• adjuvants
• biodistribution
• mRNA vaccines
• microRNA

• gene expression regulation
• maize
• microRNA
• ribosome
• ribosome profiling
• translation

• Zea mays/genetics
• Zea mays/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Gene Expression Regulation, Plant
• RNA, Plant/genetics
• Protein Biosynthesis/genetics
• Ribonuclease III/genetics
• Ribonuclease III/metabolism
• Mutation
• Plant Proteins/genetics
• Plant Proteins/metabolism
• RNA, Messenger/genetics
• RNA, Messenger/metabolism

• IOS-1148971 Division of Integrative Organismal Systems

• Epigenetics
• Geroprotector
• Senescence
• Skin Aging
• Traditional Chinese Medicine

• Humans
• Epigenesis, Genetic/drug effects
• Skin Aging/drug effects
• Skin Aging/genetics
• Animals
• Skin/metabolism
• Skin/drug effects
• Medicine, Chinese Traditional/methods
• Protective Agents/pharmacology

• NF-kB signaling pathway
• cingulin
• claudin
• dysbiosis
• gut permeability
• mRNA sequencing
• neuroinflammation
• occludin
• tight junctions

• Animals
• Cattle
• Female
• Male
• Mice
• Pregnancy
• Colostrum
• Intestinal Mucosa/metabolism
• Mice, Transgenic
• Tight Junctions/metabolism
• Transcriptome
• Haptoglobins/genetics
• Protein Precursors/genetics

• Atheroma
• Chemotaxis
• MMPs
• MSC
• MicroRNA

• Mice
• Animals
• Humans
• MicroRNAs/genetics
• Plaque, Atherosclerotic
• Atherosclerosis/genetics
• Cytokines
• Immunologic Factors
• Mesenchymal Stem Cells

• M/SABX/BA002 to C.R. German Federal Ministry of Defense
• RI 808/6-1 to C.R. Deutsche Forschungsgemeinschaft
• Sonderforschungsbereich 1123 project B10 to A.B. and TRR267-A02 to C.W.
• Deutsches Zentrum für Herz-Kreislauf-Forschung Junior Research Group Grant
• ERC AdG 692511 to C.W. European Research Council

• N-Cadherin
• Zeb1
• cardiac mesenchymal cells
• cell adhesion
• homing
• miR-200c/429

• SDF-1
• bone marrow stromal cells
• miRNA

Bone marrow-derived human mesenchymal stem cells (hMSCs) are recruited to damaged or inflamed tissues where they contribute to tissue repair. This multi-step process involves chemokine-directed invasion of hMSCs and on-site release of factors that influence target cells or tumor tissues. However, the underlying molecular mechanisms are largely unclear. Previously, we described that microRNA let-7f controls hMSC differentiation. Here, we investigated the role of let-7f in chemotactic invasion and paracrine anti-tumor effects. Incubation with stromal cell-derived factor-1α (SDF-1α) or inflammatory cytokines upregulated let-7f expression in hMSCs. Transfection of hMSCs with let-7f mimics enhanced CXCR4-dependent invasion by augmentation of pericellular proteolysis and release of matrix metalloproteinase-9. Hypoxia-induced stabilization of the hypoxia-inducible factor 1 alpha in hMSCs promoted cell invasion via let-7f and activation of autophagy. Dependent on its endogenous level, let-7f facilitated hMSC motility and invasion through regulation of the autophagic flux in these cells. In addition, secreted let-7f encapsulated in exosomes was increased upon upregulation of endogenous let-7f by treatment of the cells with SDF-1α, hypoxia, or induction of autophagy. In recipient 4T1 tumor cells, hMSC-derived exosomal let-7f attenuated proliferation and invasion. Moreover, implantation of 3D spheroids composed of hMSCs and 4T1 cells into a breast cancer mouse model demonstrated that hMSCs overexpressing let-7f inhibited tumor growth in vivo. Our findings provide evidence that let-7f is pivotal in the regulation of hMSC invasion in response to inflammation and hypoxia, suggesting that exosomal let-7f exhibits paracrine anti-tumor effects.

