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Nature communications
2022 Apr 19
Wang, G;Wen, B;Deng, Z;Zhang, Y;Kolesnichenko, OA;Ustiyan, V;Pradhan, A;Kalin, TV;Kalinichenko, VV;
PMID: 35440116 | DOI: 10.1038/s41467-022-29746-y
Pulmonary endothelial progenitor cells (EPCs) are critical for neonatal lung angiogenesis and represent a subset of general capillary cells (gCAPs). Molecular mechanisms through which EPCs stimulate lung angiogenesis are unknown. Herein, we used single-cell RNA sequencing to identify the BMP9/ACVRL1/SMAD1 pathway signature in pulmonary EPCs. BMP9 receptor, ACVRL1, and its downstream target genes were inhibited in EPCs from Foxf1WT/S52F mutant mice, a model of alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV). Expression of ACVRL1 and its targets were reduced in lungs of ACDMPV subjects. Inhibition of FOXF1 transcription factor reduced BMP9/ACVRL1 signaling and decreased angiogenesis in vitro. FOXF1 synergized with ETS transcription factor FLI1 to activate ACVRL1 promoter. Nanoparticle-mediated silencing of ACVRL1 in newborn mice decreased neonatal lung angiogenesis and alveolarization. Treatment with BMP9 restored lung angiogenesis and alveolarization in ACVRL1-deficient and Foxf1WT/S52F mice. Altogether, EPCs promote neonatal lung angiogenesis and alveolarization through FOXF1-mediated activation of BMP9/ACVRL1 signaling.
Nature communications
2022 Mar 31
Kemenesi, G;Tóth, GE;Mayora-Neto, M;Scott, S;Temperton, N;Wright, E;Mühlberger, E;Hume, AJ;Suder, EL;Zana, B;Boldogh, SA;Görföl, T;Estók, P;Lanszki, Z;Somogyi, BA;Nagy, Á;Pereszlényi, CI;Dudás, G;Földes, F;Kurucz, K;Madai, M;Zeghbib, S;Maes, P;Vanmechelen, B;Jakab, F;
PMID: 35361761 | DOI: 10.1038/s41467-022-29298-1
Some filoviruses can be transmitted to humans by zoonotic spillover events from their natural host and filovirus outbreaks have occured with increasing frequency in the last years. The filovirus Lloviu virus (LLOV), was identified in 2002 in Schreiber's bats (Miniopterus schreibersii) in Spain and was subsequently detected in bats in Hungary. Here we isolate infectious LLOV from the blood of a live sampled Schreiber's bat in Hungary. The isolate is subsequently sequenced and cultured in the Miniopterus sp. kidney cell line SuBK12-08. It is furthermore able to infect monkey and human cells, suggesting that LLOV might have spillover potential. A multi-year surveillance of LLOV in bats in Hungary detects LLOV RNA in both deceased and live animals as well as in coupled ectoparasites from the families Nycteribiidae and Ixodidae. This correlates with LLOV seropositivity in sampled Schreiber's bats. Our data support the role of bats, specifically Miniopterus schreibersii as hosts for LLOV in Europe. We suggest that bat-associated parasites might play a role in the natural ecology of filoviruses in temperate climate regions compared to filoviruses in the tropics.
The Journal of clinical investigation
2022 Apr 19
Duhen, R;Fesneau, O;Samson, KA;Frye, AK;Beymer, M;Rajamanickam, V;Ross, D;Tran, E;Bernard, B;Weinberg, AD;Duhen, T;
PMID: 35439168 | DOI: 10.1172/JCI156821
CD4 T helper (Th) cells play a key role in orchestrating immune responses, but the identity of the CD4 Th cells involved in the anti-tumor immune response remains to be defined. We analyzed the immune cell infiltrates of head and neck squamous cell carcinoma and colorectal cancers and identified a subset of CD4 Th cells distinct from FOXP3+ regulatory T cells that co-express PD-1 and ICOS. These tumor-infiltrating CD4 Th cells (CD4 Th TIL) have a tissue-resident memory phenotype, are present in MHC class II-rich areas and proliferate in the tumor suggesting local antigen recognition. The T-cell receptor repertoire of the PD-1+ICOS+ CD4 Th TIL is oligoclonal, with T-cell clones expanded in the tumor, but present at low frequencies in the periphery. Finally, these PD-1+ICOS+ CD4 Th TIL were shown to recognize both tumor-associated antigens and tumor-specific neoantigens. Our findings provide an approach for isolating tumor-reactive CD4 Th TIL directly ex vivo that will help define their role in the anti-tumor immune response and potentially improve future adoptive T-cell therapy approaches.
