Differential Signal Research Articles

A Differential Signal and Extended-Kalman-Filter-Based Anti-Interference Magnetic Tracking Method for Surgical Scenes

A Differential Signal and Extended-Kalman-Filter-Based Anti-Interference Magnetic Tracking Method for Surgical Scenes

Heightened TPD52 linked to metabolic dysfunction and associated abnormalities in zebrafish

The tumor protein D52 (TPD52) gene encodes a proto-oncogene protein associated with various medical conditions, including breast and prostate cancers. It plays a role in multiple biological pathways such as cell growth, differentiation, and apoptosis. The function of TPD52 in lipid droplet biosynthesis has been investigated in vitro. However, its precise role in lipid metabolism in animal models is not fully understood. To investigate the functions of TPD52 in vivo, we performed a conditional TPD52 protein expression analysis using a Tet-off transgenic system to establish conditionally expressed Tpd52 transgenic zebrafish. The effect of Tpd52 on lipogenesis was assessed using various methods, including whole-mount Oil Red O staining, histological examination, and measurement of inflammatory markers and potential targets using real-time quantitative polymerase chain reaction and immunoblotting in Tpd52 fish. Zebrafish with increased Tpd52 levels exhibited notable weight gain and the enlargement of fat deposits, which were mainly attributed to an increase in the volume of adipocytes. Moreover, Tpd52 overexpression was correlated with the triggering of the adipocyte differentiation signaling pathway. During adipocytic differentiation in response to nutrient status, our observations revealed adipogenesis, nonalcoholic fatty liver disease, and metabolic cardiomyopathy (MCM) in Tpd52 transgenic zebrafish. To gain a deeper understanding of the contribution of these proteins to the regulation of cellular growth, we investigated the expression of their corresponding genes and proteins in zebrafish. In the present study, the activated protein kinase pathway was identified as the primary target of TPD52. Adult Tpd52 zebrafish showed increased lipid accumulation, resulting in the development of visceral obesity, nonalcoholic fatty liver disease, and MCM. These findings strongly suggest that TPD52 actively contributes to adipose tissue expansion and its subsequent effects. This investigation provides compelling evidence that Tpd52 facilitates adipocyte development and related metabolic comorbidities in zebrafish.

A 24–30‐GHz Modified Gilbert‐Cell Downconverter With High Linearity and Isolation

ABSTRACTThis paper introduces a downconverter mixer employing a modified double‐balanced Gilbert‐cell topology, designed using IHP's 0.13‐m SiGe BiCMOS technology. Distinct from the conventional topology, a resonator was employed at the emitter of the transconductance stage, which enables the utilization of transconductance stage as an active balun, allowing for direct feeding of the single‐ended input without sacrificing the advantageous of the double‐balanced topology. The integration of the resonator reduces the amplitude and phase errors within the active balun segment, thereby enhancing port‐to‐port isolation. The area occupied by the resonator is approximately 1.7 times smaller than that of an RF transformer balun typically employed in conventional double‐balanced topologies. The LO and IF differential signals are converted to single‐ended ones through transformer baluns for measurement purposes. The frequencies of operation for RF, LO, and IF are 24–30, 18–24, and 6 GHz, respectively. The conversion loss is 7.7 dB at 26 GHz, with port‐to‐port isolations exceeding 35 dB. The input 1‐dB compression point is 5.7 dBm, while the circuit consumes 65‐mW power from a 3.3‐V voltage supply. Excluding the pads, the active area of the design spans 1 mm2.

