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Biology subjects

Arora, H.

Publications and source records attributed to Arora, H..

11 recordsLinked to original sources

Derivation of functional early gestation decidual natural killer cell subtypes from induced pluripotent stem cells

Abnormal decidual natural killer cell (dNK) function is linked to pregnancy complications occurring in both early and late gestation, including recurrent pregnancy loss, preeclampsia, and preterm birth. Exploration of dNK heterogeneity as it relates to function is an active area of research; however, most of this work has focused on early gestation. Using flow cytometric and transcriptomic single-cell definitions of dNK subtypes, we characterized dNK heterogeneity in term dNK within both chorioamniotic membranes and basal plate. We also applied aptamer-based secretome profiling to first trimester and term dNK, and found dNK-specific proteins - VEGF and PLGF - to be reduced at term. We further determined that, compared to first trimester dNK, term dNK have reduced cytoxicity against target cells. Finally, we applied this knowledge to establish a protocol for differentiation of induced pluripotent stem cells (iPSC) into functional dNK. We found that treatment with TGF{beta} enriched for dNK2 subtype, while inducing dNK markers, CD9 and CD103. We evaluated function using cytokine and degranulation assays, aptamer-based secretome profiling, and cytotoxicity assays. We found that iPSC-dNK are functionally most similar to primary dNK. Further, TGF{beta} iPSC-dNK had reduced GM-CSF in response to PMA/I and increased secretion of VEGF and other first trimester-specific proteins - supportive of a shift towards an early gestation, dNK2-dominant, phenotype. We conclude that changes in dNK function across gestation reflect shifts in dNK subtypes that can be reproducibly derived from iPSC, providing a new method for modeling dNK and laying the foundation for cell-based therapeutics for reproductive disease. Significance StatementAlterations in maternal decidual natural killer cells (dNK) are associated with pregnancy complications - from recurrent pregnancy loss to preeclampsia and preterm birth. We found dNK from different regions of the term placenta to be distinct from peripheral blood NK and early gestation dNK, based on gene and surface marker expression, subtype composition, secretome, and cytotoxicity. We report a novel, reproducible protocol to generate dNK resembling the most abundant dNK subtype in early gestation from induced pluripotent stem cells. Our study lays the foundation for in vitro modeling of the maternal-fetal interface and therapeutic development for reproductive disease.

cell biology↗

Adult-type diffuse gliomas share recurring cell states driven by a common astrocyte-like glioma stem cell population

Adult-type diffuse gliomas are a family of aggressive brain tumours with few effective treatments. Their complex cellular makeup adds to the challenge of finding successful therapies. This intratumoural heterogeneity is fuelled by a subpopulation of glioma stem-like cells (GSCs) that drive tumour growth and resistance to standard treatments. Previous research focused on the three glioma types (astrocytoma, oligodendroglioma, glioblastoma) individually revealed malignant cells mimic the transcriptional profiles of normal brain cell types. Whether these diverse cellular states stem from a shared biological origin is unknown. Here, we show through single-cell RNA sequencing of 40 glioma tumours that all gliomas are described by seven recurring cell states. We also identify a shared astrocyte-like GSC population. Our unique method of identifying GSCs, based on reconstructed tumour phylogenies, repositions astrocyte-like cells at the apex of a differentiation hierarchy in glioma. Our findings indicate the transcriptional heterogeneity observed in gliomas stems from a GSC population recapitulating lineages of healthy adult neural stem cells. These results suggest a shared lineage drives the intratumoural heterogeneity observed in adult-type diffuse gliomas. We anticipate that a deeper understanding of the molecular mechanisms maintaining the GSC state will provide a new framework for future therapeutic development and research into glioma cell biology. HighlightsO_LIRecurring cell states are shared across adult-type diffuse gliomas C_LIO_LIReconstructed tumour phylogenies identify an astrocyte-like glioma stem cell population C_LIO_LITumour subclones are segregated non-randomly across cell states C_LI

cancer biology↗

Protein Translation Dysregulation and Immune Cell Evasion Define Metastatic Clones in HPV-related Cancer of the Oropharynx

