Publications by authors named "Koki Hiura"

Patients with inflammatory bowel disease (IBD) who experience long-term chronic inflammation of the colon are at an increased risk of developing colorectal cancer (CRC). Mitotic spindle positioning (MISP), an actin-binding protein, plays a role in mitosis and spindle positioning. MISP is found on the apical membrane of the intestinal mucosa and helps stabilize and elongate microvilli, offering protection against colitis.

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  • Adriamycin nephropathy (ADR) is a common model used to study chronic kidney disease in mice, particularly in the BALB/c strain, while the C57BL/6J strain does not develop this condition.
  • A study found that the C57BL/6N strain (B6N) is susceptible to ADR nephropathy, with significant symptoms observed in C57BL/6NCrl (NCrl) mice, but not in C57BL/6NJcl (NJcl) mice.
  • The study also revealed that the severity of ADR nephropathy varies based on the route of administration, with more severe effects seen when ADR is administered through the tail vein rather than the orbital vein.
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Adriamycin (ADR) is an effective chemotherapy drug for various cancers but has serious side effects. ADR-induced liver damage is a common problem during therapy, but the underlying mechanism remains to be fully understood. In contrast, ADR-induced glomerular damage is well studied in rodents, and sensitivity to ADR-induced nephropathy is because of the R2140C polymorphism of Prkdc gene.

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Most mitochondrial diseases are hereditary and highly heterogeneous. Cattle born with the V79L mutation in the isoleucyl-tRNA synthetase 1 (IARS1) protein exhibit weak calf syndrome. Recent human genomic studies about pediatric mitochondrial diseases also identified mutations in the IARS1 gene.

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Inflammatory bowel disease (IBD) is classified into two types: Crohn's disease and ulcerative colitis. In IBD, the imbalance between the pro-inflammatory and anti-inflammatory cytokines prevents recovery from the inflammatory state, resulting in chronic inflammation in the colon. The mitotic spindle positioning protein (MISP) is localized to the apical membrane in the colon.

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  • Animal models are crucial for studying podocytopathy and chronic kidney diseases (CKD), with Adriamycin (ADR)-induced nephropathy being a key rodent model.
  • BALB/c mice are sensitive to ADR, whereas the commonly used C57BL/6 (B6) mice are resistant, necessitating the creation of a B6 strain that can develop ADR nephropathy.
  • The study shows that the newly developed B6-Prkdc mutants progress to CKD after ADR treatment and reveals differences in gene expressions related to inflammation between B6-Prkdc and BALB/c mice, indicating a need for further research.
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Cystinuria is an autosomal metabolic disorder caused by mutations in the SLC3A1 and SLC7A9 genes, encoding the amino acid transporter proteins rBAT and bAT, respectively. Based on the causative gene, cystinuria is classified into 3 types: type A (SLC3A1), type B (SLC7A9), and type AB (SLC3A1 and SLC7A9). Patients with cystinuria exhibit hyperexcretion of cystine and dibasic amino acids in the urine and develop cystine crystals due to its low solubility in the urine, often resulting in calculus formation.

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Adriamycin (ADR)-induced nephropathy is frequently utilized in rodent models of podocytopathy. However, the application of this model in mice is limited to a few strains, such as BALB/c mice. The most commonly used mouse strain, C57BL/6 (B6), is resistant to ADR-induced nephropathy, as are all mouse strains with a B6 genetic background.

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Mast cell-deficient mice are helpful for understanding the roles of mast cells in vivo. To date, a dozen mouse models for mast cell deficiency have been reported. However, mice with a specific depletion of all populations of mast cells have not been reported.

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The number of patients with chronic kidney disease (CKD) is growing continuously globally. In order to study pathogenesis and mechanisms, many animal models have been developed, including spontaneous, genetic, and induced models. Although each type of CKD shows disease-specific tissue changes in the early stages, tubular disorder and interstitial fibrosis histologically occur in the course of progression to end-stage renal failure.

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Diabetic animal models have made significant contributions to understanding the etiology of diabetes and to the development of new medications. Our research group recently developed a novel diabetic mouse strain, the insulin hyposecretion (ihs)mouse. The strain involves neither obesity nor insulitis but exhibits notable pancreatic β-cell dysfunction, distinguishing it from other well-characterized animal models.

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Article Synopsis
  • Tensins2 (TNS2) is a protein involved in maintaining podocytes, crucial for kidney function, with specific domains influencing its role.
  • Genetic mutations in TNS2, specifically the deletion of the SH2-PTB domain, led to significant kidney damage and protein loss in mice, while other mutations did not show these effects.
  • The study indicates that the SH2-PTB domain of TNS2 is essential for its localization at focal adhesions and the overall maintenance of podocytes postnatally.
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