Impact of cannabinoids on synapse markers in an SH-SY5Y cell culture model

Patients suffering from schizophrenic psychosis show reduced synaptic connectivity compared to healthy individuals, and often, the use of cannabis precedes the onset of schizophrenic psychosis. Therefore, we investigated if different types of cannabinoids impact methylation patterns and expression of schizophrenia candidate genes concerned with the development and preservation of synapses and synaptic function in a SH-SY5Y cell culture model. For this purpose, SH-SY5Y cells were differentiated into a neuron-like cell type as previously described. Effects of the cannabinoids delta-9-THC, HU-210, and Anandamide were investigated by analysis of cell morphology and measurement of neurite/dendrite lengths as well as determination of methylation pattern, expression (real time-qPCR, western blot) and localization (immunocytochemistry) of different target molecules concerned with the formation of synapses. Regarding the global impression of morphology, cells, and neurites appeared to be a bit more blunted/roundish and to have more structures that could be described a bit boldly as resembling transport vesicles under the application of the three cannabinoids in comparison to a sole application of retinoic acid (RA). However, there were no obvious differences between the three cannabinoids. Concerning dendrites or branch lengths, there was a significant difference with longer dendrites and branches in RA-treated cells than in undifferentiated control cells (as shown previously), but there were no differences between cannabinoid treatment and exclusive RA application. Methylation rates in the promoter regions of synapse candidate genes in cannabinoid-treated cells were in between those of differentiated cells and untreated controls, even though findings were significant only in some of the investigated genes. In other targets, the methylation rates of cannabinoid-treated cells did not only approach those of undifferentiated cells but were also valued even beyond. mRNA levels also showed the same tendency of values approaching those of undifferentiated controls under the application of the three cannabinoids for most investigated targets except for the structural molecules (NEFH, MAPT). Likewise, the quantification of expression via western blot analysis revealed a higher expression of targets in RA-treated cells compared to undifferentiated controls and, again, lower expression under the additional application of THC in trend. In line with our earlier findings, the application of RA led to higher fluorescence intensity and/or a differential signal distribution in the cell in most of the investigated targets in ICC. Under treatment with THC, fluorescence intensity decreased, or the signal distribution became similar to the dispersion in the undifferentiated control condition. Our findings point to a decline of neuronal differentiation markers in our in vitro cell-culture system under the application of cannabinoids.

7-Ketocholesterol Effects on Osteogenic Differentiation of Adipose Tissue-Derived Mesenchymal Stem Cells

Some oxysterols were shown to promote osteogenic differentiation of mesenchymal stem cells (MSCs). Little is known about the effects of 7-ketocholesterol (7-KC) in this process. We describe its impact on human adipose tissue-derived MSC (ATMSC) osteogenic differentiation. ATMSCs were incubated with 7-KC in osteogenic or adipogenic media. Osteogenic and adipogenic differentiation was evaluated by Alizarin red and Oil Red O staining, respectively. Osteogenic (ALPL, RUNX2, BGLAP) and adipogenic markers (PPARƔ, C/EBPα) were determined by RT-PCR. Differentiation signaling pathways (SHh, Smo, Gli-3, β-catenin) were determined by indirect immunofluorescence. ATMSCs treated with 7-KC in osteogenic media stained positively for Alizarin Red. 7-KC in adipogenic media decreased the number of adipocytes. 7-KC increased ALPL and RUNX2 but not BGLAP expressions. 7-KC decreased expression of PPARƔ and C/EBPα, did not change SHh, Smo, and Gli-3 expression, and increased the expression of β-catenin. In conclusion, 7-KC favors osteogenic differentiation of ATMSCs through the expression of early osteogenic genes (matrix maturation phase) by activating the Wnt/β-catenin signaling pathway, while inhibiting adipogenic differentiation. This knowledge can be potentially useful in regenerative medicine, in treatments for bone diseases.

SUMOylation regulates the aggressiveness of breast cancer-associated fibroblasts.

