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Epigenetic and Assisted Reproduction Experimental Studies
Published in Cristina Camprubí, Joan Blanco, Epigenetics and Assisted Reproduction, 2018
Celia Corral-Vazquez, Ester Anton
Several studies have revealed that hundreds of different miRNAs are expressed in mammalian testes. Also, nearly 40% of them are expressed differentially in comparison with somatic tissues (19,21). Many of the coding sequences of these prominently testicular miRNAs are placed on the X chromosome (19). Besides, the characterization of human sperm miRNAs has revealed the existence of a specific expression profile in fertile males. A study performed in 10 fertile individuals showed a panel of 221 miRNAs that were present in all their sperm samples. The regulatory pathways of these ncRNAs were found to be involved in biological processes related to spermatogenesis and embryogenesis (22). Another characterization of sperm ncRNA of fertile men revealed the presence of 35 enriched miRNAs that were involved in embryo development and cell growth processes (13). Regarding other expression studies performed in fertile men, it has been found that several miRNAs, such as hsa-miR-34b-3p, hsa-miR-375, and hsa-miR-191-5p, are overexpressed in human sperm cells (22,23).
Liver, Gallbladder, and Exocrine Pancreas
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Russell C. Cattley, James A. Popp, Steven L. Vonderfecht
Because of the infrequency of xenobiotic-induced exocrine injury, even less attention has been given to biomarkers of pancreatic injury in laboratory animals. Recently, proteomics techniques were used to identify two novel peptides that show promise as safety markers of pancreatic toxicity (Walgren et al. 2007a,b). These peptides, referred to as RA1609 and RT2864, were initially investigated as alternative biomarkers to address the deficiencies of serum amylase and lipase as markers of acute pancreatic injury in rats (Walgren et al. 2007a). Peptide RA1609 is a fragment of rat albumin and decreases with acute pancreatic injury, while RT2864 is a portion of rat trypsin III and increases with acute pancreatic injury. A subsequent study showed that the same peptide markers were altered in mice with acute pancreatic injury and suggested that corresponding peptides were also altered in humans with acute pancreatitis (Walgren et al. 2007b). Another novel approach is the measurement of organ-specific microRNA (miRNA) biomarkers in the circulation. In this regard, levels of a pancreas-enriched miRNA, designated miR-216a, were elevated in the sera of rats with arginine-induced pancreatitis but not in sera from rats with acute peritonitis and sepsis. Amylase and lipase levels were elevated in both conditions (Kong et al. 2010). Pancreas-specific miR-216a, miR-216b, miR-217, and a less specific marker of exocrine pancreas, miR-375, were evaluated against traditional biomarkers of exocrine pancreatic injury, that is, amylase and/or lipase, in several models of exocrine pancreatic injury in rodents (Endo et al. 2013; Goodwin et al. 2014; Usborne et al. 2014; Wang et al. 2017). In general, the pancreas-specific miRNAs showed a greater dynamic range and persisted longer than the traditional biomarkers. Further studies with pancreas-specific miRNAs will be needed before their utility is fully understood.