• N6-methyladenosine
• RNA metabolism
• developmental biology
• lineage specification
• miCLIP
• mouse
• skin epithelial morphogenesis

• Adenosine/analogs & derivatives
• Adenosine/chemistry
• Adenosine/genetics
• Adenosine/metabolism
• Animals
• Computational Biology
• Female
• Methylation
• Methyltransferases/metabolism
• Mice
• Organogenesis/genetics
• RNA, Messenger/chemistry
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Signal Transduction
• Skin/chemistry
• Skin/metabolism
• Transcriptome/genetics

• R21 CA224391 NCI NIH HHS
• R01 AR027883 NIAMS NIH HHS
• DRG-2263-16 Damon Runyon Cancer Research Foundation
• R35 NS111631 NINDS NIH HHS
• Howard Hughes Medical Institute
• R01 CA186702 NCI NIH HHS
• National Institutes of Health
• HHMI

• Cell reprogramming
• Clinical-grade
• Induced pluripotent stem cells
• Non-integrative approaches
• Reprogramming factors
• Transgene-free

• Dermal papilla cell
• Hair follicle density
• Ocu-miR-205
• Rex rabbit

• Animals
• Bone Morphogenetic Protein Receptors/genetics
• Bone Morphogenetic Protein Receptors/metabolism
• Gene Products, rex/genetics
• Gene Products, rex/metabolism
• Glycogen Synthase Kinase 3 beta/genetics
• Glycogen Synthase Kinase 3 beta/metabolism
• Hair Follicle/growth & development
• Hair Follicle/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Phosphorylation
• Rabbits
• Receptors, Notch/genetics
• Receptors, Notch/metabolism
• beta Catenin/genetics
• beta Catenin/metabolism

• CARS-43-B-1 Earmarked Fund for Modern Agro-industry Technology Research System
• 31972594 National Natural Science Foundation of China
• SYL2017YSTD11 Funds of Shandong "Double Tops" Programme
• Funds of Shandong “Double Tops” Programme

• Biomarker
• Male
• MicroRNA
• Non-invasive
• Unexplained infertility

• Epidermal stem cells
• Epithelial regeneration
• Signaling pathway
• Wound healing

Vitamins B9 (folate) and B12 act as methyl donors in the one-carbon metabolism which influences epigenetic mechanisms. We previously showed that an embryofetal deficiency of vitamins B9 and B12 in the rat increased brain expression of let-7a and miR-34a microRNAs involved in the developmental control of gene expression. This was reversed by the maternal supply with folic acid (3 mg/kg/day) during the last third of gestation, resulting in a significant reduction of associated birth defects. Since the postnatal brain is subject to intensive developmental processes, we tested whether further folate supplementation during lactation could bring additional benefits. Vitamin deficiency resulted in weaned pups (21 days) in growth retardation, delayed ossification, brain atrophy and cognitive deficits, along with unchanged brain level of let-7a and decreased expression of miR-34a and miR-23a. Whereas maternal folic acid supplementation helped restore the levels of affected microRNAs, it led to a reduction of structural and functional defects taking place during the perinatal/postnatal periods, such as learning/memory capacities. Our data suggest that a gestational B-vitamin deficiency could affect the temporal control of the microRNA regulation required for normal development. Moreover, they also point out that the continuation of folate supplementation after birth may help to ameliorate neurological symptoms commonly associated with developmental deficiencies in folate and B12.

• development
• folate
• maternal folate supplementation during lactation
• microRNAs
• postnatal brain maturation
• vitamin B12

• Aging
• Cellular senescence
• Stem cells
• microRNAs

• EZH2
• Hair follicles stem cells
• Transit-amplifying cells
• Wnt/β-catenin signal
• miR-214

MicroRNAs (miRNAs) are small (18–25 nucleotides), noncoding RNAs that have been identified as potential regulators of bone marrow stromal cell (BMSC) proliferation, differentiation, and musculoskeletal development. Vitamin C is known to play a vital role in such types of biological processes through various different mechanisms by altering mRNA expression. We hypothesized that vitamin C mediates these biological processes partially through miRNA regulation. We performed global miRNA expression analysis on human BMSCs following vitamin C treatment using microarrays containing human precursor and mature miRNA probes. Bioinformatics analyses were performed on differentially expressed miRNAs to identify novel target genes and signaling pathways. Our bioinformatics analysis suggested that the miRNAs may regulate multiple stem cell-specific signaling pathways such as cell adhesion molecules (CAMs), fatty acid biosynthesis and hormone signaling pathways. Furthermore, our analysis predicted novel stem cell proliferation and differentiation gene targets. The findings of the present study demonstrate that vitamin C can have positive effects on BMSCs in part by regulating miRNA expression.