Cancer-associated fibroblasts (CAFs) are the most abundant stromal cellular component in the tumor microenvironment (TME). CAFs contribute to tumorigenesis and have been proposed as targets for anticancer therapies. Similarly, dysregulation of SUMO machinery components can disrupt the balance of SUMOylation, contributing to tumorigenesis and drug resistance in various cancers, including breast cancer. We explored the role of SUMOylation in breast CAFs and evaluated its potential as a therapeutic strategy in breast cancer. We used pharmacological and genetic approaches to analyse the functional crosstalk between breast tumor cells and CAFs. We treated breast CAFs with the SUMO1 inhibitor ginkgolic acid (GA) at two different concentrations and conditioned media was used to analyse the proliferation, migration, and invasion of breast cancer cells from different molecular subtypes. Additionally, we performed quantitative proteomics (SILAC) to study the differential signalling pathways expressed in CAFs treated with low or high concentrations of GA. We confirmed these results both in vitro and in vivo. Moreover, we used samples from metastatic breast cancer patients to evaluate the use of GA as a therapeutic strategy. Inhibition of SUMOylation with ginkgolic acid (GA) induces death in breast cancer cells but does not affect the viability of CAFs, indicating that CAFs are resistant to this therapy. While CAF viability is unaffected, CAF-conditioned media (CM) is altered by GA, impacting tumor cell behaviour in different ways depending on the overall degree to which SUMO1-SUMOylated proteins are dysregulated. Breast cancer cell lines exhibited a concentration-dependent response to conditioned media (CM) from CAFs. At a low concentration of GA (10µM), there was an increase in proliferation, migration and invasion of breast cancer cells. However, at a higher concentration of GA (30µM), these processes were inhibited. Similarly, analysis of tumor development revealed that at 10µM of GA, the tumors were heavier and there was a greater degree of metastasis compared to the tumors treated with the higher concentration of GA (30µM). Moreover, some of these effects could be explained by an alteration in the activity of the GTPase Rac1 and the activation of the AKT signalling pathway. The results obtained using SILAC suggest that different concentrations of GA affected cellular processes differentially, possibly influencing the secretome of CAFs. Treatment of metastatic breast cancer with GA demonstrated the use of SUMOylation inhibition as an alternative therapeutic strategy. The study highlights the importance of SUMOylation in the tumor microenvironment, specifically in cancer-associated fibroblasts (CAFs). Targeting SUMOylation in CAFs affects their signalling pathways and secretome in a concentration-dependent manner, regulating the protumorigenic properties of CAFs.

Study on the mechanism of Xinmailong injection against chronic heart failure based on transcriptomics and proteomics

Xinmailong (XML), a traditional Chinese medicine derived from Periplaneta americana, is commonly used in China to treat chronic heart failure (CHF). However, its pharmacological mechanism remains unclear. In our research, we employed Doxorubicin (Dox) to create a CHF animal model and administered XML treatment to investigate the pharmacological effects of XML on CHF rats by combining transcriptomic and proteomic analyses. XML improved dox-induced CHF and improved cardiac function, and a joint multi-omics analysis demonstrated that it reduced cardiomyocyte fibrosis during CHF. There is further evidence that XML may alleviate cardiomyocyte fibrosis through its effects on the cGMP-PKG signaling pathway or by reducing the expression levels of COL1A1, COL3A1, MMP9, and CXCR2. In this study, the effects of XML on rats with CHF are examined at the transcriptional and protein levels, as well as its mechanism and mode of action in treating CHF. There may be novel therapeutic targets or clinical indications for XML-based CHF therapy resulting from the study's identification of significant differential genes and signaling pathways.

Effect of Hydroxyapatite Nanowires on Formation and Bioactivity of Osteoblastic Cell Spheroid.

Compared with traditional high-density cell spheroids, which are more prone to core necrosis, nanowires effectively improve the biological activity of core cells in spheroids, emanating more innovations for optimizing the internal cell survival environment and providing differentiation signals. In this study, hydroxyapatite nanowires (HAW), which provide numerous material exchange channels for internal cells by interpenetrating into cell spheroids, were added to osteoblast precursor (MC3T3-E1) cell spheroids. HAW, synthesized using the hydrothermal method, was used as a regulatory material to prepare uniformly sized 3D composite spheroids with good biological activity. Subsequently, material characterization and biocompatibility tests were performed on HAW, and the biological activity and osteogenic differentiation ability of the cell spheroids were tested. Notably, in 2D coculture, HAW displayed a certain attraction to MC3T3-E1 cells and promoted cell aggregation toward it. The content of HAW determined whether composite cell spheroids can form aggregated spherical structures, and incorporation of HAW alleviated core necrosis and enhanced the osteogenic phenotype. In summary, these findings indicate that the prepared HAW-bone cell composite spheroids can potentially be used as building blocks for the construction of large high-density biomimetic tissues and organoids using 3D bioprinting technology.