Head and neck cancers, representing the seventh most common malignancy globally, have seen a shift in causative factors from traditional smoking and alcohol use to human papillomavirus (HPV) infection, now accounting for up to 80% of oropharyngeal cancers. We identify the cellular and clonal mechanisms underlying immune avoidance and metastasis by analysing single-cell and spatial genomic data from primary and metastatic cancers. We first map the clonal evolution of malignant cells based on the accumulation of mutations. We identify metastasising clones based on mutational similarity scores between cells in the primary and lymph node metastasis. Genomic analysis of metastasising and non-metastasising clones identified virally mediated protein translation relief (P=4.24x10-24) pathway underlying metastatic expansion. We show that in metastatic clones, this process is driven through upregulation of transition-initiating factors, EIF4E (P=1.5x10-13) and EIFG1 (P<2.22x10-16), and suppression of regulatory kinases EIF4EBP1 (P=2.1x10), EIF2AK2 (P<2.22x10-16), and EIF2S1 (P<2.22x10-16). We subsequently identify that metastatic clones have a corresponding downregulation of the JAK/STAT pathway and immunoproteasome genes PSMB8 (P<2.22x10- 16) and PSMB9 (P<2.22x10-16), suggesting these clones escape immune surveillance through decreased INF inflammatory response and antigen presentation. We validate these results using spatial RNA-seq data, where metastatic cancer clones show decreased cell-to-cell interactions with CD4 T-effector memory cells (CD4TEM) (P=0.0077), CD8 T-exhausted cells (CD8Ex) (P=0.0191), and innate lymphoid cells (ILC) (P=0.04). Finally, we demonstrate that the upregulation of cap-independent translational drives cell proliferation in metastatic clones through the expression of translation initiation factors (EIF4G1: P<2.22x10-16). Our results provide evidence of the mechanisms by which virally induced cancer clones lead to advanced disease and poor prognosis in patients.

cancer biology↗

Synthetic Histology Images for Training AI Models: A Novel Approach to Improve Prostate Cancer Diagnosis

Prostate cancer (PCa) poses significant challenges for timely diagnosis and prognosis, leading to high mortality rates and increased disease risk and treatment costs. Recent advancements in machine learning and digital imagery offer promising potential for developing automated and objective assessment pipelines that can reduce human capital and resource costs. However, the reliance of AI models on large amounts of clinical data for training presents a significant challenge, as this data is often biased, lacking diversity, and not readily available. Here we aim to address this limitation by employing customized generative adversarial network (GAN) models to produce high-quality synthetic images of different PCa grades (radical prostatectomy (RP)) and needle biopsies, which were customized to account for the granularity associated with each Gleason grade. The generated images were subjected to multiple rounds of benchmarking, quantifications and quality control assessment before being used to train an AI model (EfficientNet) for grading digital histology images of adenocarcinoma specimens (RP sections) and needle biopsies obtained from the PANDA challenge repository. Validation was performed using the AI model trained with synthetic data to grade digital histology from the cancer genome atlas (TCGA) (RP sections) and needle biopsy data from Radboud University Medical Center and Karolinska Institute. Results demonstrated that the AI model trained with a combination of image patches derived from original and enhanced synthetic images outperformed the model trained with original digital histology images. Together, this study demonstrates the potential of customized GAN models to generate a large cohort of synthetic data that can train AI models to effectively grade PCa specimens. This approach could potentially eliminate the need for extensive clinical data for training any AI model in the domain of digital imagery, leading to cost and time-effective diagnosis and prognosis.

cancer biology↗

An ATP-Binding Cassette Transporter Gene Links Innate and Adaptive Immune Responses

Positive-strand RNA viruses and DNA viruses generate double-stranded RNA (dsRNA) during their replication processes and innate immune responses against viral infections are orchestrated by numerous interferon-stimulating genes, yet the detailed coordination of downstream signaling of anti-viral immune responses is not fully understood. Recent studies suggest 2-5- Oligoadenylate Synthetase 1 (OAS1) may have a protective role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections; however, the mechanism regulating OAS1 remains uninvestigated. Our aim is to understand the regulation of OAS1 and its modulation of RNaseL activity, as this has significant implications for responses to RNA viruses, including Vesicular stomatitis virus (VSV) and SARS-CoV-2. We explore the hypothesis that ABCF1 an ATP-binding cassette family member protein, a key regulator of innate immune responses and macrophage polarization and cytokine storm, play a role in regulating the antiviral responses and downstream dsRNA signaling revealed by measuring responses to the synthetic dsRNA analog termed poly (I:C). We utilize ABCF1 haplo-insufficient mice to discover that ABCF1 modulates the amplitude and frequency of VSV-specific Cytolytic T lymphocyte in anti-viral immune responses and suggests that innate immune responses underpin this process. To understand this mechanism, we describe that ABCF1 interacts with 2-5-oligoadenylate synthetase 1 (OAS1) which in turn modulates essential proteins that leads to the modulation of RNaseL activity via ABCE1. Furthermore, we find that ABCF1 also influences the production of interferon- (IFN-) and interferon-{beta} (IFN-{beta}) in bone marrow-derived macrophages. Overall,, we unexpectedly discovered that ABCF1 acts as a crucial link between innate and adaptive immunity, regulating the development of adaptive Cytolytic T lymphocyte responses and interacting with OAS1, a key regulator of innate immune responses against viral infections. Exploring pharmacological agents that target ABCE1 or ABCF1 may lead to the discovery of novel modalities for countering SARS CoV-2 and other viruses where OAS1 is a crucial innate immune response gene.

