mir-233 Modulates the Unfolded Protein Response in C. elegans during Pseudomonas aeruginosa Infection

Dai, Lili; Gao, Jinxia; Zou, Cheng‐Gang; Ma, Yi‐Cheng; Zhang, Ke‐Qin

doi:10.1371/journal.ppat.1004606

Cited by 45 publications

(31 citation statements)

References 44 publications

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“…In addition, increased autophagy can result in C. elegans lifespan extension (56)(57)(58)(59)(60)(61). To test the connection between trehalose, daf-16, and autophagy, first we examined the animals with increased internal trehalose, similar to previous C. elegans autophagy studies (60,62,63). Wild-type animals fed 5 mM trehalose had increased mRNA expression of autophagy-related genes (Fig.…”

Section: Disruption Of Glycogen Synthesis Extends Lifespan and Promotesmentioning

confidence: 88%

Metabolic shift from glycogen to trehalose promotes lifespan and healthspan in Caenorhabditis elegans

Seo

Kingsley

Walker

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

114

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As Western diets continue to include an ever-increasing amount of sugar, there has been a rise in obesity and type 2 diabetes. To avoid metabolic diseases, the body must maintain proper metabolism, even on a high-sugar diet. In both humans and , excess sugar (glucose) is stored as glycogen. Here, we find that animals increased stored glycogen as they aged, whereas even young adult animals had increased stored glycogen on a high-sugar diet. Decreasing the amount of glycogen storage by modulating the glycogen synthase, , a key enzyme in glycogen synthesis, can extend lifespan, prolong healthspan, and limit the detrimental effects of a high-sugar diet. Importantly, limiting glycogen storage leads to a metabolic shift whereby glucose is now stored as trehalose. Two additional means to increase trehalose show similar longevity extension. Increased trehalose is entirely dependent on a functional FOXO transcription factor DAF-16 and autophagy to promote lifespan and healthspan extension. Our results reveal that when glucose is stored as glycogen, it is detrimental, whereas, when stored as trehalose, animals live a longer, healthier life if DAF-16 is functional. Taken together, these results demonstrate that trehalose modulation may be an avenue for combatting high-sugar-diet pathology.

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Section: Disruption Of Glycogen Synthesis Extends Lifespan and Promotesmentioning

confidence: 88%

Metabolic shift from glycogen to trehalose promotes lifespan and healthspan in Caenorhabditis elegans

Seo

Kingsley

Walker

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

114

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“…Studies have reported that increasing miR-233 levels can induce apoptosis 48 and activate the unfolded protein response (UPR). 49 Specifically, miR-233 can target IGF-1R, which has a protective effect on Fas-induced hepatocyte apoptosis and liver injury. Although these studies were performed in other tissues, they have important implications in pathologic progress including apoptosis and UPR response in the retina.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Patterns Involved in Amyloid Beta–Induced Retinal Degeneration

Huang

Sun

Wang

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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Citation: Huang P, Sun J, Wang F, et al. MicroRNA expression patterns involved in amyloid beta-induced retinal degeneration. Invest Ophthalmol Vis Sci. 2017;58:172658: -173558: . DOI: 10.1167 PURPOSE. Dry age-related macular degeneration (AMD) is characterized by the accumulation of drusen under Bruch's membrane, and amyloid beta (Ab) is speculated to be one of the key pathologic factors. While the detrimental effects of Ab on retinas have been widely explored, Ab-induced epigenetic regulatory changes have yet to be fully investigated. We therefore aimed to identify the microRNA (miRNA) expression profiles in an Ab-induced mouse model of retinal degeneration.METHODS. C57BL/6 mice were intravitreally injected with Ab 1-40 or PBS and the eye tissues were collected for hematoxylin and eosin (H&E) staining, apoptosis immunofluorescence staining, and miRNA profiling. After filtering, 10 miRNAs and their target genes were chosen for quantitative RT-PCR (qRT-PCR) confirmations. Pathway analyses were employed for further bioinformatic analyses.RESULTS. Hematoxylin and eosin-stained sections of retinal pigment epithelium (RPE)/neural retina tissue demonstrated degenerative alterations, and immunofluorescence testing revealed apoptosis within the retina after Ab treatments. MicroRNA profiling revealed 61 miRNAs that were differentially expressed between the model and the control group. Among these, 38 miRNAs were upregulated (fold change > 1.5, P < 0.05) and 23 miRNAs were downregulated (fold change < 0.667, P < 0.05). Five of the 10 selected miRNAs (miR-142, miR-216, miR-155, miR-223, and miR-433) as well as several key target genes (CFH, IGF-1R, c-MET, and ABCA1) were confirmed by qRT-PCR analyses.CONCLUSIONS. Our study is the first to profile the miRNA expression patterns and suggests that Ab accumulation could lead to relevant biochemical alternations such as complement activation, barrier impairment, apoptosis, and positive feedback of Ab production.

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“…In recent years, some evidence has demonstrated that miRNAs may play important roles in the regulation of innate immunity1718. In C. elegans , some specific miRNAs have been shown to be involved in the control of innate immune response to bacterial pathogens192021. However, the role of miRNAs in the control of the C. elegans innate immune response to C. albicans infection is still unclear.…”

mentioning

confidence: 99%

microRNAs Involved in the Control of Innate Immunity in Candida Infected Caenorhabditis elegans

Sun

Zhi

Shakoor

et al. 2016

Sci Rep

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The role of microRNAs (miRNAs) in regulating innate immune response to Candida albicans infection in Caenorhabditis elegans is still largely unclear. Using small RNA SOLiD deep sequencing technique, we profiled the miRNAs that were dysregulated by C. albicans infection. We identified 16 miRNAs that were up-regulated and 4 miRNAs that were down-regulated in nematodes infected with C. albicans. Bioinformatics analysis implied that these dysregulated miRNAs may be involved in the control of many important biological processes. Using available mutants, we observed that mir-251 and mir-252 loss-of-function mutants were resistant to C. albicans infection, whereas mir-360 mutants were hypersensitive to C. albicans infection. The expression pattern of antimicrobial genes suggested that mir-251, mir-252, and mir-360 played crucial roles in regulating the innate immune response to C. albicans infection. Fungal burden might be closely associated with altered lifespan and innate immune response in mir-251, mir-252, and mir-360 mutants. Moreover, mir-251 and mir-252 might function downstream of p38 mitogen activated protein kinase (MAPK) or IGF-1/insulin-like pathway to regulate the innate immune response to C. albicans infection. Our results provide an important molecular basis for further elucidating how miRNA-mRNA networks may control the innate immune response to C. albicans infection.

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mir-233 Modulates the Unfolded Protein Response in C. elegans during Pseudomonas aeruginosa Infection

Cited by 45 publications

References 44 publications

Metabolic shift from glycogen to trehalose promotes lifespan and healthspan in Caenorhabditis elegans

Metabolic shift from glycogen to trehalose promotes lifespan and healthspan in Caenorhabditis elegans

MicroRNA Expression Patterns Involved in Amyloid Beta–Induced Retinal Degeneration

microRNAs Involved in the Control of Innate Immunity in Candida Infected Caenorhabditis elegans

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