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Modi, D.

Publications and source records attributed to Modi, D..

10 recordsLinked to original sources

Real-time, label-free assessment of cell fusion dynamics by high-content imaging

Cell-cell fusion is a fundamental biological process underlying diverse physiological and pathological phenomena, yet its quantitative analysis remains methodologically challenging due to its dynamic, heterogeneous, and multistep nature. Existing approaches to assess fusion largely rely on endpoint assays or manual scoring, limiting temporal resolution, scalability, and reproducibility. Here, we present a label-free, high-content live-cell imaging pipeline for real-time quantification of cell fusion dynamics, developed and validated using trophoblast syncytialization as a model system. The method integrates automated image acquisition with a reproducible, stepwise analysis workflow combining supervised texture-based segmentation, morphology-based measurements, and intensity-independent texture analysis. We define quantitative metrics, including the ratio of total cluster area to the number of detected clusters and cytoplasmic granularity features, that together discriminate bona fide fusion events from non-fusion-related cellular clustering or proliferation. Using canonical pharmacological inducers and inhibitors of fusion, we demonstrate the specificity and sensitivity of these parameters for detecting fusion-associated remodeling over time. We further demonstrate the scalability of the pipeline through high-throughput screening of biologically relevant growth factors, hormones, and inhibitors, enabling classification of modulators based on their independent, synergistic, or antagonistic effects on fusion dynamics. Consistent results obtained in an independent model further support its potential applications to additional fusion systems. By providing a robust, reproducible, and adaptable framework for time-resolved fusion analysis, this methodology bridges the gap between qualitative observation and quantitative kinetic assessment. Thus, the approach could be readily extended to other cell fusion systems following system-specific parameter optimization, offering a versatile platform for both mechanistic studies and discovery-driven screening applications.

developmental biology↗

A Functional Placenta-On-Chip Model For Maternal-Fetal Transport

The human placenta functions as a highly specialised barrier that integrates trophoblast differentiation, endocrine activity, and regulated transport of molecules to sustain fetal development. Experimental interrogation of placental barrier function remains challenging due to limited access to human placental tissue and the complexity of existing in vitro models. Here, we report a static, two-chamber placenta-on-chip platform designed to recapitulate key structural and functional attributes of the human placental barrier within an experimentally accessible format. The device design prioritises open maternal compartmentalisation and diffusion-dominated transport, reflecting the haemochorial nature of human placentation. It also remains compatible with standard multi-well plate formats for parallel experimentation. In this two-chambered device, separated by an extracellular matrix-loaded/coated microporous membrane, the trophoblast supports trophoblast syncytialisation, sustained {beta}-human chorionic gonadotropin secretion, and selective barrier function. The engineered barrier restricts macromolecular transport while permitting controlled diffusion of small solutes. Glucose transport across the device is strongly dependent on cellular configuration, with inclusion of the endothelial layer significantly modulating nutrient flux and yielding fetal-to-maternal glucose ratios comparable to those reported in vivo. The platform further supports directional transfer of urea from the fetal to the maternal compartment, demonstrating bidirectional metabolite exchange relevant to placental waste clearance. Under hyperglycemic conditions, glucose transport across the barrier increases without evidence of barrier breakdown, indicating sensitivity to metabolic perturbation. This scalable design of a placenta-on-chip platform provides a robust framework for studying placental transport, metabolic regulation, and barrier integrity. It offers broad application in placental biology, pregnancy-associated pathologies, and screening for pregnancy-safe drugs.

bioengineering↗

HOXA10 is a Temporal Switch in Controlling Decidual Inflammation and Its Dysregulation is Associated with Early Pregnancy Loss

Successful implantation requires precisely timed endometrial inflammation. Although an initial inflammatory burst is essential for implantation, this response must be rapidly resolved for placentation and pregnancy to progress. The mechanisms that coordinate this temporal switch remain poorly understood. Here, we identify the transcription factor HOXA10 as a key regulator of inflammatory transitions in decidual stromal cells and examine how its dysregulation contributes to implantation failure and early pregnancy loss. In mice, HOXA10 expression decreases transiently at implantation and rises again post-implantation. Silencing HOXA10 in human decidualized stromal cells induced a robust pro-inflammatory state, altered integrin and cytoskeletal gene expression, and impaired stromal substrate adhesion. In non-pregnant Hoxa10 hypomorphs, stromal cells exhibited elevated IL1β and TXNIP, activation of the NLRP3/ASC inflammasome, and dysregulation of receptivity markers. During pregnancy, persistent HOXA10 deficiency prevented the resolution of inflammation, resulting in disorganized decidua, defective placentation, infertility, or progressive reproductive decline. To assess translational relevance, we analyzed publicly available bulk and single-cell RNA-seq datasets from first-trimester human decidua and from women with recurrent pregnancy loss (RPL). Single-cell analysis revealed that HOXA10 is selectively low in inflammatory decidual stromal cell clusters, which display concordant upregulation of IL1B, PYCARD, TXNIP, and inflammasome components. Consistently, both bulk and single-cell datasets from women with RPL showed reduced HOXA10 accompanied by increased inflammatory gene expression. Overall, HOXA10 functions as a temporal switch that enables the initial inflammatory activation required for implantation and subsequently suppresses inflammation to support decidual organization, adhesion, and placentation. Loss of this switch leads to persistent decidual inflammation and is associated with pregnancy loss in both mouse models and humans. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=171 SRC="FIGDIR/small/691844v1_ufig1.gif" ALT="Figure 1"> View larger version (62K): org.highwire.dtl.DTLVardef@ee81b6org.highwire.dtl.DTLVardef@85d84eorg.highwire.dtl.DTLVardef@13c1b6aorg.highwire.dtl.DTLVardef@12bed9b_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