• bone marrow stromal cells
• miRNA
• vitamin C

• Animals
• Biomarkers, Tumor/genetics
• Carcinoma, Squamous Cell/genetics
• Carcinoma, Squamous Cell/pathology
• Humans
• MicroRNAs/genetics
• Prognosis
• Skin Neoplasms/genetics
• Skin Neoplasms/pathology

Intestinal regeneration and tumorigenesis are believed to be driven by intestinal stem cells (ISCs). Elucidating mechanisms underlying ISC activation during regeneration and tumorigenesis can help uncover the underlying principles of intestinal homeostasis and disease including colorectal cancer. Here we show that miR-31 drives ISC proliferation, and protects ISCs against apoptosis, both during homeostasis and regeneration in response to ionizing radiation injury. Furthermore, miR-31 has oncogenic properties, promoting intestinal tumorigenesis. Mechanistically, miR-31 acts to balance input from Wnt, BMP, TGFβ signals to coordinate control of intestinal homeostasis, regeneration and tumorigenesis. We further find that miR-31 is regulated by the STAT3 signaling pathway in response to radiation injury. These findings identify miR-31 as a critical modulator of ISC biology, and a potential therapeutic target for a broad range of intestinal regenerative disorders and cancers.

Cells lining the inner wall of the gut help to absorb nutrients and to protect the body against harmful microbes and substances. Being on the front line of defense means that these cells often sustain injuries. Specialized cells called intestinal stem cells keep the tissues healthy by replacing the damaged and dying cells.

The intestinal stem cells can produce copies of themselves and generate precursors of the gut cells. They also have specific mechanism to protect themselves from cell death. These processes are regulated by different signals that are generated by the cell themselves or the neighboring cells. If these processes get out of control, cells can easily be depleted or develop into cancer cells. Until now, it remained unclear how intestinal stem cells can differentiate between and respond to multiple and simultaneous signals.

It is known that short RNA molecules called microRNA play an important role in the signaling pathways of damaged cells and during cancer development. In the gut, different microRNAs, including microRNA-31,help to keep the gut lining intact. However, previous research has shown that bowel cancer cells also contain high amounts of microRNA-31.

To see whether microRNA-31 plays a role in controlling the signaling systems in intestinal stem cells, Tian, Ma, Lv et al. looked at genetically modified mice that either had too much microRNA-31 or none. Mice with too much microRNA-31 produced more intestinal stem cells and were able to better repair any cell damage. Mice without microRNA-31 gave rise to fewer intestinal stem cellsand had no damage repair, but were able to stop cancer cells in the gut from growing.

The results showed that microRNA-31 in intestinal stem cells helps the cells to divide and to protect themselves from cell death. It controlled and balanced the different types of cell signaling by either repressing or activating various signals. When Tian et al. damaged the stem cells using radiation, the cells increased their microRNA-31 levels as a defense mechanism. This helped the cells to survive and to activate repair mechanisms. Furthermore, Tian et al. discovered that microRNA-31 can enhance the growth of tumors.

These results indicate that microRNA-31 plays an important role both in repairing gut linings and furthering tumor development. A next step will be to see whether cancer cells use microRNA-31 to protect themselves from chemo- and radiation therapy. This could help scientists find new ways to render cancerous cells more susceptible to existing cancer therapies.

• BMP
• Wnt
• colorectal cancer
• developmental biology
• intestinal stem cell
• miR-31
• mouse
• regeneration
• stem cells

• Cancer stem cells (CSCs)
• Cardiovascular diseases (CVDs)
• MicroRNAs
• Regeneration
• Signaling pathway

The micronutrients folate and vitamin B12 are essential for the proper development of the central nervous system, and their deficiency during pregnancy has been associated with a wide range of disorders. They act as methyl donors in the one-carbon metabolism which critically influences epigenetic mechanisms. In order to depict further underlying mechanisms, we investigated the role of let-7 and miR-34, two microRNAs regulated by methylation, on a rat model of maternal deficiency. In several countries, public health policies recommend periconceptional supplementation with folic acid. However, the question about the duration and periodicity of supplementation remains. We therefore tested maternal supply (3 mg/kg/day) during the last third of gestation from embryonic days (E) 13 to 20. Methyl donor deficiency-related developmental disorders at E20, including cerebellar and interhemispheric suture defects and atrophy of selective cerebral layers, were associated with increased brain expression (by 2.5-fold) of let-7a and miR-34a, with subsequent downregulation of their regulatory targets such as Trim71 and Notch signaling partners, respectively. These processes could be reversed by siRNA strategy in differentiating neuroprogenitors lacking folate, with improvement of their morphological characteristics. While folic acid supplementation helped restoring the levels of let-7a and miR-34a and their downstream targets, it led to a reduction of structural and functional defects taking place during the perinatal period. Our data outline the potential role of let-7 and miR-34 and their related signaling pathways in the developmental defects following gestational methyl donor deficiency and support the likely usefulness of late folate supplementation in at risk women.

