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Biology subjects

Kamata, M.

Publications and source records attributed to Kamata, M..

8 recordsLinked to original sources

Human skin fibrosis with iPSC-derived organoids reveals RUNX2-mediated fibroblast reprogramming

Fibrotic skin diseases are characterized by persistent fibroblast activation and extracellular matrix remodeling, yet the mechanisms governing fibroblast state transitions remain incompletely understood. Here, we established a human iPSC-derived skin organoid model of fibrosis through chronic TGF-{beta} stimulation. Single-cell RNA sequencing combined with immunofluorescence-based spatial analysis revealed dynamic fibroblast state transitions, spatial reorganization, and expansion of activated fibroblast populations during fibrotic remodeling. Integration with human scleroderma single-cell datasets demonstrated conserved fibroblast states and transcriptional programs between organoids and patient tissues. We further identified broad induction of RUNX2 in the dermal compartment during fibrosis, and RUNX2 depletion attenuated fibrotic marker expression. CUT&RUN profiling revealed RUNX2 occupancy at fibrosis-associated loci, including RUNX1 and LOXL2. Using a machine learning-guided screening approach, we identified F0565-0303, a small molecule that suppressed RUNX2-dependent fibrotic programs in vitro and reduced fibrosis in a bleomycin-induced mouse model. Together, these findings establish human skin organoids as a platform for modeling fibrosis and nominate RUNX2 as a potential therapeutic target.

bioengineering↗

JNK knockdown enhances CAR-T cell cytotoxicity

BackgroundBoosting the performance of chimeric antigen receptor T (CAR-T) cell therapy in solid tumors may provide a substantial advantage for cancer patients. Recognizing the vital role of the nuclear factor of activated T cells (NFAT) in T cell function, we hypothesized that the strategic regulation of NFAT activity by targeting c-Jun N-terminal Kinases (JNK) can bolster the tumor-eradicating potential of CAR-T cells. MethodsWe developed a lentivirally encoded short-hairpin RNA (shRNA) for stable knockdown of JNK in CAR-T cells. CAR-T cells targeting human epidermal growth factor receptor 2 (HER2) were produced from human peripheral blood. Functionality was tested in vitro and in two xenograft models of human ovarian cancer. ResultsJNK knockdown in CAR-T cells suppressed antigen-induced stimulation and helper T cell cytokine production, while enhancing anti-tumor cytotoxicity in vitro and in ovarian cancer xenograft experiments. Mechanistically, JNK knockdown led to elevated levels of granzyme B expression which could be recapitulated through overexpression of NFATc1, suggesting an NFATc1 dependent mechanism of action. ConclusionsJNK signaling is a significant regulator of CAR-T cell cytotoxicity, offering a potential strategy to directly enhance CAR-T effectiveness in human cancer therapies.

immunology↗

Exploring the immune environment of glioblastoma through single-cell RNA sequencing in humanized mouse models

BackgroundGlioblastoma (GBM) is the deadliest primary brain tumor in adults, where current therapies fail to meaningfully extend survival. Available animal GBM tumor models, especially therapy-resistant and recurrent ones with unique immunological aspects, are restricted, impeding innovative treatment research. To confront this critical obstacle we established a unique GBM mouse model that utilizes patient-derived xenografts (PDXs) within humanized mice. MethodsWe selected two immune-deficient mouse models to facilitate the reconstitution of myeloid lineage cells. After undergoing myeloablation, mice received CD34+ hematopoietic stem progenitor cells derived from human umbilical cord blood for humanization. Upon confirming the reconstitution of human blood cells, mice were xenografted with PDXs resistant to radiation. Tumor profiles and immune cell infiltration were analyzed via flow cytometry, immunohistochemistry, and single-cell RNA sequencing (scRNA-seq). The findings were evaluated against scRNA-seq data from recurrent human GBM. ResultsA diverse range of human immune cells, including T, NK, and myeloid lineage cells, infiltrated PDX tumors in humanized mice. Notably, gene expression profiles in these immune cells resembled that of recurrent human GBM. Unlike conventional xenograft models, this model highlighted enhanced tumor diversity, particularly a high fraction of neural progenitor-like cells. ConclusionsOur humanized GBM mouse model displayed an immune cell signature similar to recurrent GBM. This model is a valuable resource for analyzing the tumor immune landscape and assessing new therapies, particularly immunotherapies. By enabling effective evaluation of novel treatments, our model has the potential to significantly advance GBM research. Key PointsO_LIA wide array of human immune cells infiltrates GBM-PDX tumors in humanized mice. C_LIO_LIThe tumor heterogeneity of GBM-PDX is more evident in humanized mouse xenografts. C_LI Importance of the studyCurrent GBM treatment development is primarily constrained by the absence of appropriate animal models that can enhance our understanding of human GBM biology and its immune dynamics. We created a specialized GBM mouse model using humanized mice with patient-derived xenografts resistant to radiation. Detailed immune cell analysis showed various human blood cells in the GBM-PDX derived from humanized mice. Single-cell RNA sequencing uncovered crucial T-cell subgroups, notably regulatory and exhausted T cells, which matched those observed in recurrent GBM patient tumors. Moreover, the model outperformed standard xenograft approaches in tumor heterogeneity, resembling the intricate diversity observed in recurrent GBM samples. Our humanized GBM mouse model provides a powerful platform to study the interactions between human tumors and immune cells. This tool will facilitate the discovery of immunosuppressive mechanisms and accelerate the assessment of immunotherapies applicable to various brain tumors.