Epithelial to Mesenchymal Transition in the Endometrium Mediated by HOXA10 drives Embryo Implantation

In mammalian reproduction, a significant proportion of embryos fail to implant despite a receptive uterus, suggesting that defects in epithelial remodelling at the embryo-uterine interface contribute to implantation failure. The molecular programs enabling such remodelling remain incompletely understood. Here, we identify a conserved transcriptional circuit involving HOXA10 and TWIST2 that regulates epithelial plasticity in the endometrium via partial epithelial-to-mesenchymal transition (pEMT). HOXA10, a transcription factor essential for uterine receptivity, is specifically downregulated in the luminal epithelium at implantation in mice, hamsters, and monkeys. Integrated CUT&RUN and transcriptomic profiling in human endometrial epithelial cells reveal that HOXA10 directly activates epithelial gene networks and represses mesenchymal programs. HOXA10 loss, both in vitro and in vivo, induces a pEMT state with increased cell motility. Mechanistically, HOXA10 represses TWIST2, a core EMT regulator; its derepression promotes mesenchymal gene expression and epithelial cell displacement. TWIST2 knockdown restores epithelial identity and impairs implantation. These findings establish a mutually antagonistic HOXA10-TWIST2 circuit as a key regulator of pEMT and epithelial remodelling during implantation. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=144 SRC="FIGDIR/small/631632v2_ufig1.gif" ALT="Figure 1"> View larger version (46K): org.highwire.dtl.DTLVardef@1ea7b16org.highwire.dtl.DTLVardef@136f3c5org.highwire.dtl.DTLVardef@be47a8org.highwire.dtl.DTLVardef@5283b2_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

LHX2 in germ cells control tubular organization in the developing mouse testis

In the gonads of mammalian XY embryos, the organization of cords is the hallmark of testis development. This organization is thought to be controlled by interactions of the Sertoli cells, endothelial and interstitial cells with little or no role of germ cells. Challenging this notion, herein we show that the germ cells play an active role in the organization of the testicular tubules. We observed that the LIM-homeobox gene, Lhx2 is expressed in the germ cells of the developing testis between E12.5-E15.5. In Lhx2 knockout-fetal testis there was altered expression of several genes not just in germ cells but also in the supporting (Sertoli) cells, endothelial cells, and interstitial cells. Further, loss of Lhx2 led to disrupted endothelial cell migration and expansion of interstitial cells in the XY gonads. The cords in the developing testis of Lhx2 knockout embryos are disorganized with a disrupted basement membrane. Together, our results show an important role of Lhx2 in testicular development and imply the involvement of germ cells in the tubular organization of the differentiating testis. HighlightO_LILhx2 is expressed in germ cells of developing mouse testis but is dispensable for germ cell and Sertoli cell specification C_LIO_LILoss of Lhx2 disrupts testicular vascularization, leads to the expansion of interstitial cells, and alters the tubular organization C_LIO_LIGerm cells govern the tubular organization in the developing testis C_LI Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=105 SRC="FIGDIR/small/522214v2_ufig1.gif" ALT="Figure 1"> View larger version (38K): org.highwire.dtl.DTLVardef@1a1761dorg.highwire.dtl.DTLVardef@1519f12org.highwire.dtl.DTLVardef@1a263baorg.highwire.dtl.DTLVardef@4167f2_HPS_FORMAT_FIGEXP M_FIG C_FIG

developmental biology↗

The G-protein-coupled estrogen receptor, a gene co-expressed with ERα in breast tumors, is regulated by estrogen-ERα signalling in ERα positive breast cancer cells.