Self-referencing refractive index sensor based on graphene-assisted TAMM plasmon cavity resonance.

In this Letter, we report TAMM plasmonic polaritons (TPPs) generated by few-layer MoS2 with a distributed Bragg reflector (DBR) structure in the terahertz frequency region by utilizing the transfer matrix method (TMM) and finite element method (FEM). By inserting a mono-graphene embedded cavity layer, we realize the graphene-induced mode strong coupling (GCM), which is a strategy of a refractive index sensor by optimizing the cavity layer spacing. By adjusting the chemical potential of graphene, GCM is modulated. μc = 0.1 eV and μc = 0.9 eV are selected as the on-off-state parameters, respectively. The difference in reflectance spectra presents a differential signal and a self-reference operation. The sensitivity of the designed refractive index sensor is 7.8 THz/RIU and a figure of merit (FOM) of 882 RUI-1 can be obtained. The proposed structure in our Letter demonstrates its potential application in high-performance self-reference refractive index sensors.

Cell-cell interaction determines cell fate of mesoderm-derived cell in tongue development through Hh signaling.

Dysfunction of primary cilia leads to genetic disorder, ciliopathies, which shows various malformations in many vital organs such as brain. Multiple tongue deformities including cleft, hamartoma, and ankyloglossia are also seen in ciliopathies, which yield difficulties in fundamental functions such as mastication and vocalization. Here, we found these tongue anomalies in mice with mutation of ciliary protein. Abnormal cranial neural crest-derived cells (CNCC) failed to evoke Hh signal for differentiation of mesoderm-derived cells into myoblasts, which resulted in abnormal differentiation of mesoderm-derived cells into adipocytes. The ectopic adipose subsequently arrested tongue swelling formation. Ankyloglossia was caused by aberrant cell migration due to lack of non-canonical Wnt signaling. In addition to ciliopathies, these tongue anomalies are often observed as non-familial condition in human. We found that these tongue deformities could be reproduced in wild-type mice by simple mechanical manipulations to disturb cellular processes which were disrupted in mutant mice. Our results provide hints for possible future treatment in ciliopathies.

Exploring the Role of Secondary Metabolites from Plants and Microbes as Modulators of Macrophage Differentiation.

Recent research has uncovered that secondary metabolites-biologically active compounds produced by plants, microbes, and other organisms-play a significant role in regulating the differentiation and function of macrophages. Macrophages, key components of the innate immune system, are crucial for a wide range of physiological processes, including immune response modulation, tissue homeostasis, and host defense against pathogens. This research delves into the mechanisms by which secondary metabolites influence macrophage differentiation signaling pathways, with a focus on how specific compounds affect macrophage polarization and functional phenotypes. Understanding these effects can open new avenues for developing therapeutic strategies that target macrophage-mediated immune responses. Secondary metabolites, such as nitrogen (N) and sulfur (S) containing compounds, terpenoids, and phenolic compounds from plants and microbes, can modulate macrophage differentiation by influencing cytokine production and activity. The activation of signaling pathways in macrophages involves multiple receptors and transcription factors, including IFN-γ receptor activation leading to STAT1 activation, TLR4 triggering IRF5, NFκB, and AP1, IL-4 receptor activation leading to STAT6 and IRF4 activation, PPARγ activation via the fatty acid receptor, TLR4 increasing CREB and C/EBP levels. The complex interplay between transcription factors and cytokines is crucial for maintaining the balance between the M1 and M2 states of macrophages. Despite these insights, further research is needed to unravel the specific molecular mechanisms involved and to identify promising secondary metabolites that could be translated into clinical applications.

