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12. Molecular Mechanisms of Aggregation of Canine SOD1 E40K Amyloidogenic Mutant Protein.

Author

Wakayama, Kento, Kimura, Shintaro, Kobatake, Yui, Kamishina, Hiroaki, Nishii, Naohito, Takashima, Satoshi, Honda, Ryo, and Kamatari, Yuji O.

Subjects
MUTANT proteins, AMYOTROPHIC lateral sclerosis, AMINO acid residues, AMYLOID beta-protein, SUPEROXIDE dismutase, STRUCTURAL stability, NEURODEGENERATION
Abstract

Canine degenerative myelopathy (DM) is a human amyotrophic lateral sclerosis (ALS)-like neurodegenerative disease. It is a unique, naturally occurring animal model of human ALS. Canine DM is associated with the aggregation of canine superoxide dismutase 1 (cSOD1), which is similar to human ALS. Almost 100% of cases in dogs are familial, and the E40K mutation in cSOD1 is a major causative mutation of DM. Therefore, it is important to understand the molecular mechanisms underlying cSOD1(E40K) aggregation. To address this, we first analyzed the structural model of wild type cSOD1. Interactions were evident between amino acid E40 and K91. Therefore, the mutation at residue E40 causes loss of the interaction and may destabilize the native structure of cSOD1. Differential scanning fluorimetry revealed that the E40K mutant was less stable than the wild type. Moreover, stability could be recovered by the E40K and K91E double mutation. Acceleration of amyloid fibril formation in vitro and aggregate formation in cells of cSOD1(E40K) was also suppressed by the introduction of this double mutation in thioflavin T fluorescence assay results and in transfectant cells, respectively. These results clearly show the importance of the interaction between amino acid residues E40 and K91 in cSOD1 for the stability of the native structure and aggregation. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Usefulness of Pain Scales for Postoperative Pain in Dogs

Author

KAWAHARADA, Mika, primary, OGAWA, Mizuho, additional, HASEGAWA, Tomomi, additional, FUCHIGAMI, Hitomi, additional, TAKASHIMA, Satoshi, additional, NISHII, Naohito, additional, OZAWA, Tsuyoshi, additional, NAGAHAMA, Shotaro, additional, and SHIBATA, Sanae, additional

Published
2022
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16. Stillbirth rates and their association with swine leucocyte antigen class II haplotypes in Microminipigs

Author

Imaeda, Noriaki, primary, Ando, Asako, additional, Matsubara, Tatsuya, additional, Takasu, Masaki, additional, Nishii, Naohito, additional, Miyamoto, Asuka, additional, Ohshima, Shino, additional, Kametani, Yoshie, additional, Suzuki, Shingo, additional, Shiina, Takashi, additional, Ono, Tetsushi, additional, Kulski, Jerzy K., additional, and Kitagawa, Hitoshi, additional

Published
2021
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18. The long-term clinical course of canine degenerative myelopathy and therapeutic potential of curcumin

Author

KOBATAKE, Yui, NAKATA, Kohei, SAKAI, Hiroki, SASAKI, Jun, YAMATO, Osamu, TAKASHIMA, Satoshi, NISHII, Naohito, MAEDA, Sadatoshi, ISLAM, Md Shafiqul, KAMISHINA, Hiroaki, KOBATAKE, Yui, NAKATA, Kohei, SAKAI, Hiroki, SASAKI, Jun, YAMATO, Osamu, TAKASHIMA, Satoshi, NISHII, Naohito, MAEDA, Sadatoshi, ISLAM, Md Shafiqul, and KAMISHINA, Hiroaki

Abstract

Canine degenerative myelopathy (DM), recognized as a spontaneous model of amyotrophic lateral sclerosis, is known as a late-onset progressive degenerative disease of the spinal cord. Because of the progressive nature of DM, many dogs are elected to be euthanized, resulting in limited information on the end-stage clinical presentation. We investigated the long-term clinical course from diagnosis to natural death to further deepen our understanding of the entire clinical picture of this disease. Because curcumin was administered in some cases, the therapeutic effect of curcumin on DM was also examined. Forty dogs included in this study were client-owned Pembroke Welsh Corgis with a definitive diagnosis of DM by necropsy and histopathology. Dogs were excluded from this study if they died from another disease or were elected to be euthanized. Information on the long-term clinical symptoms of DM was investigated based on a questionnaire, which was collected from the dog owners. Urinary incontinence and respiratory disorder were observed in most dogs, as was respiratory impairment-correlated death. In contrast, signs consistent with brainstem dysfunction were noticed at the terminal stage in a small portion of dogs. Although further studies with more cases are needed, the results of this study suggest that administration of curcumin is effective in slowing the progression of DM.