immunology↗

Within-subject changes in DNA-methylome profile identify individual signatures of early-life adversity, with a potential to predict neuropsychiatric outcome.

BackgroundAdverse early-life experiences (ELA), including poverty, trauma and neglect, affect a majority of the worlds children. Whereas the impact of ELA on cognitive and emotional health throughout the lifespan is well-established, it is not clear how distinct types of ELA influence child development, and there are no tools to predict for an individual child their vulnerability or resilience to the consequences of ELAs. Epigenetic markers including DNA-methylation profiles of peripheral cells may encode ELA and provide a predictive outcome marker. However, the rapid dynamic changes in DNA methylation in childhood and the inter-individual variance of the human genome pose barriers to identifying profiles predicting outcomes of ELA exposure. Here, we examined the relation of several dimensions of ELA to changes of DNA methylation, using a longitudinal within-subject design and a high threshold for methylation changes in the hope of mitigating the above challenges. MethodsWe analyzed DNA methylation in buccal swab samples collected twice for each of 110 infants: neonatally and at 12 months. We identified CpGs differentially methylated across time, calculated methylation changes for each child, and determined whether several indicators of ELA associated with changes of DNA methylation for individual infants. We then correlated select dimensions of ELA with methylation changes as well as with measures of executive function at age 5 years. We examined for sex differences, and derived a sex-dependent impact score based on sites that most contributed to the methylation changes. FindingsSetting a high threshold for methylation changes, we discovered that changes in methylation between two samples of an individual child reflected age-related trends towards augmented methylation, and also correlated with executive function years later. Among the tested factors and ELA dimensions, including income to needs ratios, maternal sensitivity, body mass index and sex, unpredictability of parental and household signals was the strongest predictor of executive function. In girls, an interaction was observed between a measure of high early-life unpredictability and methylation changes, in presaging executive function. InterpretationThese findings establish longitudinal, within-subject changes in methylation profiles as a signature of some types of ELA in an individual child. Notably, such changes are detectable beyond the age-associated DNA methylation dynamics. Future studies are required to determine if the methylation profile changes identified here provide a predictive marker of vulnerabilities to poorer cognitive and emotional outcomes. FundingSupported by NIH P50 MH096889, a Precision Medicine Initiative grant from the State of California (OPR20141) and the Bren Foundation. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSIdentification of individuals at risk for cognitive and emotional problems is required for targeted interventions. At the population level, experiencing early-life adversity has been consistently linked to an elevated susceptibility to various mental illnesses. However, recent studies have revealed a significant limitation in the ability of early-life adversity to predict individual-level risk, and there is presently no reliable tool available to determine whether a child experiencing adversity will develop future mental health problems. Promising efforts to discover predictive markers by examining DNA methylation in peripheral cells are challenged by extensive genetic and epigenetic population variability and the rapid methylation changes taking place during childhood, rendering the identification of clinically valuable predictive markers a complex endeavor. Added value of this studyThis study examined neurodevelopmental outcomes following several dimensions of ELA, including a recently identified dimension-unpredictability of parental and environmental signals to the child. It demonstrates changes in DNA methylation in children exposed to a spectrum of ELA dimensions and severity using alternative approaches to those used previously: It employs a longitudinal within-subject design, enabling assessment of DNA changes within an individual over time rather than a cross section comparison of different groups, and focuses on the first year of life, an understudied epoch of development. The study uses reduced representation bisulfite sequencing to measure methylation, an approach compromising between targeted sequencing and a whole genome approach, and sets a high threshold for methylation changes, in consideration of the large changes of DNA methylation during childhood. Finally, in accord with emerging discoveries of the differential effects of ELA on males and females, the study uncovers sex-effects arising already before puberty. Implications of all the available evidenceCollectively, our study, together with a robust existing literature (1) identifies early-life unpredictability as an additional determinant of DNA methylation changes, (2) indicates that within-subject changes in methylation profiles of peripheral cells hold promise as precision medicine tools for predicting risk and resilience to the adverse consequences of early-life hardships on mental health, and (3) suggests that sex-differences should be explored even prior to puberty. Our study contributes significantly to the important goal of early identification of predictive "epigenetic scars" caused by adverse early-life experiences. Such markers are required for targeting interventions to those most at need.