The Journal of clinical investigation
2022 Apr 15
Zou, HY;Guo, L;Zhang, B;Chen, S;Wu, XR;Liu, XD;Xu, XY;Li, BY;Chen, S;Xu, NJ;Sun, S;
PMID: 35426376 | DOI: 10.1172/JCI149160
Mushroom spine loss and calcium dyshomeostasis are early hallmark events of age-related neurodegeneration, such as Alzheimer's disease (AD), that are connected with neuronal hyperactivity in early pathology of cognitive brain areas. However, it remains elusive how these key events are triggered at the molecular level for the neuronal abnormality that occurs at the initial stage of disease. Here, we identify downregulated miR-339-5p and its upregulated target protein, neuronatin (Nnat), in cortex neurons from the presenilin-1 M146V knockin (PSEN1-M146V KI) mouse model of familial AD (FAD). Inhibition of miR-339-5p or overexpression of Nnat recapitulates spine loss and endoplasmic reticulum calcium overload in cortical neurons with the PSEN1 mutation. Conversely, either overexpression of miR-339-5p or knockdown of Nnat restores spine morphogenesis and calcium homeostasis. We used fiber photometry recording during the object-cognitive process to further demonstrate that the PSEN1 mutant causes defective habituation in neuronal reaction in the retrosplenial cortex and that this can be rescued by restoring the miR-339-5p/Nnat pathway. Our findings thus reveal crucial roles of the miR-339-5p/Nnat pathway in FAD that may serve as potential diagnostic and therapeutic targets for early pathogenesis.
The Journal of experimental medicine
2022 May 02
Churchill, MJ;du Bois, H;Heim, TA;Mudianto, T;Steele, MM;Nolz, JC;Lund, AW;
PMID: 35353138 | DOI: 10.1084/jem.20211830
Lymphatic vessels are often considered passive conduits that flush antigenic material, pathogens, and cells to draining lymph nodes. Recent evidence, however, suggests that lymphatic vessels actively regulate diverse processes from antigen transport to leukocyte trafficking and dietary lipid absorption. Here we tested the hypothesis that infection-induced changes in lymphatic transport actively contribute to innate host defense. We demonstrate that cutaneous vaccinia virus infection by scarification activates dermal lymphatic capillary junction tightening (zippering) and lymph node lymphangiogenesis, which are associated with reduced fluid transport and cutaneous viral sequestration. Lymphatic-specific deletion of VEGFR2 prevented infection-induced lymphatic capillary zippering, increased fluid flux out of tissue, and allowed lymphatic dissemination of virus. Further, a reduction in dendritic cell migration to lymph nodes in the absence of lymphatic VEGFR2 associated with reduced antiviral CD8+ T cell expansion. These data indicate that VEGFR2-driven lymphatic remodeling is a context-dependent, active mechanism of innate host defense that limits viral dissemination and facilitates protective, antiviral CD8+ T cell responses.