Different inflammatory, fibrotic, and immunologic signatures between pre-fibrotic and overt primary myelofibrosis.

Primary myelofibrosis (PMF) is a myeloid proliferative neoplasm (MPN) characterized by bone marrow (BM) fibrosis. Pre-fibrotic PMF (pre-PMF) progresses to overt PMF. Megakaryocytes (MKs) play a primary role in PMF; however, the functions of MK subsets and those of other hematopoietic cells during PMF progression remain unclarified. Therefore, we analyzed BM aspirates in pre-PMFs, overt PMFs, and other MPNs using single-cell RNA sequencing (scRNA-seq). We identified 14 cell types with subsets, including hematopoietic stem and progenitor cells (HSPCs) and MKs. HSPCs in overt PMF were MK-biased and inflammation/fibrosis-enriched. Among MKs, the epithelial-mesenchymal transition (EMT)-enriched subset was abruptly increased in overt PMF. MKs in non-fibrotic/non-PMF MPN were MK differentiation-enriched, whereas those in fibrotic/non-PMF MPN were inflammation/fibrosis-enriched. Overall, the inflammation/fibrosis signatures of the HSPC, MK, and CD14+ monocyte subsets increased from pre-PMF to overt PMF. Cytotoxic and dysfunctional scores also increased in T and NK cells. Clinically, MK and HSPC subsets with high inflammation/fibrosis signatures were frequent in the patients with peripheral blood blasts ≥1%. scRNA-seq predicted higher cellular communications of MK differentiation, inflammation/fibrosis, immunologic effector/dysfunction, and tumor-associated signaling in overt PMF than pre-PMF. However, no decisive subset emerged during PMF progression. Our study demonstrated that HSPCs, monocytes, and lymphoid cells contribute to PMF progression, and subset specificity existed regarding inflammation/fibrosis and immunologic dysfunction. PMF progression may depend on multiple cell types' alterations, and EMTenriched MKs may be potential targets for the diagnosis and therapy of the progression.

MiR-27 and MiR-145 mediate neural differentiation signaling pathways in dental pulp stem cells

MiR-27 and MiR-145 mediate neural differentiation signaling pathways in dental pulp stem cells

Screening core genes for minimal change disease based on bioinformatics and machine learning approaches.

Based on bioinformatics and machine learning methods, we conducted a study to screen the core genes of minimal change disease (MCD) and further explore its pathogenesis. First, we obtained the chip data sets GSE108113 and GSE200828 from the Gene Expression Comprehensive Database (GEO), which contained MCD information. We then used R software to analyze the gene chip data and performed functional enrichment analysis. Subsequently, we employed Cytoscape to screen the core genes and utilized machine learning algorithms (random forest and LASSO regression) to accurately identify them. To validate and analyze the core genes, we conducted immunohistochemistry (IHC) and gene set enrichment analysis (GSEA). Our results revealed a total of 394 highly expressed differential genes. Enrichment analysis indicated that these genes are primarily involved in T cell differentiation and p13k-akt signaling pathway of immune response. We identified NOTCH1, TP53, GATA3, and TGF-β1 as the core genes. IHC staining demonstrated significant differences in the expression of these four core genes between the normal group and the MCD group. Furthermore, GSEA suggested that their up-regulation may be closely associated with the pathological changes in MCD kidneys, particularly in the glycosaminoglycans signaling pathway. In conclusion, our study highlights NOTCH1, TP53, GATA3, and TGF-β1 as the core genes in MCD and emphasizes the close relationship between glycosaminoglycans and pathogenesis of MCD.