neuroscience↗

Phagocytosis in macrophages is regulated by the ATP-binding cassette family gene ABCF1

Phagocytosis is a conserved biological mechanism that is integral to tissue remodeling, clearance of apoptotic cells, and immune defense in animals. Additionally, it serves as a pivotal means of sustenance for diverse unicellular eukaryotes. In the context of mammals, this crucial role is fulfilled by specific cell types such as macrophages, monocytes, dendritic cells, and neutrophils. It is orchestrated by an array of receptors, kinases, cytoskeletal elements, and enzymes, working collaboratively to enable the recognition, engulfment, and internalization of particles. Despite its profound significance, the intricate mechanisms underpinning the regulation of this phenomenon remains enigmatic. In this study, we present compelling evidence indicating the involvement of ABCF1, a member of the ATP-binding cassette family, in the Fc{gamma}RIIA phagocytic pathway. ABCF1s contribution lies in facilitating downstream signal activation through interactions with Src family members and SYK, pivotal players in this cascade. Additionally, our findings highlight ABCF1s essentiality in the biosynthesis of various SFKs (Src family kinases) and MAPKs (mitogen-activated protein kinases). These molecules collectively oversee the orchestration of phagocytic cup formation, a pivotal step governing the engulfment process within macrophages. Consequently, the regulation of ABCF1 presents a potential avenue for modulating phagocytosis, allowing for the precise modulation of this fundamental process to either enhance or attenuate according to the specific physiological demands.

immunology↗

S-nitrosoglutathione Inhibits the Growth of Androgen-Receptor Dependent and Castration Resistant Prostate Cancer by Modulating FOXM1 Signaling

Castration resistant prostate cancer (CRPC) is an advanced form of prostate cancer associated with loss of androgen receptor activity and resistance to AR-targeted therapies. CRPC is often associated with higher metastasis, invasion, and proliferation. Thus, theres a strong need for additional molecular markers in CRPC, and therapies that target them directly. Transcriptomic profiling of prostate cancer patients revealed an upregulated signature specific to high-grade tumors in cell cycle progression, E2F targets, G2M checkpoint, DNA repair, Aurora Kinase B, and FOXM1 pathway. Validation in a separate cohort of neuroendocrine prostate cancer patients, the most resistant and invasive form of CRPC which lacks AR expression, showed CCP signature as a dominant driver gene set for NEPC. Moreover, high expression of mRNA targets in each of these pathways is associated with poor overall survival in NEPC patients. Gene set variation analysis revealed a strong inverse correlation between AR signaling and CCP.31, set of 31 markers associated with high proliferation, and a positive correlation between CCP.31 and NEPC signature. FOXM1, a prioritized candidate in CCP is shown to be upregulated in CRPC cell lines and human clinical sections of Gleason 9 patients. GSNO, a nitric oxide donor, known for its inhibitory effect on cell proliferation and an effective inhibitor of cell cycle checkpoints, was able to reverse CCP signature both in-vitro and in-vivo. GSNO exhibits a dependence on AR signaling in-vitro by showing mild effect on CRPC clones, but successfully inhibits tumor growth of AR-null CRPC xenografts. FOXM1 is also targeted by GSNO in-vivo and in-vitro models of both CRPC and AD prostate cancer. This establishes an important link between androgen receptor status in prostate cancer and proposes nitric oxide donors as therapeutic intervention. GSNO is effective against AR-null castration resistant prostate cancer. SignificanceNitric oxide donor, S-glutathione-transferase inhibits tumor growth of castration resistant prostate cancer, regardless of androgen receptor expression status by targeting FOXM1, a critical regulator of cell cycle progression. O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY

cancer biology↗

One Scaffold - Different Organelles Sensors: pH-Activable Fluorescent Probes for Targeting Live Primary Microglial Cell Organelles