• Belated folate supplementation
• Brain development
• Epigenetics
• Folate
• Vitamin B12
• microRNAs

• Gene Expression Profiling
• Gene Expression Regulation
• Gene Regulatory Networks
• Humans
• MicroRNAs/chemistry
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Models, Genetic

• Agence Nationale de la Recherche Investissements d’avenir (FR)
• CEA

• Adeno-associated virus
• Gene therapy
• MicroRNA
• MicroRNA regulation
• MicroRNA target sites
• RNA interference
• Vector targeting
• Viral vectors

• miRNAs
• oral cavity and oropharynx squamous cell carcinoma
• real-time PCR
• stem cell

Bone transplantation is one of the most widely performed clinical procedures. Consequently, bone regeneration using mesenchymal stem cells and tissue engineering strategies is one of the most widely researched fields in regenerative medicine. Recent scientific consensus indicates that a biomimetic approach is required to achieve proper regeneration of any tissue. Exosomes are nanovesicles secreted by cells that act as messengers that influence cell fate. Although exosomal function has been studied with respect to cancer and immunology, the role of exosomes as inducers of stem cell differentiation has not been explored. We hypothesized that exosomes can be used as biomimetic tools for regenerative medicine. In this study we have explored the use of cell-generated exosomes as tools to induce lineage specific differentiation of stem cells. Our results indicate that proosteogenic exosomes isolated from cell cultures can induce lineage specific differentiation of naïve MSCs in vitro and in vivo. Additionally, exosomes can also bind to matrix proteins such as type I collagen and fibronectin enabling them to be tethered to biomaterials. Overall, the results from this study show the potential of cell derived exosomes in bone regenerative medicine and opens up new avenues for future research.

As an actively renewable tissue, changes in skin architecture are subjected to the regulation of stem cells that maintain the population of cells responsible for the formation of epidermal layers. Stems cells retain their self-renewal property and express biomarkers that are unique to this population. However, differential regulation of the biomarkers can initiate the pathway of terminal cell differentiation. Although, pockets of non-clarity in stem cell maintenance and differentiation in skin still exist, the influence of epigenetics in epidermal stem cell functions and differentiation in skin homeostasis and wound healing is clearly evident. The focus of this review is to discuss the epigenetic regulation of confirmed and probable epidermal stem cell biomarkers in epidermal stratification of normal skin and in diseased states. The role of epigenetics in wound healing, especially in diseased states of diabetes and cancer, will also be conveyed.

• biomarkers
• epidermal stem cells
• epigenetics
• microRNA
• skin
• wound healing

• Animals
• Cell Differentiation/genetics
• Cell Lineage/genetics
• Cells, Cultured
• Enteroendocrine Cells/cytology
• Enteroendocrine Cells/metabolism
• Gene Expression Profiling
• Immunohistochemistry
• In Situ Hybridization
• Intestinal Mucosa/cytology
• Intestinal Mucosa/metabolism
• Luminescent Proteins/genetics
• Luminescent Proteins/metabolism
• Male
• Mice, Inbred C57BL
• Mice, Transgenic
• MicroRNAs/genetics
• Microvilli/metabolism
• Reverse Transcriptase Polymerase Chain Reaction

• Hypoxia
• Keratinocyte proliferation and differentiation
• MicroRNA
• Sulfur mustard
• Wound healing

