BACKGROUNDEnterovirus71 (EV71), the major cause of hand, foot, and-mouth disease (HFMD), has increasingly become a public health challenge. Type I interferons (IFNs) can regulate innate and adaptive immune responses to pathogens. MicroRNAs (miRNAs) play regulatory roles in host innate immune responses to viral infections. However, the roles of miR-103 and miR-107 in EV71 infection remain unclear.METHODSQuantitative real-time polymerase chain reaction (qRT-PCR) was employed to determine the expression of miR-103, miR-107, suppressor of cytokine signaling 3 (SOCS3), VP1, IFN-α, and IFN-β. Virus titers were measured by 50% tissue culture infectious dose (TCID₅₀) assay. Western blot assay was conducted to detect the protein levels of VP1, IFN-α, IFN-β, SOCS3, signal transducer and activator of transcription 3 (STAT3), and phospho-STAT3 (p-STAT3). Immunofluorescence assay was used to detect the protein level of VP1. The concentrations of IFN-α and IFN-β were examined by Enzyme-linked immunosorbent assay (ELISA). The interaction between SOCS3 and miR-103/miR-107 was predicted by starBase and verified by dual-luciferase reporter assay and RNA pull-down assay.RESULTSMiR-103 and miR-107 were downregulated and SOCS3 was upregulated in serum from patients with EV71 and EV71-infected cells. Overexpression of miR-103 and miR-107 repressed EV71 replication by inhibiting EV71 titers and VP1 expression. Moreover, upregulation of miR-103 and miR-107 enhanced EV71-triggered the production of type I IFNs. In addition, miR-103 and miR-107 directly targeted SOCS3, and SOCS3 upregulation reversed the effects of miR-103 and miR-107 on EV71 replication and type I IFN response. Importantly, miR-103 and miR-107 increased STAT3 phosphorylation by targeting SOCS3 after EV71 infection.CONCLUSIONMiR-103 and miR-107 suppressed EV71 replication and increased the production of type I IFNs by regulating SOCS3/STAT3 pathway, which might provide a novel strategy for developing effective antiviral therapy.

01 Jan 2020·Journal of Clinical Laboratory AnalysisQ4 · MEDICINE

An investigation of microRNA‐103 and microRNA‐107 as potential blood‐based biomarkers for disease risk and progression of Alzheimer's disease

Q4 · MEDICINE

ArticleOA

Author: Chen, Chunyan ; Wang, Jie ; Zhang, Yun

AbstractBackgroundThis study aimed to assess the correlation of circulating microRNA‐103 (miR‐103) and microRNA‐107 (miR‐107) with disease risk and cognitive impairment of Alzheimer's disease (AD).MethodsPlasma samples from 120 AD patients, 120 Parkinson's disease (PD) patients (served as disease control), and 120 healthy controls were collected for miR‐103 and miR‐107 detections using real‐time quantitative polymerase chain reaction. Mini‐Mental State Examination (MMSE) score was documented and was used to accordingly assess the dementia severity.ResultsmiR‐103 expression was decreased in AD patients compared with PD patients and healthy controls, and receiver operating characteristic (ROC) curve analyses illustrated that it was able to differentiate AD patients from PD patients and healthy controls. Additionally, miR‐103 positively correlated with MMSE score and negatively correlated with dementia severity in AD patients. miR‐107 expression was lower in AD patients compared with healthy controls but similar between AD patients and PD patients, and ROC curve analyses revealed that it was able to differentiate AD patients from healthy controls but not AD patients from PD patients. miR‐107 was positively correlated with MMSE score and negatively correlated with dementia severity in AD patients, while the correlation coefficient of miR‐107 with MMSE score was lower than that of miR‐103 with MMSE score. Besides, miR‐103 was positively correlated with miR‐107 in AD patients, PD patients, and healthy controls.ConclusionmiR‐103 may be a better choice than miR‐107 to serve as a potential biomarker for disease risk and disease progression of AD.

01 Mar 1995·European Journal of ImmunologyQ3 · MEDICINE

The distribution of CD10 (NEP 24.11, CALLA) in humans and mice is similar in non‐lymphoid organs but differs within the hematopoietic system: absence on murine T and B lymphoid progenitors

Q3 · MEDICINE

Article

Author: Ellis L. Reinherz ; Susan L. Kalled ; Niranjan Siva ; Harald Stein

AbstractPrior studies in the human have implied an important function for CD10 (CALLA, neutral endopeptidase 24.11) in early lymphoid development. To examine the role of this ectoenzyme in an experimental system, a rat mAb specific for mouse CD10, termed R103, was generated. Immunohistological and flow cytometric analyses indicate that the distribution of CD10 in non‐lymphoid anatomical compartments is virtually identical in human and mouse. However, CD10 expression within the hematopoietic system is strikingly different. In contrast to human spleen, lymph node and thymus, the corresponding mouse organs contain no detectable CD10+ cells. Mouse granulocytes, unlike human granulocytes, also lack CD10 expression. Five‐color flow cytometric studies of adult bone marrow (BM) from C57BL/6 and BALB/c mice with mAb specific for CD43, B220, HSA, BP‐1 and immunoglobulin M fail to detect any significant number of CD10+ cells at pro‐B, pre‐B or B cell stages. In addition, lymphoid cells in both (rIL‐7) independent and rIL‐7‐dependent in vitro pro‐B cell cultures lack CD10 expression. Consistent with this result, CD10 mRNA is not detected. Unlike the AA4.1+ population from day 13 and 14 fetal liver, the CD10+ subset is unable to reconstitute T and B lymphoid compartments in RAG‐2−/− mice. Nevertheless, mouse CD10 is readily found on BM stromal elements known to support early B lineage lymphoid development. Given the common expression of CD10 on human and mouse BM stromal elements, this enzyme may have an important function in the stromal cell‐dependent phase of hematopoiesis.

100 Deals associated with ABS-103

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Indication	Highest Phase	Country/Location	Organization	Date
Migraine Disorders	Phase 2	US	QHSLab, Inc.	-
Epilepsy	Preclinical	US	QHSLab, Inc.	-
Epilepsy	Preclinical	US	Abbott Laboratories (Philippines), Inc.	-
Bipolar Disorder	Discovery	US	QHSLab, Inc.	-
Migraine Disorders	Discovery	US	Abbott Laboratories (Philippines), Inc.	-

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