Published
2021

19. Additional file 1 of PCR-based genotyping assays to detect germline APC variant associated with hereditary gastrointestinal polyposis in Jack Russell terriers

Author

Yoshizaki, Kyoko, Hirata, Akihiro, Matsushita, Hiroyuki, Nishii, Naohito, Mifumi Kawabe, Mori, Takashi, and Sakai, Hiroki

Abstract

Additional file 1: Figure S1. PCR-RFLP assay conducted to determine the optimal digestion time. Acrylamide gel electrophoresis of MseI-digested PCR products amplified from synthetic wild-type and mutant DNA (A), and blood-derived DNA samples of a carrier and a non-carrier of germline APC variant (B). PCR products amplified from each sample were digested with MseI for 0, 1, 2, 4, 8, 12, and 24 h.

Published
2021
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31. Familial adenomatous polyposis in dogs: hereditary gastrointestinal polyposis in Jack Russell Terriers with germline APC mutations.

Author

Yoshizaki, Kyoko, Hirata, Akihiro, Nishii, Naohito, Kawabe, Mifumi, Goto, Minami, Mori, Takashi, and Sakai, Hiroki

Subjects
ADENOMATOUS polyposis coli, DOGS, GERM cells, DOG diseases, COLON polyps, ADENOMATOUS polyps, DESMOID tumors
Abstract

Many hereditary disorders in dogs have equivalents in humans and thus attract attention as natural animal models. Breed predisposition to certain diseases often provides promising clues to explore novel hereditary disorders in dogs. Recently, cases of gastrointestinal (GI) polyps in Jack Russell Terriers (JRTs) have increased in Japan. In 21 affected JRTs, polyps were found in either or both the stomach and colorectum, with a predilection for the gastric antrum and rectum. Multiple polyps were found in 13 of 21 examined dogs, including 5 dogs with both gastric and colorectal polyps. Some dogs were found to have GI polyps at an early age, with the youngest case being 2.3 years old. Histopathologically, 43 of 46 GI polyps (93.5%) were diagnosed as adenomas or adenocarcinomas. Immunohistochemical analysis revealed cytoplasmic and nuclear accumulation of β-catenin in the tumor cells. As in the case of human patients with familial adenomatous polyposis, all examined JRTs with GI polyps (n = 21) harbored the identical heterozygous germline APC mutations, represented by a 2-bp substitution (c.[462A>T; 463A>T]). The latter substitution was a non-sense mutation (p.K155X) resulting in a truncated APC protein, thus suggesting a strong association with this cancer-prone disorder. Somatic mutation and loss of the wild-type APC allele were detected in the GI tumors of JRTs, suggesting that biallelic APC inactivation was involved in tumor development. This study demonstrated that despite differences in the disease conditions between human and dog diseases, germline APC mutation confers a predisposition to GI neoplastic polyps in both dogs and humans. [ABSTRACT FROM AUTHOR]

Published
2021
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33. Influence of swine leukocyte antigen haplotype on serum antibody titers against swine erysipelas vaccine and reproductive and meat production traits of SLA-defined selectively bred Duroc pigs

Author

IMAEDA, Noriaki, primary, ANDO, Asako, additional, TAKASU, Masaki, additional, MATSUBARA, Tatsuya, additional, NISHII, Naohito, additional, TAKASHIMA, Satoshi, additional, SHIGENARI, Atsuko, additional, SHIINA, Takashi, additional, and KITAGAWA, Hitoshi, additional

Published
2018
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38. Identification and characterization of two CD4 alleles in Microminipigs

Author

Matsubara, Tatsuya, primary, Nishii, Naohito, additional, Takashima, Satoshi, additional, Takasu, Masaki, additional, Imaeda, Noriaki, additional, Aiki-Oshimo, Kayo, additional, Yamazoe, Kazuaki, additional, Kakisaka, Michinori, additional, Takeshima, Shin-nosuke, additional, Aida, Yoko, additional, Kametani, Yoshie, additional, Kulski, Jerzy K., additional, Ando, Asako, additional, and Kitagawa, Hitoshi, additional

Published
2016
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49. Dirofilariasis

Author

KITAGAWA, Hitoshi, primary, SASAKI, Yoshihide, additional, NISHII, Naohito, additional, and KITOH, Katsuya, additional

Published
2014
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