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Transcriptome Dynamics of the Stomatal Lineage: Birth, Amplification, and Termination of a Self-Renewing Population

DEVELOPMENTAL CELL 2015年第1期33卷 107-118页

作者： Adrian, Jessika Chang, Jessica Ballenger, Catherine E. Bargmann, Bastiaan O. R. Alassimone, Julien Davies, Kelli A. Lau, On Sun Matos, Juliana L. Hachez, Charles Lanctot, Amy Vaten, Anne Birnbaum, Kenneth D. Bergmann, Dominique C. Stanford Univ Dept Biol Stanford CA 94305 USA NYU Dept Biol Ctr Genom & Syst Biol New York NY 10003 USA Stanford Univ Howard Hughes Med Inst Stanford CA 94305 USA

Developmental transitions can be described in terms of morphology and the roles of individual genes, but also in terms of global transcriptional and epigenetic changes. Temporal dissections of transcriptome changes, however, are rare for intact, developing tissues. We used RNA sequencing and microarray platforms to quantify gene expression from labeled cells isolated by fluorescence-activated cell sorting to generate cell-type-specific transcriptomes during development of an adult stem-cell lineage in the Arabidopsis leaf. We show that regulatory modules in this early lineage link cell types that had previously been considered to be under separate control and provide evidence for recruitment of individual members of gene families for different developmental decisions. Because stomata are physiologically important and because stomatal lineage cells exhibit exemplary division, cell fate, and cell signaling behaviors, this dataset serves as a valuable resource for further investigations of fundamental developmental processes.

关键词： EPIGENETICS RNA-seq microarray technology GENE expression FLOW cytometry STOMATA CELL determination CELL differentiation

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A Longitudinal Biomarker for the Extent of Skin Disease in Patients With Diffuse Cutaneous Systemic Sclerosis

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ARTHRITIS & RHEUMATOLOGY 2015年第11期67卷 3004-3015页

作者： Rice, Lisa M. Ziemek, Jessica Stratton, Eric A. McLaughlin, Sarah R. Padilla, Cristina M. Mathes, Allison L. Christmann, Romy B. Stifano, Giuseppina Browning, Jeffrey L. Whitfield, Michael L. Spiera, Robert F. Gordon, Jessica K. Simms, Robert W. Zhang, Yuqing Lafyatis, Robert Boston Univ Sch Med Boston MA 02118 USA Geisel Sch Med Dartmouth Univ Med Sch Hanover NH USA Hosp Special Surg New York NY 10021 USA

Objective. To define a pharmacodynamic biomarker based on gene expression in skin that would provide a biologic measure of the extent of disease in patients with diffuse cutaneous systemic sclerosis (dcSSc) and could be used to monitor skin disease longitudinally. Methods. Skin biopsy specimens obtained from a cohort of patients with dcSSc (including longitudinal specimens) were analyzed by microarray. Expression of genes correlating with the modified Rodnan skin thickness score (MRSS) were examined for change over time using a NanoString platform, and a generalized estimating equation (GEE) was used to define and validate longitudinally measured pharmacodynamic biomarkers composed of multiple genes. Results. microarray analysis of genes parsed to include only those correlating with the MRSS revealed prominent clusters of profibrotic/transforming growth factor beta-regulated, interferon-regulated/proteasome, macrophage, and vascular marker genes. Using genes changing longitudinally with the MRSS, we defined 2 multigene pharmacodynamic biomarkers. The first was defined mathematically by applying a GEE to longitudinal samples. This modeling method selected cross-sectional THBS1 and longitudinal THBS1 and MS4A4A. The second model was based on a weighted selection of genes, including additional genes that changed statistically significantly over time: CTGF, CD163, CCL2, and WIF1. In an independent validation data set, biomarker levels calculated using both models correlated highly with the MRSS. Conclusion. Skin gene expression can be used effectively to monitor changes in SSc skin disease over time. We implemented 2 relatively simple models on a NanoString platform permitting highly reproducible assays that can be applied directly to samples from patients or collected as part of clinical trials.