Micronutrients in Prevention and Improvement of the Standard Therapy in Diabetes
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Several studies on the levels of circulating microRNAs have been published with a suggestion that their alterations could be of diagnostic value in diabetes. Only the results of a few selected investigations are presented (Table 6.1). The expression of miR-23a, let-7i, miR-486, miR-186, miR-191, miR-192, and miR-146a was lower in patients with type 2 diabetes and pre-diabetes than in normal glucose tolerance control subjects. Furthermore, the expression of miR-23a in the serum of patients with type 2 diabetes was lower than in pre-diabetic patients.68 Serum concentrations of miR-101, miR-375, and miR-802 were higher in type 2 diabetic patients compared to normal glucose tolerance control subjects.69 In serum of newly diagnosed patients with type 2 diabetes, the expression of seven miR-9, miR-29a, miR-30d, miR-34a, miR-124a, miR-146a, and miR-375 was elevated compared with pre-diabetes and type 2 diabetes susceptible individuals with normal glucose tolerance.70 Plasma and urine levels of miR-21 and miR-210 were unregulated, while urine level of miR-126 was downregulated in patients with type 1 diabetes compared with control subjects; however, plasma level of miR-126 was similar in both groups. Additionally, decreased urine levels of miR-126 were associates with increased levels of A1c.71 Circulating expression of miR-142-3p was enhanced; while the expression of miR-126a and miR-30e was reduced in type 2 diabetic patients compared with normal glucose tolerance individuals.72 In streptozotocin- (STZ) induced diabetes mouse model, circulating concentrations of miR-375 were elevated before the onset of hyperglycemia. This was confirmed by experiments in which cytokine- and STZ induced cell death in cultured mouse islets, which was associated with a rise in the extracellular level of miR-375.73
Dual regulation of miR-375 and CREM genes in pancreatic beta cells
Published in Islets, 2022
David M. Keller, Isis G. Perez
MiR-375 may play a role in the pathogenesis of type 2 diabetes mellitus in humans as well. In a small cohort of patients, Zhao et al.6 discovered that miR-375 expression in the pancreas was increased approximately 4-fold in diabetic patients compared with non-diabetic control individuals. While additional patient studies need to be done, it suggests that the miR-375 gene can be misregulated in the pathogenic state. Intriguingly, diabetic patients exhibit decreased β-cell mass and increased α-cell mass due in part to dedifferentiation of β-cells.7 In patients, the gain of miR-375 expression correlates with the decrease in β-cell to α-cell ratio.6 It is therefore at least a possibility that miR-375 contributes to the pathogenicity of diabetes by decreasing insulin secretion in β-cells,4 and by decreasing insulin levels through the reduction in β-cell numbers.5,6
Dietary Intake is Associated with miR-31 and miR-375 Expression in Patients with Head and Neck Squamous Cell Carcinoma
Published in Nutrition and Cancer, 2022
Tathiany Jéssica Ferreira, Caroline Castro de Araújo, Ana Carolina da Silva Lima, Larissa Morinaga Matida, Ana Flávia Mendes Griebeler, Alexandre Siqueira Guedes Coelho, Antônio Paulo Machado Gontijo, Cristiane Cominetti, Eneida Franco Vêncio, Maria Aderuza Horst
Increased expression of miR-375 has been observed in the plasma of healthy humans after an oral glucose test (25); however, there are no studies assessing HNSCC patients. It is speculated that miR-375 acts as a glucose sensor and regulates insulin secretion and blood glucose. El Ouaamari et al. found that glucose represses the expression of miR-375 in both insulinoma-1E cells (INS-1E) and primary rat islets, although the precise mechanism remains unclear (26). Keller et al. showed that miR-375 is transcriptionally repressed by the cAMP-dependent protein kinase (PKA) pathway, an important modulator of glucose homeostasis. The authors believe that cAMP and glucose share some downstream signaling pathways for PKA in the regulation of miR-375 (27). However, it is not known whether the PKA pathway is responsible for the deregulation of miR-375 in cancer. Our results reinforce the negative relationship between sugar consumption and the expression of miR-375 in HNSCC, but no studies explaining this association were found.
MiRNA-375 inhibits retinoblastoma progression through targeting ERBB2 and inhibiting MAPK1/MAPK3 signalling pathway
Published in Cutaneous and Ocular Toxicology, 2022
Lei Liu, Chunlin Xiao, Qiuyun Sun
In previous studies, numerous miRNAs such as miR-488, miR-137, and miR-4319, have been found to take part in the progression of RB32–34. These observations have attracted intense investigation into miRNA-based therapies for RB. In particular, miR-375 is a well-known cancer-related miRNA which has become the hotspot of current studies. For example, miR-375 suppressed the tumorigenesis of colorectal cancer35. Another study showed that up-regulation of miR-375 inhibited the proliferation and invasion of glioblastoma36. More importantly, Venkatesan N. et al discovered that miR-375 was down-regulated in RB37. This is in line with the results of the present study which showed that miR-375 was down-regulated in RB. Moreover, it was demonstrated that miR-375 was significantly correlated with the differentiation, N classification, and largest tumour base. Furthermore, up-regulation of miR-375 suppressed RB cell viability, invasion, and migration.