Cutaneous microRNA expression in healthy Labrador and Golden retrievers and retrievers with allergic and inflammatory skin diseases

Abstract

Background -MicroRNAs (miRNA) are short, single-stranded RNA molecules that regulate gene expression in a post-transcriptional manner. Their expression is proposed to be tissue-specific and alterations in miRNA expression have been detected in many diseases.Objective -To compare miRNA expression in the skin of healthy Labrador and golden retrievers, and those with allergic and nonallergic dermatitis.Methods and materials -Formalin-fixed and paraffin-embedded (FFPE) skin specimens from seven healthy Labrador and golden retrievers, and seven dogs with allergic skin disease were collected. A further mixed nonallergic inflammation group consisted of samples from five dogs with fungal infection, demodicosis and mast cell tumours. Total RNA was extracted and miRNA primer assays for 18 target miRNAs (miR-142, miR-363, miR-18b, miR-451, miR-146a, miR-124, miR-409, miR-193b, miR-223, miR-215, miR-155, miR-423a, miR-143, miR-1839, miR-21, miR-34b, miR-146b and miR-202) were performed, with RNU6-2 and SNORD95 as miRNAs for normalisation. The selection of miRNAs for investigation was based on reported data and a pilot study evaluating miRNA extraction from FFPE tissue specimens.Results -In the two dogs with mast cell tumours, miRNA expression was undetermined for most miRNAs, so both were excluded from analysis. Although there were differences in the miRNA expression between healthy and inflamed skin, allergic and nonallergic inflammation showed similar expression patterns. Conclusion and clinical relevance -Although the number of included dogs was small, based on this study, none of the evaluated miRNAs allowed differentiation of allergic dermatitis from other inflammatory skin diseases in retriever dogs.

Update on the role of genetic factors, environmental factors and allergens in canine atopic dermatitis

“…Potential genetic biomarkers of cAD are miR-141, miR-187, miR-200a, miR-203, miR-215 and miR-429, and the genes PDE4D, PIAS1, RORA and SH2B1. [22][23][24] However, further studies are needed to confirm that these genetic biomarkers are specific to cAD and not an upregulation caused by other nonallergic inflammatory skin responses. The protective or detrimental role of environmental factors such as living environment during early life, and exposure to bacterial, fungal and parasitic components have undergone continued investigation.…”

“…23 In a more recent study in golden and Labrador retrievers, 18 selected miRNAs were compared between atopic dogs, dogs with nonallergic inflammatory skin diseases and a group of healthy dogs. 24 Four miRNAs (miR-142, miR-146a, miR-155 and miR-21) were overexpressed in the atopic compared to the healthy dogs. However, the same miRNAs were overexpressed in a similar way in other nonallergic inflammatory skin samples, suggesting that those miRNAs have a rather general role in the inflammatory skin response rather than being associated with atopic disease or an allergic reaction.…”

“…However, the same miRNAs were overexpressed in a similar way in other nonallergic inflammatory skin samples, suggesting that those miRNAs have a rather general role in the inflammatory skin response rather than being associated with atopic disease or an allergic reaction. 24…”

Translocator protein 18 kDa regulates retinal neuron apoptosis and pyroptosis in glaucoma

“…This is the first study to report the role of miR-1839 in rats. Previous studies have shown that miR-1839 is a highly conserved lncRNA in pigs and dogs [ [24] , [25] , [26] ], and some studies have shown that miR-1839 is significantly altered in allergic and inflammatory skin [ 27 ], suggesting a strong association between miR-1839 and inflammation and immunity.…”

MiR-193b-3p Regulates TLR4 Expression to Inhibit Inflammation by Targeting ETS1 in Allergic Rhinitis

“…Moreover, a review mentioned that miR-193b-3p level was downregulated in allergic diseases but did not provide substantial evidence [9]. In addition, miR-193b was notably underexpressed in the allergic dermatitis group compared to healthy controls [10]. Yet the function and specific mechanism of miR-193b-3p in AR have hardly been reported currently.…”