关键词： SYSTEMIC scleroderma DIAGNOSIS THERAPEUTIC use of biochemical markers ACADEMIC medical centers BIOPSY CONFIDENCE intervals CORRELATION (Statistics) PATIENT monitoring PUBLIC health surveillance REGRESSION analysis FINANCING of research STATISTICS INTER-observer reliability microarray technology GENE expression profiling

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BRIEF REPORT Defining the Nasal Transcriptome in Granulomatosis With Polyangiitis (Wegener's)

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ARTHRITIS & RHEUMATOLOGY 2015年第8期67卷 2233-2239页

作者： Grayson, Peter C. Steiling, Katrina Platt, Michael Berman, Jeffrey S. Zhang, Xiaohui Xiao, Ji Alekseyev, Yuriy O. Liu, Gang Monach, Paul A. Kaplan, Mariana J. Spira, Avrum Merkel, Peter A. NIAMSD NIH Bethesda MD 20892 USA Boston Univ Boston MA 02215 USA Univ Penn Philadelphia PA 19104 USA

Objective. To determine whether disease processes related to granulomatosis with polyangiitis (Wegener's) (GPA) are reflected in gene expression profiles of the nasal mucosa. Methods. Nasal brushings of the inferior turbinate were obtained from 32 patients with GPA (10 with active nasal disease, 13 with prior nasal disease, and 9 with no history of nasal disease) and a composite comparator group with and without inflammatory nasal disease (12 healthy people, 15 with sarcoidosis, and 8 with allergic rhinitis). Differential gene expression was assessed between subgroups of GPA and comparators. Results. A total of 339 genes were differentially expressed between the GPA and comparator groups (absolute fold change >1.5;false discovery rate <0.05). Top canonical pathways up-regulated in nasal brushings from patients with GPA included granulocyte adhesion and diapedesis (P=8.6(-22)), agranulocyte adhesion and diapedesis (P=1.3(-14)), IL10 signaling (P=3.0(-11)), LXR/RXR activation (P=4.3(-11)), and TREM1 signaling (P=9.0(-11)). A set of genes differentially expressed in GPA independently of nasal disease activity status included genes related to epithelial barrier integrity (fibronectin 1, desmosomal proteins) and several matricellular proteins (e.g., osteonectin, osteopontin). Significant overlap of differentially expressed genes was observed between active and prior nasal disease GPA subgroups. Peripheral blood neutrophil and mononuclear gene expression levels associated with GPA were similarly altered in the nasal gene expression profiles of patients with active or prior nasal disease. Conclusion. Profiling the nasal transcriptome in GPA reveals gene expression signatures related to innate immunity, inflammatory cell chemotaxis, extracellular matrix composition, and epithelial barrier integrity. Thus, airway-based expression profiling is feasible and informative in GPA.

关键词： SINUSITIS PROGNOSIS WEGENER'S granulomatosis NOSE diseases ACADEMIC medical centers IMMUNITY POLYMERASE chain reaction REGRESSION analysis FINANCING of research REVERSE transcriptase polymerase chain reaction microarray technology GENE expression profiling

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Myofibroblasts in Murine Cutaneous Fibrosis Originate From Adiponectin-Positive Intradermal Progenitors

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ARTHRITIS & RHEUMATOLOGY 2015年第4期67卷 1062-1073页

作者： Marangoni, Roberta Goncalves Korman, Benjamin D. Wei, Jun Wood, Tammara A. Graham, Lauren V. Whitfield, Michael L. Scherer, Philipp E. Tourtellotte, Warren G. Varga, John Northwestern Univ Feinberg Sch Med Chicago IL 60611 USA Geisel Sch Med Dartmouth Sch Med Hanover NH USA Univ Texas SW Med Ctr Dallas Dallas TX 75390 USA

Objective. Accumulation of myofibroblasts in fibrotic skin is a hallmark of systemic sclerosis (SSc;scleroderma), but the origins of these cells remain unknown. Because loss of intradermal adipose tissue is a consistent feature of cutaneous fibrosis, we sought to examine the hypothesis that myofibroblasts populating fibrotic dermis derive from adipocytic progenitors. Methods. We performed genetic fate mapping studies to investigate the loss of intradermal adipose tissue and its potential role in fibrosis in mice with bleomycin-induced scleroderma. Modulation of adipocytic phenotypes ex vivo was investigated in adipose tissue-derived cells in culture. Results. A striking loss of intradermal adipose tissue and its replacement with fibrous tissue were consistently observed in mice with bleomycin-induced fibrosis. Loss of adipose tissue and a decline in the expression of canonical adipogenic markers in lesional skin preceded the onset of dermal fibrosis and expression of fibrogenic markers. Ex vivo, subcutaneous adipocytes were driven by transforming growth factor to preferentially undergo fibrogenic differentiation. Cell fate mapping studies in mice with the adiponectin promoter-driven Cre recombinase transgenic construct indicated that adiponectin-positive progenitors that are normally confined to the intradermal adipose tissue compartment were distributed throughout the lesional dermis over time, lost their adipocytic markers, and expressed myofibroblast markers in bleomycin-treated mice. Conclusion. These observations establish a novel link between intradermal adipose tissue loss and dermal fibrosis and demonstrate that adiponectin-positive intradermal progenitors give rise to dermal myofibroblasts. Adipose tissue loss and adipocyte-myofibroblast transition might be primary events in the pathogenesis of cutaneous fibrosis that represent novel potential targets for therapeutic intervention.

