scholarly journals Age-Related Cell Proliferation and Apoptosis in the Kidney of Male Fischer 344 Rats With Observations on a Spontaneous Tubular Cell Adenoma

2000 ◽  
Vol 28 (6) ◽  
pp. 802-806 ◽  
Author(s):  
Rosanna Cardani ◽  
Teresa Zavanella
Keyword(s):  
Cell Proliferation ◽  
Tubular Cell ◽  
Fischer 344 Rats ◽  
Cell Adenoma ◽  
Fischer 344 ◽  
Related Cell ◽  
Age Related ◽  
Proliferation And Apoptosis

R403 – Epidermal Proliferating Cell Nuclear Antigen in Aging Rats

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P178-P178 ◽  
Author(s):  
Tapan K Bhattacharyya ◽  
Paula Jackson ◽  
J Regan Thomas
Keyword(s):  
Cell Proliferation ◽  
Proliferating Cell Nuclear Antigen ◽  
Nuclear Antigen ◽  
Proliferation Index ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Age Related ◽  
Two Parameters ◽  
Proliferating Cell ◽  
Effect Of Age

Problem To determine if epidermal cell proliferation in colony-raised Fischer 344 rats changes with age and diet. Methods Fischer 344 rats fed ad libitum and calorie-restricted (CR) diets were obtained from the NIA colonies, and young, young adult, and old animals from both groups were used for this study (six in each group). Tissue sections from the dorsal skin (DS) and foot plate (FP) were used for immunohistochemical staining of proliferating cell nuclear antigen (PCNA). The proliferation index (PCNA-I) was computed from counts of stained and total number of keratinocytes. Simultaneous measurements of epidermal thickness were obtained from same sections. Data were analyzed with Excel and SPSS 14.0 software for statistics. Results Two-way analysis of variance (ANOVA) was applied to the data to probe the effect of age, diet, and age-diet interaction. A significant effect of age was noticed in the two parameters i.e., DS PCNA (F 3.96, P .011), FP epidermal width (F 3.37, P .021) and FP PCNA-I (F 9.0, P .000). A significant correlation between DS width and PCNA values was also noted (r 0.5, P .01). Conclusion There is a trend of reduction of PCNA positive cells with increasing age irrespective of thickness of epidermis, and this trend is more apparent in CR rats. Significance This cell proliferation study has implications in relation to CR effect on age-related disease conditions, and biogerontology. Support The study was partially funded by the 2007 Leslie Bernstein grant from AAFPRS foundation.

Interactive effects of methyl-deficiency and dietary restrictionon liver cell proliferation and telomerase activity in Fischer 344 rats pretreated with aflatoxin B1

2000 ◽  
Vol 152 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Ming W Chou ◽  
Marina V Mikhailova ◽  
Jasyl Nichols ◽  
Lionel A Poirier ◽  
Alan Warbritton ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Liver Cell ◽  
Aflatoxin B1 ◽  
Telomerase Activity ◽  
Interactive Effects ◽  
Fischer 344 Rats ◽  
Fischer 344

scholarly journals Phrenic motor neuron loss in aged rats

2018 ◽  
Vol 119 (5) ◽  
pp. 1852-1862 ◽  
Author(s):  
Matthew J. Fogarty ◽  
Tanya S. Omar ◽  
Wen-Zhi Zhan ◽  
Carlos B. Mantilla ◽  
Gary C. Sieck
Keyword(s):  
Motor Neuron ◽  
Surface Area ◽  
Motor Neurons ◽  
Fiber Type ◽  
Dendritic Morphology ◽  
Diaphragm Muscle ◽  
Specific Force ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Age Related

Sarcopenia is the age-related reduction of muscle mass and specific force. In previous studies, we found that sarcopenia of the diaphragm muscle (DIAm) is evident by 24 mo of age in both rats and mice and is associated with selective atrophy of type IIx and IIb muscle fibers and a decrease in maximum specific force. These fiber type-specific effects of sarcopenia resemble those induced by DIAm denervation, leading us to hypothesize that sarcopenia is due to an age-related loss of phrenic motor neurons (PhMNs). To address this hypothesis, we determined the number of PhMNs in young (6 mo old) and old (24 mo old) Fischer 344 rats. Moreover, we determined age-related changes in the size of PhMNs, since larger PhMNs innervate type IIx and IIb DIAm fibers. The PhMN pool was retrogradely labeled and imaged with confocal microscopy to assess the number of PhMNs and the morphometry of PhMN soma and proximal dendrites. In older animals, there were 22% fewer PhMNs, a 19% decrease in somal surface area, and a 21% decrease in dendritic surface area compared with young Fischer 344 rats. The age-associated loss of PhMNs involved predominantly larger PhMNs. These results are consistent with an age-related denervation of larger, more fatigable DIAm motor units, which are required primarily for high-force airway clearance behaviors. NEW & NOTEWORTHY Diaphragm muscle sarcopenia in rodent models is well described in the literature; however, the relationship between sarcopenia and frank phrenic motor neuron (MN) loss is unexplored in these models. We quantify a 22% loss of phrenic MNs in old (24 mo) compared with young (6 mo) Fischer 344 rats. We also report reductions in phrenic MN somal and proximal dendritic morphology that relate to decreased MN heterogeneity in old compared with young Fischer 344 rats.

