Animal Models in Aging Research

Masoro, Edward J.

doi:10.1016/b978-0-12-627871-2.50011-4

Cited by 10 publications

(12 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The life span of SAMP mice is shorter than that of other mouse models used for aging research (CBA, C57BL, RFM and NZB strains) [3], and agedependent changes in reproductive functions are more severe in SAMP mice than in other murine models [4][5][6][7]. Previously, we found that some LBs in the ovaries of SAMP mice with regular estrus cycles were abnormally accumulated [8].…”

Section: Discussionmentioning

confidence: 99%

“…SAM-prone (SAMP) mice show accelerated changes in many of the signs of aging including a moderate to severe loss of activity, hair loss and lack of hair glossiness, skin coarseness, periophthalmic lesions, increased lordokyphosis of the spine and a shortened life span as compared with SAM-resistant (SAMR) mice, which is the control strain that ages normally. A lt h o u gh ph ys i o l o gi c al , pa t ho lo g ic a l and biochemical changes associated with aging in SAMP mice with advancing age have been studied by m any investigato rs [3], there hav e been insufficient data on reproductive properties in SAM mice. We previously compared male [4,5] and female reproductive properties and the early embryonic development of SAMP mice with those of SAMR mice [6,7].…”

mentioning

confidence: 99%

See 1 more Smart Citation

Abnormal Structural Luteolysis in Ovaries of the Senescence Accelerated Mouse (SAM): Expression of Fas Ligand/Fas-Mediated Apoptosis Signaling Molecules in Luteal Cells

Kiso

Manabe

Komatsu

et al. 2003

Journal of Reproduction and Development

View full text Add to dashboard Cite

Abstract. Senescence accelerated mouse-prone (SAMP) mice with a shortened life span show accelerated changes in many of the signs of aging and a shorter reproductive life span than SAMresistant (SAMR) controls. We previously showed that functional regression (progesterone dissimilation) occurs in abnormally accumulated luteal bodies (aaLBs) of SAMP mice, but structural regression of luteal cells in aaLB is inhibited. A deficiency of luteal cell apoptosis causes the abnormal accumulation of LBs in SAMP ovaries. In the present study, to show the abnormality of Fas ligand (FasL)/Fas-mediated apoptosis signal transducing factors in the aaLBs of the SAMP ovaries, we assessed the changes in the expression of FasL, Fas, caspase-8 and caspase-3 mRNAs by reverse transcription-polymerase chain reaction, and in the expression and localization of FasL, Fas and activated caspase-3 proteins by Western blotting and immunohistochemistry, respectively, during the estrus cycle/luteolysis. These mRNAs and proteins were expressed in normal LBs of both SAMP and SAMR ovaries, but not at all or only in trace amounts in aaLBs of SAMP, indicating that structural regression is inhibited by blockage of the expression of these transducing factors in luteal cells of aaLBs in SAMP mice. Key words: Apoptosis, Fas ligand/Fas system, Intracellular signal transduction, Luteolysis, Senescence accelerated mouse (SAM) (J. Reprod. Dev. 49: [457][458][459][460][461][462][463] 2003) he senescence accelerated mouse (SAM) strain, which is an inbred strain of AKR mice, was bred and established in Kyoto University by Takeda et al. [1,2] and is a useful animal model for studying senescence. SAM-prone (SAMP) mice show accelerated changes in many of the signs of aging including a moderate to severe loss of activity, hair loss and lack of hair glossiness, skin coarseness, periophthalmic lesions, increased lordokyphosis of the spine and a shortened life span as compared with SAM-resistant (SAMR) mice, which is the control strain that ages normally. A lt h o u gh ph ys i o l o gi c al , pa t ho lo g ic a l and biochemical changes associated with aging in SAMP mice with advancing age have been studied by m any investigato rs [3], there hav e been insufficient data on reproductive properties in SAM mice. We previously compared male [4,5] and female reproductive properties and the early embryonic development of SAMP mice with those of SAMR mice [6,7]. During the investigations on the reproductive properties of SAM mice, we found abnormally accumulated luteal bodies (aaLBs) in the ovaries of SAMP mice [8]. During the estrous cycle, no differences between the kinetics of 17β-

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Abnormal Structural Luteolysis in Ovaries of the Senescence Accelerated Mouse (SAM): Expression of Fas Ligand/Fas-Mediated Apoptosis Signaling Molecules in Luteal Cells

Kiso

Manabe

Komatsu

et al. 2003

Journal of Reproduction and Development

View full text Add to dashboard Cite

show abstract

“…1 The applicability of rodents and other nonprimate animals as models in cardiovascular physiology and aging research has been debated in a number of publications. [2][3][4][5] Significant dissimilarities between different taxonomic groups of mammals also exist at the cellular level. For instance, rodent and human cells differ in responses to carcinogens in vivo and in cell culture.…”

Section: Andrei B Borisov Phdmentioning

confidence: 99%

“…The paraphrase “to muddle or to model, that is the question” was used as the epigraph to one of the recent reviews concerning the principles and philosophy of modeling in present‐day experimental biology and medicine 1 . The applicability of rodents and other nonprimate animals as models in cardiovascular physiology and aging research has been debated in a number of publications 2‐5 . Significant dissimilarities between different taxonomic groups of mammals also exist at the cellular level.…”

mentioning

confidence: 99%

Regeneration of skeletal and cardiac muscle in mammals: do nonprimate models resemble human pathology?