PurposeThe purpose of this study was to assess the relationship between GPER, a seven transmembrane G-protein coupled estrogen receptor, and ER in breast tumors, and to make inroads into the mechanistic basis and clinical significance. MethodsTCGA-BRCA data was mined to examine the relationship between GPER and ER expression. GPER mRNA, and protein expression were analyzed in ER-positive or -negative breast tumors from two cohorts using immunohistochemistry, western blotting, or RT-qPCR. The Kaplan-Meier Plotter was employed for survival analysis. The influence of estrogen in vivo was studied by examining GPER expression levels in estrus or diestrus mouse mammary tissues, and the impact of 17{beta}-estradiol (E2) administration in juvenile or adult mice. The effect of E2, or propylpyrazoletriol (PPT, an ER agonist) stimulation on GPER expression was studied in MCF-7 and T47D cells, with or without tamoxifen or ER knockdown. ER-binding to the GPER locus was explored by analysing ChIP-seq data (ERP000380), in silico prediction of estrogen response elements, and chromatin immunoprecipitation assay. ResultsClinical data revealed significant positive association between GPER and ER expression in breast tumors. The median GPER expression in ER-positive tumors was significantly higher than ER-negative tumors. High GPER expression was significantly associated with longer overall survival of patients with ER-positive tumors. In vivo experiments showed a positive effect of E2 on GPER expression. E2 induced GPER expression in MCF-7 and T47D cells; an effect mimicked by PPT. Tamoxifen or ER-knockdown blocked the induction of GPER. Estrogen-mediated induction was associated with increased ER occupancy in the upstream region of GPER. ConclusionGPER expression is positively associated with ER in breast tumors, and a transcriptional target of the estrogen-ER signalling axis. More in-depth studies are required to establish the significance of GPER-ER co-expression, and their interplay in breast tumor development, progression, and treatment.

cancer biology↗

Loss of HOXA10 causes endometrial hyperplasia progressing to endometrial cancer

Endometrial cancer is the fourth most common malignancy in women and the precursor lesion is endometrial hyperplasia. HOXA10 is a transcription factor that plays key roles in endometrial functions such as the endowment of receptivity, embryo implantation, and trophoblast invasion. Herein, using testicular transgenesis, we developed transgenic mice that expressed an shRNA against HOXA10 and observed that in these animals there was nearly 70% reduction in the expression of HOXA10. We termed these animals as HOXA10 hypomorphs and observed that downregulation of HOXA10 led to the development of endometrial hyperplasia and most animals developed well-differentiated endometrial adenocarcinoma with age. There was an increased proliferation of the uterine glands and stromal cells in the hypomorphs along with a gain of OVGP1 expression and increased levels of ER and ER{beta}. In parallel, there was increased expression of Wnt4 and {beta}-Catenin, SOX9 and YAP1. We propose that chronic reduction in HOXA10 expression disrupts multiple pathways in the uterus that aids in the development of endometrial hyperplasia which progresses to endometrial cancer with age.

cancer biology↗

Lhx2 in germ cells suppresses endothelial cell migration in the developing ovary

LIM-homeobox genes play multiple roles in developmental processes, but their roles in gonad development are not completely understood. Herein, we report that Lhx2, Ils2, Lmx1a, and Lmx1b are expressed in a sexually dimorphic manner in mouse, rat, and human gonads during sex determination. Amongst these, Lhx2 has female biased expression in the developing gonads of species with environmental and genetic modes of sex determination. Single-cell RNAseq analysis revealed that Lhx2 is exclusively expressed in the germ cells of the developing mouse ovaries. To elucidate the roles of Lhx2 in the germ cells, we analyzed the phenotypes of Lhx2 knockout XX gonads. While the gonads developed appropriately in Lhx2 knockout mice and the somatic cells were correctly specified in the developing ovaries, transcriptome analysis revealed enrichment of genes in the angiogenesis pathway. There was an elevated expression of several pro-angiogenic factors in the Lhx2 knockout ovaries. The elevated expression of pro-angiogenic factors was associated with an increase in numbers of endothelial cells in the Lhx2-/-ovaries at E13.5. Gonad recombination assays revealed that the increased numbers of endothelial cells in the XX gonads in absence of Lhx2 was due to ectopic migration of endothelial cells in a cell non-autonomous manner. We also found that, there was increased expression of several endothelial cell-enriched male-biased genes in Lhx2 knockout ovaries. Also, in absence of Lhx2, the migrated endothelial cells formed an angiogenic network similar to that of the wild type testis, although the coelomic blood vessel did not form. Together, our results suggest that Lhx2 in the germ cells is required to suppress vascularization in the developing ovary. These results suggest a need to explore the roles of germ cells in the control of vascularization in developing gonads. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=143 SRC="FIGDIR/small/483280v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@59ca47org.highwire.dtl.DTLVardef@ef193eorg.highwire.dtl.DTLVardef@162651corg.highwire.dtl.DTLVardef@dc3d0f_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightO_LIMultiple LIM-HD genes are expressed in developing gonads during the window of sex determination with Lhx2 having female dominating expression in an evolutionarily conserved manner C_LIO_LILhx2 is expressed in the germ cells of developing mouse ovaries C_LIO_LILoss of Lhx2 in the developing ovaries alters the expression of genes involved in various pathways including angiogenesis C_LIO_LILhx2 in germ cells suppress endothelial cell migration in the developing ovaries C_LI

developmental biology↗

No association of mitochondrial DNA levels in trophectodermal cells with the developmental competence of the blastocyst and pregnancy outcomes