关键词： ACADEMIC medical centers ANALYSIS of variance ANIMAL experimentation BIOLOGICAL models IMMUNOHISTOCHEMISTRY MICE POLYMERASE chain reaction FINANCING of research STATISTICS SYSTEMIC scleroderma T-test (Statistics) WESTERN immunoblotting DATA analysis FIBROSIS DATA analysis software microarray technology ADIPONECTIN MANN Whitney U Test

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Transcriptomic Analysis of Human Primary Bronchial Epithelial Cells after Chloropicrin Treatment

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CHEMICAL RESEARCH IN TOXICOLOGY 2015年第10期28卷 1926-1935页

作者： Pesonen, Maija Storvik, Markus Kokkola, Tarja Rysa, Jaana Vahakangas, Kirsi Pasanen, Markku Univ Eastern Finland Fac Hlth Sci Sch Pharm Toxicol Kuopio 70211 Finland Univ Eastern Finland Pharmaceut Chem Kuopio 70211 Finland Ctr Mil Med Finnish Def Forces Res & Dev Helsinki 00301 Finland

Chloropicrin is a vaporizing toxic irritant that poses a risk to human health if inhaled, but the mechanism of its toxicity in the respiratory tract is poorly understood. Here, we exposed human primary bronchial epithelial cells (HBEpC) to two concentrations of chloropicrin (10-50 mu M) for 6 or 48 h and used genomic microarray, flow cytometry, and TEM-analysis to monitor cellular responses to the exposures. The overall number of differentially expressed transcripts with a fold-change > +/- 2 compared to controls increased with longer exposure times. The initial response was activation of genes with a higher number of up- (512 by 10 mu M and 408 by 40 mu M chloropicrin) rather than down-regulated transcripts (40 by 10 mu M and 215 by 40 mu M chloropicrin) at 6 h seen with both exposure concentrations. The number of down-regulated transcripts, however, increased with the exposure time. The differentially regulated transcripts were further examined for enriched Gene Ontology Terms (GO) and KEGG-pathways. According to this analysis, the "ribosome" and "oxidative phosphorylation" were the KEGG-pathways predominantly affected by the exposure. The predominantly affected (GO) biological processes were "protein metabolic process" including "translation," "cellular protein complex assembly," and "response to unfolded protein." Furthermore, the top pathways, "NRF2-activated oxidative stress" and "Ala-receptor signaling," were enriched in our data sets by IPA-analysis. Real time qPCR assay of six selected genes agreed with the microarray analysis. In addition, chloropicrin exposure increased the numbers of late S and/or G2/M-phase cells as analyzed by flow cytometry and induced autophagy as revealed by electron microscopy. The targets identified are critical for vital cellular functions reflecting acute toxic responses and are potential causes for the reduced viability of epithelial cells after chloropicrin exposure.

关键词： EPITHELIAL cells BRONCHI -- Physiology CHLOROPICRIN PUBLIC health microarray technology ACUTE toxicity testing

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Concurrent Whole-Genome Haplotyping and Copy-Number Profiling of Single Cells

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AMERICAN JOURNAL OF HUMAN GENETICS 2015年第6期96卷 894-912页