Enhancer landscape of lung neuroendocrine tumors reveals regulatory and developmental signatures with potential theranostic implications

Well-differentiated low-grade lung neuroendocrine tumors (lung carcinoids or LNETs) are histopathologically classified as typical and atypical LNETs, but each subtype is still heterogeneous at both the molecular level and its clinical manifestation. Here, we report genome-wide profiles of primary LNETs' cis-regulatory elements by H3K27ac ChIP-seq with matching RNA-seq profiles. Analysis of these regulatory landscapes revealed three regulatory subtypes, independent of the typical/atypical classification. We identified unique differentiation signals that delineate each subtype. The "proneuronal" subtype emerges under the influence of ASCL1, SOX4, and TCF4 transcription factors, embodying a pronounced proneuronal signature. The "luminal-like" subtype is characterized by gain of acetylation at markers of luminal cells and GATA2 activation and loss of LRP5 and OTP. The "HNF+" subtype is characterized by a robust enhancer landscape driven by HNF1A, HNF4A, and FOXA3, with notable acetylation and expression of FGF signaling genes, especially FGFR3 and FGFR4, pivotal components of the FGF pathway. Our findings not only deepen the understanding of LNETs' regulatory and developmental diversity but also spotlight the HNF+ subtype's reliance on FGFR signaling. We demonstrate that targeting this pathway with FGF inhibitors curtails tumor growth both in vitro and in xenograft models, unveiling a potential vulnerability and paving the way for targeted therapies. Overall, our work provides an important resource for studying LNETs to reveal regulatory networks, differentiation signals, and therapeutically relevant dependencies.

Quinic acid contributes to neurogenesis: Targeting Notch pathway a key player in hippocampus

Coordinated proliferation and differentiation of neural stem cells (NSCs) results in continuous neurogenesis. The present study provides novel insights into the Notch intracellular signaling in neuronal cell proliferation, maintenance, migration, and differentiation regulated by naturally based Quinic acid (QA) in primary hippocampal cell culture. Further, this study might help in the discovery and development of lead molecules that can overcome the challenges in the treatment of neurodegenerative diseases. The growth supporting effect of QA was studied using Alamar Blue assay. The migratory potential of QA was evaluated using scratch assay. The in vitro H2O2-induced oxidative stress model was used to upregulate neuronal survival after QA treatment. The RT-qPCR and immunocytochemical analysis were performed for selected markers of Notch signaling to determine the proliferation, differentiation, and maintenance of NSCs at gene and molecular levels. The Mash1 and Ngn2 are the upstream proneural genes of the Notch pathway which were included to evaluate the differentiation of NSCs into mature neurons after treatment with QA.Furthermore, regarding the role of QA in maintaining the pool of NPCs, we used Notch1 and Hes1 markers for proliferation analysis. Also, secondary neuronal markers i.e. Pax6, PCNA, and Mcm2 were included in this study and their gene expression analysis was analyzed following treatment with QA. Based on the study’s results, we suggest that naturally based QA can promote the growth and differentiation of neonatal NSCs residing in hippocampal regions into neuronal lineage. Therefore, we propose that the neurogenic potential of QA can be employed to prevent and treat neurodegenerative diseases.

Differential Gene Expression and Signal Pathways Activation Lead to Differences in Cell Proliferation and Migration of Venous and Arterial Pig Smooth Muscle Cells

Differential Gene Expression and Signal Pathways Activation Lead to Differences in Cell Proliferation and Migration of Venous and Arterial Pig Smooth Muscle Cells

A fluorescence-electrochemical dual-mode aptasensor for ultrasensitive detection of lead based on exonuclease-catalyzed recycling and hybridization chain reaction amplification

