic encephalopathy.

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Section: Discussionmentioning

confidence: 99%

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

et al. 2019

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“…DAPI (dilution 1:10) was used to stain the nucleus. Images were captured using an Olympus Fluorescence microscope (cellSens standard software version 1.6, DP80, Olympus Corporation, Tokyo, Japan) [ 13 , 14 ].…”

Section: Methodsmentioning

confidence: 99%

MiR-4463 inhibits the migration of human aortic smooth muscle cells by AMOT

Wang

et al. 2018

Bioscience Reports

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Aberrant vascular smooth muscle cell (VSMC) migration has been implicated in a variety of vascular disorders, while the signal pathways governing this process remain unclear. Here, we investigated whether miRNAs, which are strong post-transcriptional regulators of gene expression, could alter VSMC migration. We detected the expression of miR-4463 in the plasma of patients with atherosclerosis and in human aortic smooth muscle cells under hypoxia–ischemia condition, and investigated the migration effect and its downstream pathways. The results have shown that whether in clinical AS patients or hypoxic cells, the expression of miR-4463 was lower than that of normal group, then the number of migrating cells in the miR-4463 mimic intervention group was significantly decreased compared with the normal group and miR-4463 inhibitor instead. Furthermore, the expression of angiomotin (AMOT) in gastrocnemius muscle and femoral artery of patients was significantly higher than that of the control group. The protein level of AMOT in miR-4463 mimic intervention group was significantly decreased, and its level was reversed by inhibiting miR-4463. In summary, these results indicate that miR-4463 is a novel modulator of VSMC migration by targetting AMOT expression. Regulating miR-4463 or its specific downstream target genes in VSMCs may represent an attractive approach for the treatment of vascular diseases.

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“…On this basis, it is highly likely that ticks inject host α1-antitrypsin and α2-macroglobulin into the feeding site as a strategy of evading the host's tissue repair defense response. It is also notable that fibrinogen and neutrophil gelantinase-associated lipocalin, which among other functions plays important roles in wound healing, were identified towards the end of feeding [153][154][155][156]. This is interesting in that the tick-feeding lesion is completely sealed, preventing leakage of blood, when a replete fed tick detaches from its feeding site.…”

Section: Secretion Of Rabbit Host Proteins In a Americanum Tick Salimentioning

confidence: 96%

Time-resolved proteomic profile of Amblyomma americanum tick saliva during feeding

et al. 2020

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Amblyomma americanum ticks transmit more than a third of human tick-borne disease (TBD) agents in the United States. Tick saliva proteins are critical to success of ticks as vectors of TBD agents, and thus might serve as targets in tick antigen-based vaccines to prevent TBD infections. We describe a systems biology approach to identify, by LC-MS/MS, saliva proteins (tick = 1182, rabbit = 335) that A. americanum ticks likely inject into the host every 24 h during the first 8 days of feeding, and towards the end of feeding. Searching against entries in GenBank grouped tick and rabbit proteins into 27 and 25 functional categories. Aside from housekeeping-like proteins, majority of tick saliva proteins belong to the tick-specific (no homology to non-tick organisms: 32%), protease inhibitors (13%), proteases (8%), glycine-rich proteins (6%) and lipocalins (4%) categories. Global secretion dynamics analysis suggests that majority (74%) of proteins in this study are associated with regulating initial tick feeding functions and transmission of pathogens as they are secreted within 24-48 h of tick attachment. Comparative analysis of the A. americanum tick saliva proteome to five other tick saliva proteomes identified 284 conserved tick saliva proteins: we speculate that these regulate critical tick feeding functions and might serve as tick vaccine antigens. We discuss our findings in the context of understanding A. americanum tick feeding physiology as a means through which we can find effective targets for a vaccine against tick feeding.

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Insulin treatment prevents wounding associated changes in tissue and circulating neutrophil MMP-9 and NGAL in diabetic rats

Cited by 20 publications

References 31 publications

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

Role of Hippocampal Lipocalin-2 in Experimental Diabetic Encephalopathy

MiR-4463 inhibits the migration of human aortic smooth muscle cells by AMOT

Time-resolved proteomic profile of Amblyomma americanum tick saliva during feeding

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