作者： Esteki, Masoud Zamani Dimitriadou, Eftychia Mateiu, Ligia Melotte, Cindy Van der Aa, Niels Kumar, Parveen Das, Rakhi Theunis, Koen Cheng, Jiqiu Legius, Eric Moreau, Yves Debrock, Sophie D'Hooghe, Thomas Verdyck, Pieter De Rycke, Martine Sermon, Karen Vermeesch, Joris R. Voet, Thierry Katholieke Univ Leuven Ctr Human Genet Univ Hosp Leuven Dept Human Genet B-3000 Leuven Belgium Katholieke Univ Leuven Dept Elect Engn ESAT STADIUS B-3000 Leuven Belgium Univ Hosp Gasthuisberg Leuven Univ Fertil Ctr B-3000 Leuven Belgium Univ Ziekenhuis Brussel Ctr Med Genet B-1090 Brussels Belgium Vrije Univ Brussel Res Grp Reprod & Genet REGE B-1090 Brussels Belgium Welcome Trust Sanger Inst Single Cell Genom Ctr Hinxton CB10 1SA Cambs England

Methods for haplotyping and DNA copy-number typing of single cells are paramount for studying genomic heterogeneity and enabling genetic diagnosis. Before analyzing the DNA of a single cell by microarray or next-generation sequencing, a whole-genome amplification (WGA) process is required, but it substantially distorts the frequency and composition of the cell's alleles. As a consequence, haplotyping methods suffer from error-prone discrete SNP genotypes (AA, AB, BB) and DNA copy-number profiling remains difficult because true DNA copy-number aberrations have to be discriminated from WGA artifacts. Here, we developed a single-cell genome analysis method that reconstructs genome-wide haplotype architectures as well as the copy-number and segregational origin of those haplotypes by employing phased parental genotypes and deciphering WGA-distorted SNP B-allele fractions via a process we coin haplarithmisis. We demonstrate that the method can be applied as a generic method for preimplantation genetic diagnosis on single cells biopsied from human embryos, enabling diagnosis of disease alleles genome wide as well as numerical and structural chromosomal anomalies. Moreover, meiotic segregation errors can be distinguished from mitotic ones.

关键词： GENE amplification microarray technology HAPLOTYPES HUMAN genome DNA copy number variations CHROMOSOME segregation

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Malondialdehyde-Acetaldehyde Adducts and Anti-Malondialdehyde-Acetaldehyde Antibodies in Rheumatoid Arthritis

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ARTHRITIS & RHEUMATOLOGY 2015年第3期67卷 645-655页

作者： Thiele, Geoffrey M. Duryee, Michael J. Anderson, Daniel R. Klassen, Lynell W. Mohring, Stephen M. Young, Kathleen A. Benissan-Messan, Dathe Sayles, Harlan Dusad, Anand Hunter, Carlos D. Sokolove, Jeremy Robinson, William H. O'Dell, James R. Nicholas, Anthony P. Tuma, Dean J. Mikuls, Ted R. VA Nebraska Western Iowa Hlth Care Syst Omaha NE USA Univ Nebraska Med Ctr Omaha NE USA VA Palo Alto Hlth Care Syst Palo Alto CA USA Stanford Univ Palo Alto CA 94304 USA Univ Alabama Birmingham Birmingham AL USA

Objective. Malondialdehyde-acetaldehyde (MAA) adducts are a product of oxidative stress associated with tolerance loss in several disease states. This study was undertaken to investigate the presence of MAA adducts and circulating anti-MAA antibodies in patients with rheumatoid arthritis (RA). Methods. Synovial tissue from patients with RA and patients with osteoarthritis (OA) were examined for the presence of MAA-modified and citrullinated proteins. Anti-MAA antibody isotypes were measured in RA patients (n = 1,720) and healthy controls (n = 80) by enzyme-linked immunosorbent assay. Antigen-specific anti-citrullinated protein antibodies (ACPAs) were measured in RA patients using a multiplex antigen array. Anti-MAA isotype concentrations were compared in a subset of RA patients (n = 80) and matched healthy controls (n = 80). Associations of anti-MAA antibody isotypes with disease characteristics, including ACPA positivity, were examined in all RA patients. Results. Expression of MAA adducts was increased in RA synovial tissue compared to OA synovial tissue, and colocalization with citrullinated proteins was found. Increased levels of anti-MAA antibody isotypes were observed in RA patients compared to controls (P < 0.001). Among RA patients, anti-MAA antibody isotypes were associated with seropositivity for ACPAs and rheumatoid factor (P < 0.001) in addition to select measures of disease activity. Higher anti-MAA antibody concentrations were associated with a greater number of positive antigen-specific ACPA analytes (expressed at high titer) (P < 0.001) and a higher ACPA score (P < 0.001), independent of other covariates. Conclusion. MAA adduct formation is increased in RA and appears to result in robust antibody responses that are strongly associated with ACPAs. These results support speculation that MAA formation may be a cofactor that drives tolerance loss, resulting in the autoimmune responses characteristic of RA.