Borisov

1999

Wound Repair Regeneration

View full text Add to dashboard Cite

Most of the available information regarding the regenerative potential and compensatory remodeling of mammalian tissues has been obtained from nonprimate animals, mainly rodent experimental models. The increasing use of transgenic mice for studies of the mechanisms controlling organogenesis and regeneration also requires a clear understanding of their applicability as experimental models for studies of similar processes in humans and other mammals. Application of modern cell biology methods to studies of regenerative processes has provided new insights into similarity and differences in cellular responses to injury in the tissues of different mammalian species. During more than 200-million years of progressive divergent evolution of mammals, cellular mechanisms of tissue regeneration and compensatory remodeling evolved together with increasingly adaptive functional specialization and structural complexity of mammalian tissues and organs. Rodents represent a phylogenetically ancient order of mammals that has conservatively retained a number of morphofunctional characteristics of early representatives of this class, which include enhanced regenerative capacity of tissues. A comparative analysis of regenerative processes in skeletal and cardiac muscle, as well as in several other mammalian tissues, shows that time courses and intensities of regeneration in response to the same type of injury vary even within taxonomically related species (e.g., rat, mouse, and hamster). The warm bloodedness of mammals facilitated the development of more complex mechanisms of metabolic, immune, and neurohumoral regulation, which resulted in a stronger dependence of regenerative processes on vascularization and innervation. For this reason, interspecies modifications of regenerative responses are limited by the capacity of the animal to resorb rapidly the foci of necrosis and to revascularize and reinnervate the volume of the regenerating tissue. These differences, among other factors, result in significantly lower rates of reparative regeneration in mammals possessing larger body sizes than rodents. A review of these data strongly indicates that the phylogenetic age and biological differences between different species should be taken into account before extrapolation of regenerative properties of nonprimate tissues on the regenerative responses in the primates.

show abstract

“…The SAM model meets most criteria for the use of mammalian models for aging research, such as life table data, short life span, defined environmental conditions, and genetic characteristics, as proposed by Masoro (1990). The use of mice to study the genetics of aging and age-associated pathologies has definite advantages: the richness of genetic information available on this species and the similarity of mouse and human genetics (Sprott 1994).…”

Section: Significance Of Sam Developmentmentioning

confidence: 99%

Senescence-accelerated Mouse (SAM): With Special Reference to Development and Pathobiological Phenotypes

Takeda

Higuchi²,

Hosokawa³

1997

ILAR Journal

View full text Add to dashboard Cite

Harrison DE. 1994. Potential misinterpretations using models of accelerated aging. J Gerontol Biol Sci 49:B245. Klinger MM, MacCarter GD, Boozer CN. 1996. Body weight and composition in the Sprague Dawley rat: Comparison of three outbred sources. Lab Anim Sci 46:67-70. Lipman RD, Chrisp CE, Hazzard DG, Branson RT. 1996. Pathologic characterization of Brown Norway, Brown Norway X Fischer 344, and Fischer 344 X Brown Norway rats with relation to age. J Gerontol Biol Sci51A:B54-B59. Masoro EJ. 1992. A dietary key to uncovering aging processes. News Physiol Sci 7:15-160. Nelson JF, Karelus K, Bergman MD, Felicio LS. 1995. Neuroendocrine involvement in aging: Evidence from studies of reproductive aging and caloric restriction. Neurobiol Aging 16:837-843.Phelan JP, Austad SN. 1994. Selecting animal models of human aging: Inbred strains often exhibit less biological uniformity than Fl hybrids.

show abstract

Animal Models in Aging Research

Cited by 10 publications

References 71 publications

Abnormal Structural Luteolysis in Ovaries of the Senescence Accelerated Mouse (SAM): Expression of Fas Ligand/Fas-Mediated Apoptosis Signaling Molecules in Luteal Cells

Abnormal Structural Luteolysis in Ovaries of the Senescence Accelerated Mouse (SAM): Expression of Fas Ligand/Fas-Mediated Apoptosis Signaling Molecules in Luteal Cells

Regeneration of skeletal and cardiac muscle in mammals: do nonprimate models resemble human pathology?

Senescence-accelerated Mouse (SAM): With Special Reference to Development and Pathobiological Phenotypes

Contact Info

Product

Resources

About