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Katagiri, M.

Publications and source records attributed to Katagiri, M..

4 recordsLinked to original sources

Bioengineered iPSC Vessels Recapitulate Human Vascular Physiological Function and Aging Phenotypes

Vascular aging contributes to multisystem diseases and limits health span. Although various animal models have contributed to aging research, their vasculatures poorly recapitulate human physiology. Even existing tissue-engineered blood vessels fail to mimic human vascular function and pathology, hindering translational advances in vascular aging studies. Here, we present a novel human physiological vascular model fabricated via the unique molding-induced circumferential alignment of human induced pluripotent stem cell (iPSC)-derived vascular smooth muscle cells with luminally seeded endothelial cells. This architecture enabled dynamic vasodiameter changes in response to vasoactive stimuli, including hormones and intraluminal pressure. Using iPSCs from a patient with Werner syndrome, the model recapitulated aging-associated phenotypes, such as hypercontractility and increased vascular compliance, possibly due to impaired nitric oxide bioavailability. Transcriptomic and metabolomic analyses revealed age-related dysregulation consistent with vascular senescence. As a key advantage of the vasculature, spatial transcriptomic analysis demonstrated upregulation of the aging marker CDKN1A near the lumen and downregulation of COL6A1 and TPM1 throughout the vessel. Treatment with mitochonic acid 5, a mitochondria-targeted compound, significantly reversed the aging phenotypes. These findings demonstrate that our engineered vascular model recapitulates key aspects of human vascular properties and provides a platform for mechanistic studies of vascular aging and drug discovery aimed at extending health span.

bioengineering↗

Kaempferol exerts anti-inflammatory effects by accelerating Treg development via AhR-mediated and PU.1/IRF4-dependent transactivation of the Aldh1a2/RALDH2 gene in dendritic cells

Retinaldehyde dehydrogenase 2 encoded in the Aldh1a2 gene (RALDH2) is expressed in intestinal dendritic cells (DCs) in mesenteric lymph nodes (MLNs) and plays a crucial role in Treg development by producing retinoic acid. In the present study, we screened food ingredients and identified kaempferol, a flavonoid, as the compound that most effectively up-regulated RALDH2 expression in DCs. The development of Foxp3+ cells from OT-II-derived naive CD4+ T cells was enhanced by a co-culture with OVA peptide-pulsed bone marrow-derived DCs (BMDCs) in the presence of kaempferol or by a pre-treatment of BMDCs with kaempferol. The involvement of the aryl hydrocarbon receptor (Ahr) in the effects of kaempferol on Aldh1a2 expression was demonstrated by in vitro experiments using siRNA and various agonistic or antagonistic compounds of AhR. AhR suppressed Aldh1a2 gene expression and kaempferol inhibited the AhR activity by functioning as an antagonist of AhR. The kaempferol treatment also increased the protein levels of PU.1 and IRF4, which are essential for transcription of the Aldh1a2 gene in DCs, and accelerated the subsequent recruitment of PU.1 to the Aldh1a2 gene. The kaempferol-induced increase in PU.1 protein levels occurred in an AhR-dependent and transcription-independent manner, whereas the kaempferol treatment transactivated the Irf4 gene in DCs. The frequency of DCs exhibiting RALDH2 activity in the MLNs of mice was increased by the intraperitoneally (i.p.) administration of an AhR antagonist or by the oral administration of astragalin, a 3-O-glucoside of kaempferol. We also observed an increase in Tregs in the Peyers patches of C57BL/6 mice i.p. administered kaempferol-treated BMDCs. We utilized an OVA-induced food allergy model of Balb/c mice to examine the effects of kaempferol in vivo and confirmed that the rapid decrease in body temperature and allergic diarrhea observed just after the OVA challenge were significantly suppressed in mice administered kaempferol.

immunology↗

NR4A3 deficiency ameliorates contact hypersensitivity and exacerbates psoriasis by regulating gene expression in dendritic cells

NR4A3 is a transcription factor that belongs to the nuclear receptor superfamily. To reveal the roles of NR4A3 in skin diseases, we constructed contact hypersensitivity (CHS)- and imiquimod-induced psoriasis models in Nr4a3-/- mice. In the CHS induced Nr4a3-/- mice, ear swelling was significantly reduced, accompanied by suppressed migration of dendritic cells (DCs), in which CCR7 expression was reduced. In contrast, ear swelling in psoriasis model Nr4a3-/- mice was enhanced. The expression levels of inflammatory cytokines in psoriasis skin lesions and in TLR7-ligand-stimulated DCs were increased by NR4A3 deficiency. Subcutaneous (s.c.) injection of hapten-treated Nr4a3+/+ DCs induced ear swelling in Nr4a3-/- mice, and s.c. injection of TLR7-ligand-stimulated Nr4a3-/- DCs caused significant ear swelling. Compared with Nr4a3+/+ DCs, Nr4a3-/- DCs expressed lower levels of CCR7 and IRF4, and higher levels of TLR7, IRF7, IFN-{beta}, and PU.1. Taken together, NR4A3 deficiency ameliorates CHS and exacerbates psoriasis by regulating the expression of CCR7, TLR7, and related transcription factors in DCs.

immunology↗

Recycling of uridylated mRNAs in starfish embryos

In eukaryotes, mRNAs with long poly(A) tails are translationally active, whereas deadenylation of the tails decreases translation and uridylation of the short poly(A) tails causes the mRNA to be degraded. In this study, we confirmed that maternal cyclin B mRNAs with long poly(A) tails in blastula embryos of invertebrate starfish were deadenylated and uridylated, followed by decay. In starfish oocytes, however, cyclin B mRNAs with uridylated short poly(A) tails are stable. They are polyadenylated and translationally active immediately following hormonal stimulation for resumption of meiosis. Similarly, maternal ribosomal protein mRNAs, Rps29 and Rpl27a, which become uridylated following deadenylation upon hormonal stimulation, remain stable even after fertilisation and early development. At the morula stage, the uridylated maternal ribosomal protein mRNAs are modified to yield non-canonical poly (A) tails rich in U and G residues in the 5 region and in A residues at the 3 end, rendering them translationally active. These results indicate that the fates of uridylated mRNAs in starfish are decay and/or recycling.

molecular biology↗