Science advances
2022 Apr 08
Tay, JK;Zhu, C;Shin, JH;Zhu, SX;Varma, S;Foley, JW;Vennam, S;Yip, YL;Goh, CK;Wang, Y;Loh, KS;Tsao, SW;Le, QT;Sunwoo, JB;West, RB;
PMID: 35394843 | DOI: 10.1126/sciadv.abh2445
Nasopharyngeal cancer (NPC) is an Epstein-Barr virus (EBV)-positive epithelial malignancy with an extensive inflammatory infiltrate. Traditional RNA-sequencing techniques uncovered only microenvironment signatures, while the gene expression of the tumor epithelial compartment has remained a mystery. Here, we use Smart-3SEQ to prepare transcriptome-wide gene expression profiles from microdissected NPC tumors, dysplasia, and normal controls. We describe changes in biological pathways across the normal to tumor spectrum and show that fibroblast growth factor (FGF) ligands are overexpressed in NPC tumors, while negative regulators of FGF signaling, including SPRY1, SPRY2, and LGALS3, are down-regulated early in carcinogenesis. Within the NF-κB signaling pathway, the critical noncanonical transcription factors, RELB and NFKB2, are enriched in the majority of NPC tumors. We confirm the responsiveness of EBV-positive NPC cell lines to targeted inhibition of these pathways, reflecting the heterogeneity in NPC patient tumors. Our data comprehensively describe the gene expression landscape of NPC and unravel the mysteries of receptor tyrosine kinase and NF-κB pathways in NPC.
Science advances
2022 Apr 01
Kato, T;Radicioni, G;Papanikolas, MJ;Stoychev, GV;Markovetz, MR;Aoki, K;Porterfield, M;Okuda, K;Barbosa Cardenas, SM;Gilmore, RC;Morrison, CB;Ehre, C;Burns, KA;White, KK;Brennan, TA;Goodell, HP;Thacker, H;Loznev, HT;Forsberg, LJ;Nagase, T;Rubinstein, M;Randell, SH;Tiemeyer, M;Hill, DB;Kesimer, M;O'Neal, WK;Ballard, ST;Freeman, R;Button, B;Boucher, RC;
PMID: 35363522 | DOI: 10.1126/sciadv.abm9718
Cystic fibrosis (CF) is characterized by abnormal transepithelial ion transport. However, a description of CF lung disease pathophysiology unifying superficial epithelial and submucosal gland (SMG) dysfunctions has remained elusive. We hypothesized that biophysical abnormalities associated with CF mucus hyperconcentration provide a unifying mechanism. Studies of the anion secretion-inhibited pig airway model of CF revealed elevated SMG mucus concentrations, osmotic pressures, and SMG mucus accumulation. Human airway studies revealed hyperconcentrated CF SMG mucus with raised osmotic pressures and cohesive forces predicted to limit SMG mucus secretion/release. Using proline-rich protein 4 (PRR4) as a biomarker of SMG secretion, CF sputum proteomics analyses revealed markedly lower PRR4 levels compared to healthy and bronchiectasis controls, consistent with a failure of CF SMGs to secrete mucus onto airway surfaces. Raised mucus osmotic/cohesive forces, reflecting mucus hyperconcentration, provide a unifying mechanism that describes disease-initiating mucus accumulation on airway surfaces and in SMGs of the CF lung.
Nature metabolism
2022 Apr 01
Haddad-Tóvolli, R;Ramírez, S;Muñoz-Moreno, E;Milà-Guasch, M;Miquel-Rio, L;Pozo, M;Chivite, I;Altirriba, J;Obri, A;Gómez-Valadés, AG;Toledo, M;Eyre, E;Bortolozzi, A;Valjent, E;Soria, G;Claret, M;
PMID: 35379970 | DOI: 10.1038/s42255-022-00557-1
Preparation for motherhood requires a myriad of physiological and behavioural adjustments throughout gestation to provide an adequate environment for proper embryonic development1. Cravings for highly palatable foods are highly prevalent during pregnancy2 and contribute to the maintenance and development of gestational overweight or obesity3. However, the neurobiology underlying the distinct ingestive behaviours that result from craving specific foods remain unknown. Here we show that mice, similarly to humans, experience gestational food craving-like episodes. These episodes are associated with a brain connectivity reorganization that affects key components of the dopaminergic mesolimbic circuitry, which drives motivated appetitive behaviours and facilitates the perception of rewarding stimuli. Pregnancy engages a dynamic modulation of dopaminergic signalling through neurons expressing dopamine D2 receptors in the nucleus accumbens, which directly modulate food craving-like events. Importantly, persistent maternal food craving-like behaviour has long-lasting effects on the offspring, particularly in males, leading to glucose intolerance, increased body weight and increased susceptibility to develop eating disorders and anxiety-like behaviours during adulthood. Our results reveal the cognitively motivated nature of pregnancy food cravings and advocates for moderating emotional eating during gestation to prevent deterioration of the offspring's neuropsychological and metabolic health.