Study questionCan mitochondrial DNA (mtDNA) levels in trophectodermal cells of the blastocyst predict the blastocyst quality, ploidy status, implantation rate and clinical outcomes?\n\nSummary answermtDNA levels in trophectodermal cells of the blastocyst do not associate with the blastocyst quality, ploidy status, implantation potential and clinical outcomes, but can differentiate between aneuploid and euploid blastocysts.\n\nWhat we already knowmtDNA levels in the trophectodermal cells have been suggested to be associated with blastocyst morphology, ploidy and implantation rates, and has been proposed as biomarker to access blastocyst quality and predict clinical outcomes. However, discrepancies exist if mtDNA levels could serve as a marker for the same.\n\nStudy design and durationRetrospective analysis of mtDNA levels in trophectodermal cells obtained from blastocysts undergoing preimplantation genetic testing for aneuploidy (PGT-A) at Craft Hospital & Research Center, Kerala from January 2016-July 2017.\n\nParticipants/materials and methodsStudy included data from 287 blastocyst from (61) couples who underwent PGT-A using next generation sequencing (NGS). Levels of mtDNA in trophectodermal cells of the blastocyst were estimated by the NGS. Comparison of mtDNA levels with maternal age, blastocyst morphology, ploidy status, implantation rates, miscarriage rates and live birth rate was done.\n\nMain resultsThe levels of mtDNA in the trophectoderm of the blastocyst did not correlate with maternal age. There was no significant difference in the mtDNA levels between grade 1 and grade 2 blastocyst. Euploid blastocyst had significantly lower amounts of mtDNA levels in trophectodermal cells of the blastocyst were compared to aneuploid blastocyst. No significant differences were seen between mtDNA levels and implanting and non-implanting blastocysts or those resulted into miscarriage or live birth.\n\nLimitationsThe study is limited by a small sample size and hence type II error cannot be ruled out.\n\nWider ImplicationsThe study does not support the potential use of mtDNA levels in the trophectodermal cells as biomarker for blastocyst quality and predicting clinical outcomes needs.\n\nStudy funding/competing interest(s)There is no external funding for the study. There is no conflict of interest.

developmental biology↗

Ontogeny and expression profiles of steroid hormone receptors in a mouse model of endometriosis

Endometriosis is a chronic incurable disorder of unknown etiology affecting a large proportion of women in reproductive age. In order to understand the pathogenesis and preclinical testing of drugs,animal models that recapitulate the key features of the disorder are highly desirous. Herein, we describe the ontogeny of the ectopic endometrial lesion in a mouse model where uterine tissue was ligated to the intestinal mesentery and the animals were followed up from day 5 to day 60 post-surgery. Out of 60 animals that underwent surgery, 58 developed endometriosis using this strategy. Most lesions were pale, fluid filled while red lesions were seen in ~10% of animals. Histologically, in most animals there was one large cystic gland with well differentiated epithelium, in 13% of animals there was mixed phenotype (well and poorly differentiated). There was extensive stromal compaction and increased number of macrophages in ectopic lesions. During the course of endometriosis, there was an increase in number of PCNA positive epithelial and stromal cells. The epithelial cells at all the time point were cytokeratin positive and the stroma was vimentin positive. However, at day 30 and 60, the stromal cells were also cytokeratin positive. The mRNA levels of estrogen receptors Esr1 and Gper1 were reduced while those of Esr2 were elevated as compared to normal endometrium, the levels of progesterone receptor (Pgr) were found to be downregulated in ectopic lesions as compared to control. However, these differences were not statistically significant due to high biological variability. Low abundance of Cyp19a1 transcripts (aromatase gene) were only detected in the ectopic endometrium. Immunohistochemically, the expression of ER and ER{beta} was significantly reduced only in stromal cells; the epithelial cell staining was maintained. GPER1 and PR immunoreactivity was significantly low in both epithelial and stromal cells. The immunostaining of all the steroid receptors was highly heterogeneous in the ectopic tissues with some areas of sections had stained intensely while others had negligible staining. We propose that temporal and spatial difference in the expression of steroid hormone receptors during the course of endometriosis development coupled with micro-heterogeneity may alter the effectiveness of steroid hormone analogues resulting in variable outcomes and often failure of therapy.

pathology↗