Characterization of Senescence-Accelerated Mouse Prone 6 (SAMP6) as an Animal Model for Brain Research

Niimi, Kimie; Takahashi, Eiki

doi:10.1538/expanim.63.1

Cited by 8 publications

(5 citation statements)

References 71 publications

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“…Among SAMP strains, SAMP1 and SAMP6 show the change of locomotor activity and motor dyscoordination in rotarod test ( Niimi et al, 2009 ; Aoyama et al, 2013 ) and are useful models of age-related motor dyscoordination. However, SAMP1 also shows skeletal muscle atrophy, senile amyloidosis, impaired immune response, hyperinflation of the lungs, hearing impairment, and lower locomotor activity ( Takeda, 1999 ; Sakakima et al, 2004 ), and SAMP6 is a model of senile osteoporosis and 1 month old SAMP8 already impairs motor coordination ( Matsushita et al, 1986 ; Niimi and Takahashi, 2014 ). Taken together, motor dyscoordination of SAMP1 and SAMP6 is likely to be susceptible to some factors in addition to aging and the cerebellum.…”

Section: Introductionmentioning

confidence: 99%

“…These SAMP lines are useful for an evaluation of putative anti-aging therapies (Takahashi, 2010). Motor dyscoordination is one of the age-related disorders and there has been several studies about age-related motor dyscoordination in SAMP strains (Niimi et al, 2009;Aoyama et al, 2013;Niimi and Takahashi, 2014). Among SAMP strains, SAMP1 and SAMP6 show the change of locomotor activity and motor dyscoordination in rotarod test (Niimi et al, 2009;Aoyama et al, 2013) and are useful models of agerelated motor dyscoordination.…”

Section: Introductionmentioning

confidence: 99%

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Motor Dyscoordination and Alteration of Functional Correlation Between DGKγ and PKCγ in Senescence-Accelerated Mouse Prone 8 (SAMP8)

Tsumagari

Maruo

Nakao

et al. 2021

Front. Aging Neurosci.

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Senescence-accelerated mouse prone 8 (SAMP8) is an animal model of age-related central nervous system (CNS) disorders. Although SAMP8 shows deficits in learning, memory, and emotion, its motor coordination has not been clarified. We have recently reported that DGKγ-regulated PKCγ activity is important for cerebellar motor coordination. However, involvement of the functional correlation between the kinases in age-related motor dyscoordination still remains unknown. Therefore, we have investigated the motor coordination in SAMP8 and involvement of the functional correlation between DGKγ and PKCγ in the age-related motor dyscoordination. Although 6 weeks old SAMP8 showed equivalent motor coordination with control mice (SAMR1) in the rotarod test, 24 weeks old SAMP8 exhibited significantly less latency in the rotarod test and more frequent slips in the beam test compared to the age-matched SAMR1. Furthermore, 24 weeks old SAMP8 showed the higher locomotor activity in open field test and Y-maze test. Western blotting revealed that DGKγ expression decreased in the cerebellum of 24 weeks old SAMP8, while PKCγ was upregulated. These results suggest that SAMP8 is a useful model of age-related motor dysfunction and that the DGKγ-regulated PKCγ activity is involved in the age-related motor dyscoordination.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Motor Dyscoordination and Alteration of Functional Correlation Between DGKγ and PKCγ in Senescence-Accelerated Mouse Prone 8 (SAMP8)

Tsumagari

Maruo

Nakao

et al. 2021

Front. Aging Neurosci.

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“…In addition, SAMP6 mice showed increased bone marrow cavity and trabecular space (Tb.Sp), decreased maximum elastic stress and load, and decreased number of osteoblasts (Ji et al, 2023) leading to an early disturbance of bone homeostasis (Chen et al, 2009;Ichioka et al, 2002;Niimi et al, 2014). Osteoblasts and osteocytes in the TB of SAMP6 mice at two and five months of age showed degenerative changes, such as mitochondrial swelling and fragmentation and myelin-like structures (Chen et al, 2004), Additionally, the mice had fewer osteoblasts on the trabecular bone and inner surface of bone (Chen et al, 2004;Jilka et al, 1996) and increased bone marrow adiposity.…”

Section: The Samp6 Premature Aging Mouse Modelmentioning

confidence: 99%

“…BMSCs are abnormally differentiated and differentiate in favor of adipogenesis rather than osteogenesis (Chen et al, 2009;Ichioka et al, 2002;Niimi et al, 2014).…”