关键词： THERAPEUTIC use of proteins RHEUMATOID arthritis diagnosis NEEDS assessment (Medical care) METHODOLOGY ALDEHYDES ANTIGENS ARTHRITIS ENZYME-linked immunosorbent assay IMMUNOGLOBULINS IMMUNOHISTOCHEMISTRY RHEUMATOID arthritis RHEUMATOLOGY SYNOVIAL membranes DATA analysis BODY mass index microarray technology DESCRIPTIVE statistics

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MicroRNA Expression Profiling and DNA Methylation Signature for Deregulated MicroRNA in Cutaneous T-Cell Lymphoma

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JOURNAL OF INVESTIGATIVE DERMATOLOGY 2015年第4期135卷 1128-1137页

作者： Sandoval, Juan Diaz-Lagares, Angel Salgado, Rocio Servitje, Octavio Climent, Fina Ortiz-Romero, Pablo L. Perez-Ferriols, Amparo Garcia-Muret, Maria P. Estrach, Teresa Garcia, Mar Nonell, Lara Esteller, Manel Pujol, Ramon M. Espinet, Blanca Gallardo, Fernando Bellvitge Biomed Res Inst IDIBELL Canc Epigenet & Biol Program PEBC Barcelona Spain Hosp Mar Serv Patol Lab Citogenet Mol Barcelona 08003 Spain Hosp Univ Bellvitge Serv Dermatol & Patol Barcelona Spain Univ Complutense Madrid Hosp 12 Octubre Serv Dermatol Madrid Spain Hosp Gen Valencia Serv Dermatol Valencia Spain Hosp Santa Creu & Sant Pau Serv Dermatol Barcelona Spain Univ Barcelona Hosp Clin IDIBAPS Serv Dermatol Barcelona Spain IMIM Hosp Mar Med Res Inst Serv Anal Microarrays Barcelona Spain Univ Barcelona Sch Med Dept Physiol Sci 2 Barcelona Spain ICREA Barcelona Spain Univ Autonoma Barcelona Serv Dermatol Hosp Mar E-08193 Barcelona Spain IMIM Hosp Mar Med Res Inst Canc Res Program Barcelona Spain

MicroRNAs usually regulate gene expression negatively, and aberrant expression has been involved in the development of several types of cancers. microarray profiling of microRNA expression was performed to define a microRNA signature in a series of mycosis fungoides tumor stage (MFt, n=21) and CD30+ primary cutaneous anaplastic large cell lymphoma (CD30+ cALCL, n=11) samples in comparison with inflammatory dermatoses (ID, n=5). Supervised clustering confirmed a distinctive microRNA profile for cutaneous T-cell lymphoma (CTCL) with respect to ID. A 40 microRNA signature was found in MFt including upregulated onco-microRNAs (miR-146a, miR-142-3p/5p, miR-21, miR-181a/b, and miR-155) and downregulated tumor-suppressor microRNAs (miR-200ab/429 cluster, miR-10b, miR-193b, miR-141/200c, and miR-23b/27b). Regarding CD30+ cALCL, 39 differentially expressed microRNAs were identified. Particularly, overexpression of miR-155, miR-21, or miR-142-3p/5p and downregulation of the miR-141/200c clusters were observed. DNA methylation in microRNA gene promoters, as expression regulatory mechanism for deregulated microRNAs, was analyzed using Infinium 450K array and approximately one-third of the differentially expressed microRNAs showed significant DNA methylation differences. Two different microRNA methylation signatures for MFt and CD30+ cALCL were found. Correlation analysis showed an inverse relationship for microRNA promoter methylation and microRNA expression. These results reveal a subgroup-specific epigenetically regulated microRNA signatures for MFt and CD30+ cALCL patients.