Nature metabolism
2022 Mar 01
Wanner, N;Andrieux, G;Badia-I-Mompel, P;Edler, C;Pfefferle, S;Lindenmeyer, MT;Schmidt-Lauber, C;Czogalla, J;Wong, MN;Okabayashi, Y;Braun, F;Lütgehetmann, M;Meister, E;Lu, S;Noriega, MLM;Günther, T;Grundhoff, A;Fischer, N;Bräuninger, H;Lindner, D;Westermann, D;Haas, F;Roedl, K;Kluge, S;Addo, MM;Huber, S;Lohse, AW;Reiser, J;Ondruschka, B;Sperhake, JP;Saez-Rodriguez, J;Boerries, M;Hayek, SS;Aepfelbacher, M;Scaturro, P;Puelles, VG;Huber, TB;
PMID: 35347318 | DOI: 10.1038/s42255-022-00552-6
Extrapulmonary manifestations of COVID-19 have gained attention due to their links to clinical outcomes and their potential long-term sequelae1. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) displays tropism towards several organs, including the heart and kidney. Whether it also directly affects the liver has been debated2,3. Here we provide clinical, histopathological, molecular and bioinformatic evidence for the hepatic tropism of SARS-CoV-2. We find that liver injury, indicated by a high frequency of abnormal liver function tests, is a common clinical feature of COVID-19 in two independent cohorts of patients with COVID-19 requiring hospitalization. Using autopsy samples obtained from a third patient cohort, we provide multiple levels of evidence for SARS-CoV-2 liver tropism, including viral RNA detection in 69% of autopsy liver specimens, and successful isolation of infectious SARS-CoV-2 from liver tissue postmortem. Furthermore, we identify transcription-, proteomic- and transcription factor-based activity profiles in hepatic autopsy samples, revealing similarities to the signatures associated with multiple other viral infections of the human liver. Together, we provide a comprehensive multimodal analysis of SARS-CoV-2 liver tropism, which increases our understanding of the molecular consequences of severe COVID-19 and could be useful for the identification of organ-specific pharmacological targets.
Biological psychiatry
2022 Apr 05
Varodayan, FP;Patel, RR;Matzeu, A;Wolfe, SA;Curley, DE;Khom, S;Gandhi, PJ;Rodriguez, L;Bajo, M;D'Ambrosio, S;Sun, H;Kerr, TM;Gonzales, RA;Leggio, L;Natividad, LA;Haass-Koffler, CL;Martin-Fardon, R;Roberto, M;
PMID: 35430085 | DOI: 10.1016/j.biopsych.2022.02.006
Alcohol use disorder (AUD) is a leading preventable cause of death. The central amygdala (CeA) is a hub for stress and AUD, while dysfunction of the noradrenaline stress system is implicated in AUD relapse.Here, we investigated whether alcohol (ethanol) dependence and protracted withdrawal alter noradrenergic regulation of the amygdala in rodents and humans. Male adult rats were housed under control conditions, subjected to chronic intermittent ethanol vapor exposure to induce dependence, or withdrawn from chronic intermittent ethanol vapor exposure for 2 weeks, and ex vivo electrophysiology, biochemistry (catecholamine quantification by high-performance liquid chromatography), in situ hybridization, and behavioral brain-site specific pharmacology studies were performed. We also used real-time quantitative polymerase chain reaction to assess gene expression of α1B, β1, and β2 adrenergic receptors in human postmortem brain tissue from men diagnosed with AUD and matched control subjects.We found that α1 receptors potentiate CeA GABAergic (gamma-aminobutyric acidergic) transmission and drive moderate alcohol intake in control rats. In dependent rats, β receptors disinhibit a subpopulation of CeA neurons, contributing to their excessive drinking. Withdrawal produces CeA functional recovery with no change in local noradrenaline tissue concentrations, although there are some long-lasting differences in the cellular patterns of adrenergic receptor messenger RNA expression. In addition, postmortem brain analyses reveal increased α1B receptor messenger RNA in the amygdala of humans with AUD.CeA adrenergic receptors are key neural substrates of AUD. Identification of these novel mechanisms that drive alcohol drinking, particularly during the alcohol-dependent state, supports ongoing new medication development for AUD.
