1Spatiotemporal study of hepatitis BSource: STOmics DB (ID: STT0000102 )

Liver cirrhosis and liver cancer caused by hepatitis B virus infection cause about 800000 deaths every year. In this study, we used Stereo-seq FFPE technology to obtain the transcriptome of liver biopsy tissues from 11 hepatitis B patients and 3 normal controls, identifying disease progression markers in each stage of hepatitis B virus infection.

2Spatial Decoding of Aortic Atherosclerosis at Single-Cell ResolutionSource: STOmics DB (ID: STT0000118 )

Atherosclerosis is a chronic process that leads to the buildup of plaque inside arterial walls and is a key factor underlying cardiovascular disease-related mortality. However, the mechanisms involved in its formation remain largely unclear. The aorta's thin, strip-like topology, combined with its complex environment and remarkable plasticity -- with the capacity for transdifferentiation between multiple cell types under physiological and pathophysiological conditions -- has hindered molecular discoveries in vascular single-cell biology. Fortunately, this intricate spatiotemporal heterogeneity, always concurrent with cell migration across the aortic layers during plaque formation, could potentially be captured through spatial transcriptomics (ST). Using ST technology at cellular resolution, we present a spatial atlas of a murine model of atherosclerosis, comprising over one million cells across multiple stages of atherogenesis. We computationally digitize the aortic stratification to record cell migration and transdifferentiation in situ, constructing molecular trajectories to account for the progression of atherosclerosis. Our systematic study explores the intricate interactions between smooth muscle cell modulation and endothelial-to-mesenchymal transition, identifying novel transcription factors involved in this process, which we validated experimentally. Based on these findings, we further verified that secreted plasma midkine (MDK) could serve as a potential biomarker for early clinical detection and therapeutic target for atherosclerosis. Taken together, we demonstrate an experimental and computational framework for the spatiotemporal investigation of atherosclerosis, fostering more comprehensive research and clinical insights.

3spatiotemporal transcriptomes of maize leaf at early stagesSource: STOmics DB (ID: STT0000121 )

Here, we constructed single cell spatial transcriptomes and single cell RNA-seq (scRNA-seq) atlases of leaf primordia for maize (Zea mays). By integrating spatial and scRNA-seq data in maize, we identified all cell types, particularly bundle sheath cells (BSC) at early developmental stages. We developed a unified pseudo-Kranz framework to integrate transcriptomics data for cells at different positions and distances from vascular bundles. We construct genetic regulatory networks for different cell types in early developing leaves and consequently identified newly recruited regulators related to Kranz anatomy.

4wing primordium of the domestic silkwormSource: STOmics DB (ID: STT0000176 )

scRNA-seq data in the wing primordium of the domestic silkworm during normal development at 5th instar, 2nd day; 5th instar, 3rd day; 5th instar, 4th day; 5th instar, 5th day; 5th instar, 6th day; 5th instar, 7th day; WD period, 1st day; WD period, 2nd day; and P period. snRNA-seq data in the wing primordium of the domestic silkworm after hormonal induction treatment following normal development until 5th instar, 2nd day; 0h; 10 min; 20 min; 30 min; 40 min; 50 min; 60 min; 4h; and 6h. stereo-seq data of single cells in the wing primordium of the domestic silkworm during normal development at 5th instar, 2nd day; 5th instar, 3rd day; and WD period, 2nd day.

5Exploring the mechanism of tumer microenvironment reconstruction in the process of breast cancer invasionSource: STOmics DB (ID: STT0000067 )

Breast cancer is a leading cause of death that seriously threatens women's life and health. Tumor invasion is a crucial event in the progression of breast cancer. However, we still know little about the specific mechanisms of tumor invasion in breast cancer. In this study, we perform single-cell and spatial RNA-sequencing on tumor samples from normal, in situ and invasive regions to explore the specific cellular and molecular mechanisms of the dynamic tumor microenvironment reconstruction during tumor invasion, thus providing new targets for clinical diagnosis and treatment of breast cancer.