关键词： T-cell lymphoma RESEARCH MICRORNA GENETIC transcription DNA methylation GENETIC regulation microarray technology

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MiR-200c regulates ROS-induced apoptosis in murine BV-2 cells by targeting FAP-1

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SPINAL CORD 2015年第3期53卷 182-189页

作者： Yu, D. S. Lv, G. Mei, X. F. Cao, Y. Wang, Y. F. Wang, Y. S. Bi, Y. L. Liaoning Med Univ Affiliated Hosp 1 Dept Orthopaed Jinzhou 121001 Peoples R China China Med Univ Affiliated Hosp 1 Dept Orthopaed Shenyang 110001 Peoples R China

Objective: Reactive oxygen species (ROS) are significantly upregulated after spinal cord injury (SCI). MicroRNAs (miRNAs) are reported to be widely involved in regulating gene expression. This paper aims to explore the correlation between ROS-induced cell apoptosis and abnormal miRNA expression after SCI. Methods: To profile the expression of miRNAs after SCI, miRNA microarray was applied and the result was verified by reverse transcription quantitative PCR (RT-qPCR). ROS production following H2O2 stimulation was examined using dihydroethidium staining and flow cytometry. The levels of miR-200c after H2O2 treatment were determined using RT-qPCR. Cell viability and apoptosis were examined in murine BV-2 cells transfected with miR-200c mimics, inhibitor or negative control. Immunofluorescence and western blot were used to further explore the effects of miR-200c on Fas-associated phosphatase-1 (FAP-1) expression. Results: MiR-200c was showed to be significantly increased after SCI by miRNA microassay and RT-qPCR. ROS production enhanced miR-200c expression in a dose-dependent manner and induced significant apoptosis in BV-2 cells. The upregulation of miR-200c reduced cell viability and induced BV-2 cell apoptosis. MiR-200c negatively regulated the expression of FAP-1, thereby inducing FAS signaling-induced apoptosis. RT-qPCR analysis showed that the FAP-1-targeting small interfering RNA (siRNA) did not affect the level of miR-200c in murine BV-2 cells. In addition, suppression of FAP-1 by siRNA promoted apoptosis, even in cells that were co-transfected with the miR-200c inhibitor. Conclusions: The current data suggested that miR-200c contributes to apoptosis in murine BV-2 cells by regulating the expression of FAP-1. This proposes a therapeutic target for enhancing neural cell functional recovery after SCI.

关键词： ACTIVE oxygen ANALYSIS of variance ANIMAL experimentation APOPTOSIS CELL culture CELL physiology FLOW cytometry FLUORESCENT antibody technique GENE expression HYDROGEN peroxide MICE PHOSPHATASES POLYMERASE chain reaction RESEARCH -- Finance RNA SPINAL cord -- Wounds & injuries STATISTICS WESTERN immunoblotting DATA analysis OXIDATIVE stress DATA analysis -- Software microarray technology DESCRIPTIVE statistics

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Hairless Up-Regulates Tgf-2 Expression via Down-Regulation of miR-31 in the Skin of "Hairpoor" (Hr^Hp) Mice

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JOURNAL OF CELLULAR PHYSIOLOGY 2015年第9期230卷 2075-2085页

作者： Kim, Bong-Kyu Yoon, Sungjoo Kim Catholic Univ Korea Dept Med Life Sci Seoul 137701 South Korea

Hairless (HR) has been shown to regulate hair follicle (HF) morphogenesis and hair cycling. The Hr mutant hair loss mouse referred to as hairpoor (Hr(Hp)) displays overexpression of the HR protein through translational derepression. In this study, we found that 64 miRNAs were differentially expressed between the skin of Hr(Hp)/Hr(Hp) and wild type mice at P7 using miRNA-microarray analysis and miR-31 displayed the most reduced expression in Hr(Hp)/Hr(Hp) skin. In vivo observation and investigation using an in vitro reporter expression system revealed that miR-31 and pri-miR-31 were consistently down-regulated in the HR over-expressed condition. In addition, we found that the transforming growth factor 2 (Tgf-2), a known catagen inducer, is the putative target of miR-31. Furthermore, Tgf-2 level was also increased in HR over-expressed keratinocyte and Hr(Hp)/Hr(Hp) mice. These study results suggest that HR controls Tgf-2 expression via regulation of miR-31, thus causing abnormal hair cycle in Hr(Hp)/Hr(Hp) mice. J. Cell. Physiol. 230: 2075-2085, 2015. (c) 2015 Wiley Periodicals, Inc.

关键词： HAIR follicles DOWN-regulation (Biology) MICRORNA MORPHOGENESIS OVEREXPRESSION (Genetics) microarray technology MICE as laboratory animals

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