• Lesch–Nyhan disease (LND)
• MicroRNAs
• Therapeutic discovery
• Transcription regulation

miRNAs, a unique class of endogenous noncoding RNAs, are highly conserved across species, repress gene translation upon binding to mRNA, and thereby influence many biological processes. As such, they have been recently recognized as regulators of virtually all aspects of cardiac biology, from the development and cell lineage specification of different cell populations within the heart to the survival of cardiomyocytes under stress conditions. Various miRNAs have been recently established as powerful mediators of distinctive aspects in many cardiac disorders. For instance, acute myocardial infarction induces cardiac tissue necrosis and apoptosis but also initiates a pathological remodelling response of the left ventricle that includes hypertrophic growth of cardiomyocytes and fibrotic deposition of extracellular matrix components. In this regard, recent findings place various miRNAs as unquestionable contributing factors in the pathogenesis of cardiac disorders, thus begging the question of whether miRNA modulation could become a novel strategy for clinical intervention. In the present review, we aim to expose the latest mechanistic concepts regarding miRNA function within the context of CVD and analyse the reported roles of specific miRNAs in the different stages of left ventricular remodelling as well as their potential use as a new class of disease-modifying clinical options.

High-throughput sequencing (HTS) has become a powerful tool for the detection of and sequence characterization of microRNAs (miRNA) and other small RNAs (sRNA). Unfortunately, the use of HTS data to determine the relative quantity of different miRNAs in a sample has been shown to be inconsistent with quantitative PCR and Northern Blot results. Several recent studies have concluded that the major contributor to this inconsistency is bias introduced during the construction of sRNA libraries for HTS and that the bias is primarily derived from the adaptor ligation steps, specifically where single stranded adaptors are sequentially ligated to the 3’ and 5’-end of sRNAs using T4 RNA ligases. In this study we investigated the effects of ligation bias by using a pool of randomized ligation substrates, defined mixtures of miRNA sequences and several combinations of adaptors in HTS library construction. We show that like the 3’ adaptor ligation step, the 5’ adaptor ligation is also biased, not because of primary sequence, but instead due to secondary structures of the two ligation substrates. We find that multiple secondary structural factors influence final representation in HTS results. Our results provide insight about the nature of ligation bias and allowed us to design adaptors that reduce ligation bias and produce HTS results that more accurately reflect the actual concentrations of miRNAs in the defined starting material.

• Animals
• Computational Biology
• Genomic Library
• High-Throughput Nucleotide Sequencing/statistics & numerical data
• Humans
• Mice
• MicroRNAs/chemistry
• MicroRNAs/genetics
• Nucleic Acid Conformation
• RNA Ligase (ATP)
• RNA, Small Untranslated/chemistry
• RNA, Small Untranslated/genetics
• Rats
• Selection Bias
• Sequence Analysis, RNA/statistics & numerical data
• Viral Proteins

miRNA-214 regulates hair follicle development and cycling by targeting β-catenin and thereby modulating Wnt pathway transduction.

Skin development is governed by complex programs of gene activation and silencing, including microRNA-dependent modulation of gene expression. Here, we show that miR-214 regulates skin morphogenesis and hair follicle (HF) cycling by targeting β-catenin, a key component of the Wnt signaling pathway. miR-214 exhibits differential expression patterns in the skin epithelium, and its inducible overexpression in keratinocytes inhibited proliferation, which resulted in formation of fewer HFs with decreased hair bulb size and thinner hair production. The inhibitory effects of miR-214 on HF development and cycling were associated with altered activities of multiple signaling pathways, including decreased expression of key Wnt signaling mediators β-catenin and Lef-1, and were rescued by treatment with pharmacological Wnt activators. Finally, we identify β-catenin as one of the conserved miR-214 targets in keratinocytes. These data provide an important foundation for further analyses of miR-214 as a key regulator of Wnt pathway activity and stem cell functions during normal tissue homeostasis, regeneration, and aging.

MiRNAs are key regulators of gene expression. By binding to many genes, they create a complex network of gene co-regulation. Here, using a network-based approach, we identified miRNA hub groups by their close connections and common targets. In one cluster containing three miRNAs, miR-612, miR-661 and miR-940, the annotated functions of the co-regulated genes suggested a role in small GTPase signalling. Although the three members of this cluster targeted the same subset of predicted genes, we showed that their overexpression impacted cell fates differently. miR-661 demonstrated enhanced phosphorylation of myosin II and an increase in cell invasion, indicating a possible oncogenic miRNA. On the contrary, miR-612 and miR-940 inhibit phosphorylation of myosin II and cell invasion. Finally, expression profiling in human breast tissues showed that miR-940 was consistently downregulated in breast cancer tissues