immunology↗

Extreme high-diversity barcoded HIV library enables single cell multi-omics analysis of viral expression and fate determination

HIV-1 persists as a global health challenge due to its ability to establish latent reservoirs that evade eradication by antiretroviral therapy (ART). This study introduces a high-diversity barcoded HIV-1 library combined with a novel peptide barcode system to enable single-cell multi-dimensional analysis of viral integration, transcription, splicing, and translation of distinct viral mRNA isoform. Our method revealed over 80 distinct HIV-1 splicing isoforms and uncovered significant temporal variation in mRNA diversity, driven by integration site and chromatin context. By linking HIV-1 5UTR with peptide barcoding, we quantified the translation efficiency of alternative 5' UTRs and demonstrated correlations with abundance of each viral mRNA isoform. Additionally, we showed that latency reversal agents, such as SAHA and Bryostatin, selectively reactivate proviruses depending on their genomic and chromatin context and leads to distinct viral RNA splicing program. This platform revealed the diversity of HIV-infected cells at levels of transcripts as well as at proteins, and subsequently the fate determination. The detailed understanding of the stochastic diversity and dynamic nature of HIV-1 latency, inform the development of targeted therapies to eliminate latent reservoirs.

microbiology↗

Immediate Modulation of the Blood Oxygenation Level-Dependent Signals by Dual-Site Transcranial Alternating Current Stimulation Propagates Across the Whole Brain

Transcranial alternating current stimulation (tACS) is assumed to target specific brain regions and modulate their activity. Recent discussions of tACS propose that, entraining the phase of brain activity to the stimulation current, stimulation effects extend globally across the whole brain based on phase differences. However, immediate online spatiotemporal propagation of resting-state blood oxygenation level-dependent (BOLD) signals within the brain due to multi-region stimulation remains unclear. The objectives of the present study were three-fold: 1) to elucidate the immediate online effect of tACS on BOLD signal, 2) to examine the extent of the influence on the brain when applying tACS, and 3) to explore whether variations in the phase difference between two brain regions result in differential effects on the stimulated areas and the whole brain. Through two experiments involving high-definition tACS with simultaneous measurements using a functional magnetic resonance imaging (fMRI), we revealed that the immediate online stimulation effects not only altered BOLD signals in the stimulated regions but also propagated across the whole brain in specific spatiotemporal patterns (functional networks). Stimulation effects were observed specifically in regions rich in neural fibres, including the grey and white matter, with no effect in regions containing cerebrospinal fluid. The timing of the signal value peaks depended on the stimulated region and functional networks, with a notable trend observed. Thus, tACS with a specific phase difference in two anatomically connected brain regions can immediately modulate online neural dynamics at both local and global scales. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/610912v2_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@124d6e1org.highwire.dtl.DTLVardef@1976b16org.highwire.dtl.DTLVardef@1f78294org.highwire.dtl.DTLVardef@9df1b7_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

CCR5 closes the temporal window for memory linking

Real world memories are formed in a particular context and are not acquired or recalled in isolation 1-5. Time is a key variable in the organization of memories, since events experienced close in time are more likely to be meaningfully associated, while those experienced with a longer interval are not1-4. How does the brain segregate events that are temporally distinct? Here, we report that a delayed (12-24h) increase in the expression of the C-C chemokine receptor type 5 (CCR5), an immune receptor well known as a co-receptor for HIV infection6,7, following the formation of a contextual memory, determines the duration of the temporal window for associating or linking that memory with subsequent memories. This delayed CCR5 expression in mouse dorsal CA1 (dCA1) neurons results in a decrease in neuronal excitability, which in turn negatively regulates neuronal memory allocation, thus reducing the overlap between dCA1 memory ensembles. Lowering this overlap affects the ability of one memory to trigger the recall of the other, thus closing the temporal window for memory linking. Remarkably, our findings also show that an age-related increase in CCL5/CCR5 expression leads to impairments in memory linking in aged mice, which could be reversed with a CCR5 knockout and an FDA approved drug that inhibits this receptor, a result with significant clinical implications. All together the findings reported here provide the first insights into the molecular and cellular mechanisms that shape the temporal window for memory linking.

neuroscience↗

Membrane-proximal external region is a superior target for mediating effector activity of HIV-1 specific chimeric antigen receptor modified T cells.