To improve the accuracy and reliability of the detection system, this study combined the exonuclease-assisted autocatalytic target cycling fluorescence strategy with an electrochemical platform to establish a dual-mode fluorescence-electrochemical aptasensor for the ultra-sensitive quantification of lead ion (Pb2+). In the fluorescence detection strategy, ssDNA could hybridize with the aptamer to form double-stranded DNA. With the addition of Pb2+, the aptamer dissociated from the double-stranded DNA to capture Pb2+ and trigger the enzymatic digestion process, leading to the target recirculation to achieve the first signal amplification. The free ssDNA could then hybridize with S1, and the released S2 was able to trigger a hybridization chain reaction (HCR) in the electrochemical system, achieving the second signal amplification. The quantification of Pb2+ was realized by measuring both the fluorescence and the differential pulse voltammetry signals with detection limits of 0.028ng/mL and 0.788pg/mL, respectively. This fluorescence-electrochemical dual-mode aptasensor overcame the limitations of complex matrices and environmental interference, and provided a valuable reference for the development of reliable multi-signal sensors in water, tea and vegetable safety monitoring.

Eupalinolide A attenuates trauma-induced heterotopic ossification of tendon in mice by promoting YAP degradation through TOLLIP-mediated selective autophagy

BackgroundInhibiting the aberrant osteogenic differentiation of tendon-derived stem cells (TDSCs) is an effective strategy for treating traumatic heterotopic ossification (HO) in tendons. PurposeThis study aimed to investigate whether eupalinolide A (EA) could prevent tendon HO progression by suppressing the osteogenic differentiation of TDSCs. MethodsThe effects of EA on osteogenic differentiation and key signaling pathways in TDSCs were examined in vitro to assess its therapeutic potential and elucidate the underlying molecular mechanisms. Furthermore, the therapeutic efficacy of EA was evaluated in a mouse model of trauma-induced tendon HO via local injection therapy. ResultsEA significantly inhibited the osteogenic differentiation of TDSCs by targeting YAP in vitro. Specifically, EA facilitated the recruitment of E3 ubiquitin ligase HECW1, which mediated K27-linked polyubiquitination of YAP, leading to its degradation via the TOLLIP-mediated selective autophagy pathway. In vivo, EA mitigated trauma-induced tendon HO by inhibiting the YAP pathway. ConclusionsEA could be a potential therapeutic agent for treating traumatic tendon HO. The therapeutic target HECW1 involved in YAP degradation via autophagy presents a new therapeutic avenue to attenuate the progression of traumatic tendon HO.

Screening and analysis of GULP1 downstream target genes based on transcriptomic sequencing.

GULP1 is an engulfment adaptor protein containing a phosphotyrosine-binding (PTB) domain, and existing studies have shown that it can promote glucose uptake in 3T3-L1 adipocytes. To further explore key metabolically related differential genes downstream of GULP1, this study conducted transcriptome analysis on adipocytes and skeletal muscle cells overexpressing GULP1. Subsequently, abnormally expressed genes were subjected to bioinformatic analysis, and real-time fluorescent quantitative PCR (qRT-PCR) was used for mutual validation with transcriptome sequencing. The results indicated that, with a threshold of P < 0.05 and |Log2FoldChange| ≥ 1 for screening differentially expressed genes, compared with control cells, there were 278 upregulated and 263 downregulated genes in adipocytes overexpressing GULP1. Metabolism-related GO (Gene Ontology) terms included cholesterol biosynthetic process, cholesterol metabolic process, response to lipopolysaccharide, lipid metabolic process, etc. A total of 52 metabolically related differentially expressed genes were enriched in 10 KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways, with lipid metabolism being highly enriched. In skeletal muscle cells overexpressing GULP1, there were 280 upregulated and 302 downregulated genes, with metabolism-related GO terms including hormone metabolic process, response to lipopolysaccharide, one-carbon metabolic process, etc. A total of 86 metabolically related differentially expressed genes were enriched in 10 KEGG pathways, with amino acid metabolism, lipid metabolism, and carbohydrate metabolism being highly enriched. GULP1's biological functions are extensive, including lipid metabolism and oncology. This study, through transcriptomics and bioinformatic analysis, identified key metabolically related differential genes downstream of GULP1, obtained metabolically related differential genes and signaling pathways after GULP1 overexpression, providing important theoretical basis for future research on GULP1 downstream target genes.