Biological Psychiatry
2022 May 01
Fox, M;Wulff, A;Franco, D;Choi, E;Engeln, M;Calarco, C;Turner, M;Chandra, R;Thompson, S;Ament, S;Lobo, M;
| DOI: 10.1016/j.biopsych.2022.02.052
Background Opioid withdrawal or abstinence generates a negative affective state and causes dendritic atrophy in nucleus accumbens (NAc) medium spiny neurons (MSNs). Based on our previous work, we hypothesized that opioid abstinence-induced atrophy is MSN subtype-specific, and blocking the subtype-specific molecular mediators can reverse behavioral changes caused by opioid abstinence. Methods All experiments were conducted in 8-10-week-old mice using sex as a biological variable. Cohorts of n=8-12 per condition were used in behavioral experiments; n=4-5 per condition for morphology or electrophysiology (3-7 cells/mouse); n=24 per condition (4 mice pooled/sample) for molecular biology. We used Cre-dependent viruses to label D1- and D2-MSNs in D1- and A2A-Cre mice for morphology or patch-clamp electrophysiology. We used D1- or A2A-Cre x RiboTag mice for subtype-specific RNAseq. We analyzed RNAseq data with weighted correlation network analysis (WGCNA), then further validated identified genes with Nanostring and RNAscope. Results Mice exhibit increased social-withdrawal and stress-like behaviors after fentanyl abstinence. (2-way ANOVA P=0.018). Stress-like behaviors after abstinence were associated with reduced dendritic complexity of NAc D1-, but not D2-MSNs (D1: 2-way ANOVA P=0.0129, D2:P=0.97). Using WGCNA, we identified 11 MSN subtype-specific gene networks altered by fentanyl abstinence (P0.05). Conclusions Our findings indicate fentanyl abstinence causes unique structural, functional, and molecular changes in NAc D1-MSNs that can be targeted to alleviate abstinence-induced dendritic atrophy and stress-like behaviors.
Allergy
2022 Mar 27
Schaller, T;Märkl, B;Claus, R;Sholl, L;Hornick, JL;Giannetti, MP;Schweizer, L;Mann, M;Castells, M;
PMID: 35340030 | DOI: 10.1111/all.15293
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| Description | ||
|---|---|---|
| sense Example: Hs-LAG3-sense | Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe. | |
| Intron# Example: Mm-Htt-intron2 | Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection | |
| Pool/Pan Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G) | A mixture of multiple probe sets targeting multiple genes or transcripts | |
| No-XSp Example: Hs-PDGFB-No-XMm | Does not cross detect with the species (Sp) | |
| XSp Example: Rn-Pde9a-XMm | designed to cross detect with the species (Sp) | |
| O# Example: Mm-Islr-O1 | Alternative design targeting different regions of the same transcript or isoforms | |
| CDS Example: Hs-SLC31A-CDS | Probe targets the protein-coding sequence only | |
| EnEm | Probe targets exons n and m | |
| En-Em | Probe targets region from exon n to exon m | |
| Retired Nomenclature | ||
| tvn Example: Hs-LEPR-tv1 | Designed to target transcript variant n | |
| ORF Example: Hs-ACVRL1-ORF | Probe targets open reading frame | |
| UTR Example: Hs-HTT-UTR-C3 | Probe targets the untranslated region (non-protein-coding region) only | |
| 5UTR Example: Hs-GNRHR-5UTR | Probe targets the 5' untranslated region only | |
| 3UTR Example: Rn-Npy1r-3UTR | Probe targets the 3' untranslated region only | |
| Pan Example: Pool | A mixture of multiple probe sets targeting multiple genes or transcripts | |
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