Section: Samp6 Micementioning

confidence: 99%

Skeletal phenotypes and molecular mechanisms in aging mice

Guan,

Zhang,

Wang

et al. 2024

Zoological Research

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Aging is an inevitable physiological process. With aging, bone often undergoes age-related bone loss, and then a series of bone-related diseases that seriously threaten the health of the human body can occur. The use of humans as the research object of studies of skeletal disease caused by aging faces many problems, such as long study duration, inconvenient sampling, significant influence by regional factors, and high investment. Mice are the first choice for studying the effects of aging on the skeletal system due to the similar structure and function of their motor system to that of humans, simple control, easy access, low cost, and short generation time. Therefore, this review summarizes the characteristics, limitations, scope of application, the bone phenotypes and the treatment methods of naturally aging mice and premature aging mouse models (including SAMP6 mice, Polg mutant mice, Lmna mice, Sirt6 mice, Zmpste24 mice, Tfam mice, Ercc1 mice, Werner mice and KL/KL-deficient mice). The molecular mechanisms of these aging mouse models, including the cellular DNA damage response, senescence-related secretory phenotype, telomere shortening, oxidative stress, bone marrow stem cell abnormalities and mitochondrial dysfunction, are summarized. We hope that this review will contribute to the understanding of the pathogenesis of aging related bone diseases.

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“…In the age of 4 months, SAM/P6 mice presents the full spectrum of senile osteoporosis symptoms: low global bone density, deteriorated osteogenesis of bone marrow, deficits in endocortical mineralizing surface, reduction of BMD index and BV/TV index, as well as reduced calcium and phosphorus level. In addition, SAM/P6 mice are characterised by age-dependent inhibition of osteoblastogenesis and osteoclastogenesis but enhanced adipogenesis, which results in early disturbances of bone homeostasis [22][23][24].…”

Section: Model Of Senescence-accelerated Mice Pronementioning

confidence: 99%

MiR-21-5p regulates the dynamic of mitochondria network and rejuvenates the senile phenotype of bone marrow stromal cells (BMSCs) isolated from osteoporotic SAM/P6 mice

et al. 2023

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Background Progression of senile osteoporosis is associated with deteriorated regenerative potential of bone marrow-derived mesenchymal stem/stromal cells (BMSCs). According to the recent results, the senescent phenotype of osteoporotic cells strongly correlates with impaired regulation of mitochondria dynamics. Moreover, due to the ageing of population and growing osteoporosis incidence, more efficient methods concerning BMSCs rejuvenation are intensely investigated. Recently, miR-21-5p was reported to play a vital role in bone turnover, but its therapeutic mechanisms in progenitor cells delivered from senile osteoporotic patients remain unclear. Therefore, the goal of this paper was to investigate for the first time the regenerative potential of miR-21-5p in the process of mitochondrial network regulation and stemness restoration using the unique model of BMSCs isolated from senile osteoporotic SAM/P6 mice model. Methods BMSCs were isolated from healthy BALB/c and osteoporotic SAM/P6 mice. We analysed the impact of miR-21-5p on the expression of crucial markers related to cells’ viability, mitochondria reconstruction and autophagy progression. Further, we established the expression of markers vital for bone homeostasis, as well as defined the composition of extracellular matrix in osteogenic cultures. The regenerative potential of miR-21 in vivo was also investigated using a critical-size cranial defect model by computed microtomography and SEM–EDX imaging. Results MiR-21 upregulation improved cells’ viability and drove mitochondria dynamics in osteoporotic BMSCs evidenced by the intensification of fission processes. Simultaneously, miR-21 enhanced the osteogenic differentiation of BMSCs evidenced by increased expression of Runx-2 but downregulated Trap, as well as improved calcification of extracellular matrix. Importantly, the analyses using the critical-size cranial defect model indicated on a greater ratio of newly formed tissue after miR-21 application, as well as upregulated content of calcium and phosphorus within the defect site. Conclusions Our results demonstrate that miR-21-5p regulates the fission and fusion processes of mitochondria and facilitates the stemness restoration of senile osteoporotic BMSCs. At the same time, it enhances the expression of RUNX-2, while reduces TRAP accumulation in the cells with deteriorated phenotype. Therefore, miR-21-5p may bring a novel molecular strategy for senile osteoporosis diagnostics and treatment.

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Characterization of Senescence-Accelerated Mouse Prone 6 (SAMP6) as an Animal Model for Brain Research

Cited by 8 publications

References 71 publications

Motor Dyscoordination and Alteration of Functional Correlation Between DGKγ and PKCγ in Senescence-Accelerated Mouse Prone 8 (SAMP8)

Motor Dyscoordination and Alteration of Functional Correlation Between DGKγ and PKCγ in Senescence-Accelerated Mouse Prone 8 (SAMP8)

Skeletal phenotypes and molecular mechanisms in aging mice

MiR-21-5p regulates the dynamic of mitochondria network and rejuvenates the senile phenotype of bone marrow stromal cells (BMSCs) isolated from osteoporotic SAM/P6 mice

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