The use of chimeric antigen receptor modified-T (CAR-T) cells in adoptive immunotherapy has been popularized through recent success in the field of cancer treatment research. CD4{zeta} CAR, which targets HIV-1-infected cells, has been developed and evaluated in patients. Though well-tolerated for over a decade, efficacy was disappointingly limited. This result encourages us to develop a novel CAR more effective than CD4{zeta} CAR. To quantitatively compare anti-HIV-1 activity of different CAR constructs in a highly sensitive and reproducible manner, we developed a multicolor flow cytometry method for assessing anti-HIV-1 effector T-cell activity. "Target" Jurkat cells inducibly expressing an HIV-1HXBC2 envelope protein and "Non-target" control cells were genetically labeled with red and blue fluorescent protein, respectively, and co-incubated with human primary T cells transduced with anti-HIV-1 "Effector" CARs at various Effector vs Target cell ratios. Absolute cell numbers of each population were collected by MACSQuant Analyzer and used for calculation of relative cytotoxicity. We successfully ranked the cytotoxicity of three previously reported single chain-antibody CARs and six newly developed single-domain antibody CARs in comparison to CD4{zeta} CAR. Interestingly, three CARs--10E8, 2E7, and 2H10--which demonstrate high cytotoxic activity were all known to target the membrane-proximal external region. Use of this novel assay will simplify assessment of new CAR constructs and in turn accelerate the development of new effective CARs against HIV-1. Author SummaryAdoptive immunotherapies that utilize autologous T cells expressing a desired antigen-specific CAR aim to elicit directed immune responses. In recent years, CAR immunotherapies have been promoted extensively in B cell malignancy treatments. The HIV-1-targeting CAR, known as CD4{zeta}, was developed over 20 years ago and has been widely and longitudinally tested in patients. However, its effectiveness was hindered by poor survival and functionality of the transduced cells. To conduct quantitative evaluation of newly designed anti-HIV-1 CARs, we developed a novel multicolor flow-based assay for HIV-1-specific cytotoxicity, enabling sensitive and quantitative assessment in a high-throughput fashion. This assay would be also useful in screening HIV-1-targeting immune receptors--including CARs and T cell receptors--and other immunotherapeutic drugs such as anti-HIV-1 antibodies.

microbiology↗

Role of the high-affinity leukotriene B4 receptor signaling in fibrosis after unilateral ureteral obstruction in mice

Leukotriene B4 (LTB4) is a lipid mediator that acts as a potent chemoattractant for inflammatory leukocytes. Kidney fibrosis is caused by migrating inflammatory cells and kidney-resident cells. Here, we examined the role of the high-affinity LTB4 receptor BLT1 during development of kidney fibrosis in wild-type (WT) mice and BLT1 knockout (BLT1-/-) mice with unilateral ureteral obstruction (UUO). We found elevated expression of 5-lipoxygenase (5-LOX), which generates LTB4, in the renal tubules of WT and BLT1-/- UUO mice. Accumulation of immunoreactive type I collagen in UUO kidneys of WT mice increased over time; however, the increase was less prominent in BLT1-/- mice. Accumulation of S100A4-positive fibroblasts also increased temporally in WT UUO kidneys, but was again less pronounced in those of BLT1-/- mice. The same was true of mRNA encoding transforming growth factor-{beta} (TGF)-{beta} and fibroblast growth factor (FGF)-2. Finally, accumulation of F4/80-positive macrophages, which secrete TGF-{beta}, also increased temporally in WT UUO and BLT1-/- kidneys, but to a lesser extent in the latter. Following LTB4 stimulation in vitro, macrophages showed increased expression of mRNA encoding TGF-{beta}/FGF-2 and Col1a1, whereas L929 fibroblasts showed increased expression of mRNA encoding smooth muscle actin (SMA). Bone marrow (BM) transplantation studies revealed that the area positive for type I collagen was significantly smaller in BLT1-/--BM[->]WT UUO kidneys than in WT-BM[->]WT kidneys. Thus, LTB4-BLT1 signaling plays a critical role in fibrosis in UUO kidneys by increasing accumulation of macrophages and fibroblasts. Therefore, blocking BLT1 may prevent renal fibrosis.

pharmacology and toxicology↗