Targeting live cell organelles is important for imaging and to understand and control specific biochemical processes. Typically, fluorescent probes with distinct structural scaffolds have been used for targeting specific cell organelle. Herein, we aimed to design modular one-step synthetic strategies using a common reaction intermediate to develop new lysosomal, mitochondrial and nucleus targeting pH-activable fluorescent probes that are all based on a single boron dipyrromethane analogs. The divergent cell organelle targeting was achieved by synthesizing pH-activable fluorescent probes with specific functional groups changes to the main scaffold resulting in differential fluorescence and pKa. Specifically, we show that the functional group transformation of the same scaffold influences cellular localization and specificity of pH-activable fluorescent probes in live primary microglial cells with pKas ranging from ~4.5-6.0. We introduce a structure-organelle-relationship (SOR) framework targeting the nucleus (NucShine), lysosomes (LysoShine) and mitochondria (MitoShine) in primary mouse microglial cells. This work will result in future applications of SOR beyond imaging to target and control organelle-specific biochemical processes in disease-specific models.

biochemistry↗

S-nitrosoglutathione reductase deficiency causes aberrant placental S-nitrosylation and preeclampsia.

Preeclampsia (PE), a leading cause of maternal and fetal mortality and morbidity, is characterized by an increase in S-nitrosylated (SNO) proteins and reactive oxygen species (ROS), suggesting a pathophysiologic role for dysregulation in nitrosylation and nitrosative stress. Here we show that mice lacking S-nitrosoglutathione reductase (GSNOR-/-), a denitrosylase regulating protein S-nitrosylation, exhibit a PE phenotype, including hypertension, proteinuria, renal pathology, cardiac concentric hypertrophy, decreased placental vascularization, and fetal growth retardation. ROS, nitric oxide (NO) and peroxynitrite levels are elevated. Importantly, mass spectrometry reveals elevated placental SNO-amino acid residues in GSNOR-/- mice. Ascorbate reverses the phenotype except for fetal weight, reduces the difference in the S-nitrosoproteome, and identifies a unique set of SNO-proteins in GSNOR-/- mice. Therefore, deficiency of GSNOR creates dysregulation of placental S-nitrosylation and preeclampsia in mice, which can be rescued by ascorbate. These findings offer valuable insights and therapeutic implications for PE. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/183012v3_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@1baa15corg.highwire.dtl.DTLVardef@1b79fe7org.highwire.dtl.DTLVardef@62f899org.highwire.dtl.DTLVardef@1af0b29_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical Abstract:C_FLOATNO Dysregulation in nitrosylation contributes to nitroso-redox imbalance and nitrosative stress contributing to clinical features of PE including hypertension, proteinuria, concentric hypertrophy in the heart, decrease placental vascularization and fetal growth restriction. Antioxidant treatment rescued the PE-like phenotype in the mother. C_FIG

physiology↗

BjuWRR1, a CC-NB-LRR gene identified in Brassica juncea, confers resistance to white rust caused by Albugo candida

White rust caused by oomycete pathogen Albugo candida is a significant disease of crucifer crops including Brassica juncea (mustard), a major oilseed crop of the Indian subcontinent. Earlier a resistance-conferring locus named AcB1-A5.1 was mapped in an east European gene pool line of B. juncea - Donskaja-IV. This line was tested along with some other lines of B. juncea (AABB), B. rapa (AA) and B. nigra (BB) for resistance to six isolates of A. candida collected from different mustard growing regions of India. Donskaja-IV was found to be completely resistant to all the tested isolates. Sequencing of a BAC spanning the locus AcB1-A5.1 showed the presence of a single CC-NB-LRR protein encoding R gene. The genomic sequence of the putative R gene with its native promoter and terminator was used for the genetic transformation of a susceptible Indian gene pool line Varuna and was found to confer complete resistance to all the isolates. This is the first white rust resistance-conferring gene described from Brassica species and has been named BjuWRR1. Allelic variants of the gene in B. juncea germplasm and orthologues in the Brassicaceae genomes were studied to understand the evolutionary dynamics of the BjuWRR1 gene.\n\nHighlightBjuWRR1, a CNL type R gene, was identified from an east European gene pool line of Brassica juncea and validated for conferring resistance to white rust by genetic transformation.

plant biology↗