• dental
• hypselodont
• renewal
• tissue regeneration
• tooth

• Animals
• Biological Evolution
• Cells, Cultured
• Epithelial Cells/metabolism
• Gene Expression Regulation, Developmental
• Incisor/cytology
• Incisor/physiology
• Phylogeny
• Regeneration
• Rodentia/genetics
• Rodentia/physiology
• Signal Transduction
• Stem Cells/cytology
• Stem Cells/metabolism

• DP2 OD007191 NIH HHS
• DP2-OD00719 NIH HHS
• R01 DE021420 NIDCR NIH HHS
• F30 DE022482 NIDCR NIH HHS
• F32-DE023705 NIDCR NIH HHS
• R01-DE021420 NIDCR NIH HHS
• F32 DE023705 NIDCR NIH HHS
• F30-DE022482 NIDCR NIH HHS

• invasion
• microRNA-145
• migration
• oral cancer cell
• proliferation

• Animals
• Cell Proliferation
• Gene Deletion
• Mice
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Phosphatidylinositol 3-Kinases/genetics
• Phosphatidylinositol 3-Kinases/metabolism
• Signal Transduction/physiology
• Skin/cytology
• Skin/metabolism
• Stem Cells/cytology
• Stem Cells/metabolism

• R01GM083300 NIGMS NIH HHS
• R01 AR066703 NIAMS NIH HHS
• T32 GM008759 NIGMS NIH HHS
• R00AR054704 NIAMS NIH HHS
• R01 AR059697 NIAMS NIH HHS
• R00 AR054704 NIAMS NIH HHS
• R01 GM083300 NIGMS NIH HHS
• P30 CA008748 NCI NIH HHS
• P30 CA046934 NCI NIH HHS
• R01AR059697 NIAMS NIH HHS
• T32 GM142607 NIGMS NIH HHS

Current research in pulmonary pathology has focused on inflammatory reactions initiated by immunological responses to allergens and irritants. In addition to these biochemical stimuli, physical forces also play an important role in regulating the structure, function, and metabolism of the lung. Hyperstretch of lung tissues can contribute to the inflammatory responses in asthma, but the mechanisms of mechanically induced inflammation in the lung remain unclear. Our results demonstrate that excessive stretch increased the secretion of inflammatory cytokines by human bronchial epithelial cells (hBECs), including IL-8. This increase of IL-8 secretion was due to an elevated microRNA-155 (miR-155) expression, which caused the suppression of Src homology 2 domain–containing inositol 5-phosphatase 1 (SHIP1) production and the subsequent activation of JNK signaling. In vivo studies in our asthmatic mouse model also showed such changes in miR-155, IL-8, and SHIP1 expressions that reflect inflammatory responses. Co-culture with human mesenchymal stem cells (hMSCs) reversed the stretch-induced hBEC inflammatory responses as a result of IL-10 secretion by hMSCs to down-regulate miR-155 expression in hBECs. In summary, we have demonstrated that mechanical stretch modulates the homeostasis of the hBEC secretome involving miR-155 and that hMSCs can be used as a potential therapeutic approach to reverse bronchial epithelial inflammation in asthma.

• Animals
• Asthma/chemically induced
• Asthma/metabolism
• Bronchi/metabolism
• Cell Line
• Coculture Techniques
• Cytokines/metabolism
• Disease Models, Animal
• Gene Expression
• Humans
• Inflammation/metabolism
• Inflammation Mediators/metabolism
• Inositol Polyphosphate 5-Phosphatases
• Lung/metabolism
• Lung/pathology
• Mechanical Phenomena
• Mesenchymal Stem Cells/metabolism
• Mice
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Ovalbumin/adverse effects
• Paracrine Communication
• Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases
• Phosphoric Monoester Hydrolases/genetics
• Phosphoric Monoester Hydrolases/metabolism
• Respiratory Mucosa/metabolism

• R01 HL108735 NHLBI NIH HHS
• AI 38425 NIAID NIH HHS
• R37 AI038425 NIAID NIH HHS
• R01 AI072115 NIAID NIH HHS
• AI 70535 NIAID NIH HHS
• HL108735 NHLBI NIH HHS
• R01 AI038425 NIAID NIH HHS
• AI 72115 NIAID NIH HHS
• R01 HL106579 NHLBI NIH HHS
• U19 AI070535 NIAID NIH HHS
• HL106579 NHLBI NIH HHS