6Single-cell and spatial transcriptomics reveal the mechanisms of bile duct injury in biliary atresiaSource: STOmics DB (ID: STT0000060 )

Biliary Atresia(BA) is a devastating pediatric cholangiopathy affecting the bile ducts of the liver. This research utilized spatial and single-cell transcriptomics to analyze the immune microenvironment of biliary atresia, revealing the mechanisms of bile duct injury that occur concurrently with inflammation and fibrosis.

7Malignant progression of pancreatic ductal adenocarcinomaSource: STOmics DB (ID: STT0000056 )

Pancreatic ductal adenocarcinoma (PDAC) is the deadliest common malignancy1. Benign lesions named pancreatic intraepithelial neoplasia (PanIN) are important precursors to PDAC, but these are extremely common in the general population2. The mechanisms underlying the lethal conversion of benign PanINs to invasive PDAC is poorly understood. Here we harness Stereo-seq, a high resolution spatial transcriptomic profiling platform3, to identify a core transcriptional program associated with invasive growth in human PDAC. This program, highly conserved in mice, is predominantly comprised of genes activated to drive reepithelialization during wound healing. Genes of this wound-like program are required for conversion of PanINs into invasive PDAC in mice. Benign PanINs continually produce a small reservoir of wound-like epithelial cells that activate key tumor suppressor genes (TSGs), keeping the incipient malignant cells in check. TSG KO in PanINs leads to rapid outgrowth of the wound-like population, unleashing invasive growth. Wound-induced AP-1 transcription factors (TFs) FOSL1 and JUNB are specifically activated in invasive PDAC cells and enforced expression of FOSL1 in PanIN drives wound-like gene expression and benign-to-malignant plasticity. Malignant PDAC cells are surrounded by a conserved population of CTHRC1-expressing cancer-associated fibroblasts (CAFs) that possess a transcriptional program strikingly similar to one activated in a population of wound-emergent fibroblasts in skin. Bidirectional interactions between malignant cancer cells and the wound-like CAFs result in a feedback loop that enforces the malignant state.

8Cross-species single-cell and spatial transcriptomic maps of the spleen reveal the origin and evolution of the GC-like moduleSource: STOmics DB (ID: STT0000158 )

Germinal center (GC) is the core microstructure of mammalian adaptive immunity, but the evolutionary origins and functional precursors in ectothermic vertebrates is still unclear. Here we systematically reconstruct the evolutionary trajectory of GC-like structures by integrating spleen single-cell and spatial transcriptomic data across six major jawed vertebrate classes (from chondrichthyans to mammals).

9A single-cell resolution spatial atlas of pancreatic ductal adenocarcinomaSource: STOmics DB (ID: STT0000061 )

In this study, we employed a spatial transcriptome stereo-seq in combine with scRNA-seq analysis on PDAC tumor and para-cancer tissues to explore the rearrangement of the TME in PDAC.

10Spatiotemporal transcriptomic maps of mouse intracerebral hemorrhage at single-cell resolutionSource: STOmics DB (ID: STT0000047 )

Intracerebral hemorrhage (ICH) is a prevalent disease with high mortality. Despite advances in clinical care, the prognosis of ICH remains poor due to an incomplete understanding of the complex pathological processes. To address this challenge, we generated single-cell resolution spatiotemporal transcriptomic maps of mouse brain after ICH. This data set is the most extended resource available that provides detailed information about temporal expression of genes together with a high resolution cellular profile and preserved cellular organization. We identified 100 distinct cellular subclasses, 17 of which were found to play significant roles in the pathophysiology of ICH. We also report similarities and differences between two experimental ICH models and human postmortem ICH brain tissue. This study advances the understanding of the local and global responses of brain cells to ICH, and provides a valuable resource that can facilitate future research and aid the development of novel therapies for this devastating condition.