Parathyroid gland volume increases with postmaturational aging in the rat

2002 ◽  
Vol 282 (3) ◽  
pp. E557-E563 ◽  
Author(s):  
Bernard Halloran ◽  
Per Udén ◽  
Quan-Yang Duh ◽  
Shoichi Kikuchi ◽  
Tracy Wieder ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Renal Insufficiency ◽  
Parathyroid Gland ◽  
Inorganic Phosphorus ◽  
Proliferation Rate ◽  
Parathyroid Cell ◽  
Fischer 344 ◽  
Gland Volume ◽  
Cell Proliferation Rate ◽  
Age Related

To examine the pathophysiology of the age-related rise in the plasma concentration of parathyroid hormone (PTH), we studied the relationships among plasma immunoreactive PTH (iPTH), parathyroid gland volume, parathyroid cell proliferation rate, renal function, and blood Ca2+ in male Fischer 344 rats aged 6–28 mo. Plasma iPTH increased 2.5-fold between 6 and 28 mo and correlated with parathyroid gland volume ( r = 0.87). Gland volume began to increase as early as 6–12 mo of age and by 28 mo was threefold greater than at 6 mo. Gland expansion was a consequence of hyperplasia stimulated in part by an increase in cell proliferative activity late in life. Blood Ca2+ and plasma inorganic phosphorus did not change significantly with age. Glomerular filtration rate decreased with age but only after the age of 24 mo. Unlike what has been observed in the human, these data suggest that the age-related increase in plasma iPTH in the rat is linked to parathyroid gland hyperplasia and that early gland growth does not appear to be associated with hypocalcemia or renal insufficiency, but rather to developmentally related metabolic changes. Later in life (>24 mo), the increase in parathyroid cell proliferation rate, further hyperplastic expansion of the gland, and increase in iPTH secretion appear to be associated with renal insufficiency.

Upregulation of G protein-linked receptor kinases with advancing age in rat aorta

2001 ◽  
Vol 280 (3) ◽  
pp. R897-R903 ◽  
Author(s):  
William E. Schutzer ◽  
John F. Reed ◽  
Michael Bliziotes ◽  
Scott L. Mader
Keyword(s):  
G Protein ◽  
Rat Aorta ◽  
Aortic Tissue ◽  
Fischer 344 Rats ◽  
Membrane Expression ◽  
Fischer 344 ◽  
Age Related ◽  
Protein Receptor ◽  
Receptor Kinases ◽  
Increased Activity

The age-related decline in β-adrenergic receptor (β-AR)-mediated vasorelaxation is associated with desensitization of β-ARs without significant downregulation. The primary mode of this homologous β-AR desensitization, in general, is via G protein receptor kinases (GRK). Therefore, we hypothesize that age-related changes in GRKs are causative to this etiology in rat aorta. Herein, we investigate the activity and cellular distribution (cytoplasmic vs. membrane) of several GRK isoforms and β-arrestin proteins. GRK activity was assessed in extracts from aortic tissue of 6-wk, 6-mo, 12-mo, and 24-mo-old male Fischer-344 rats using a rhodopsin phosphorylation assay. We also performed immunoblots on lysates from aorta with specific antibodies to GRK-2, -3, -5, and β-arrestin-1. Results show an age-related increase in GRK activity. Furthermore, expression of GRK-2 (cytoplasmic and membrane), GRK-3 (cytoplasmic and membrane), and β-arrestin (soluble) increased with advancing age, whereas GRK-5 (membrane) expression remained unchanged. These results suggest that age is associated with increased activity and expression of specific GRKs. This increase likely results in enhanced phosphorylation and desensitization of β-ARs. These biochemical changes are consistent with observed aging physiology.

Age-related increases in diaphragmatic maximal shortening velocity

1996 ◽  
Vol 80 (2) ◽  
pp. 445-451 ◽  
Author(s):  
S. K. Powers ◽  
D. Criswell ◽  
R. A. Herb ◽  
H. Demirel ◽  
S. Dodd
Keyword(s):  
Force Production ◽  
Specific Force ◽  
Fischer 344 Rats ◽  
Rat Diaphragm ◽  
Shortening Velocity ◽  
Fischer 344 ◽  
Age Related ◽  
Highly Correlated ◽  
Related Increase

Recent evidence demonstrates that aging results in an increase in fast (type IIB) myosin heavy chain (MHC) in the rat diaphragm. It is unknown whether this age-related change in fast MHC influences the diaphragmatic maximal shortening velocity (Vmax). Therefore, we tested the hypothesis that aging is associated with an increase in the diaphragmatic Vmax and that the increase in the Vmax is highly correlated with the percentage of type IIb MHC. In vitro contractile properties were measured with costal diaphragm strips obtained from young (4 mo old; n = 8) and (old 24 mo old; n = 8) male Fischer-344 rats. Diaphragmatic maximal tetanic specific force production was 14.5% lower in the old compared with the young animals (23.0 +/- 0.4 vs. 19.7 +/- 0.8 N/cm2; P < 0.05). In contrast, the diaphragmatic Vmax was significantly higher in the old compared with the young animals (5.5 +/- 0.1 vs. 4.4 +/- 0.3 lengths/s; P < 0.05). Although the percent type IIb MHC was significantly higher (approximately +14%; P < 0.05) in the old compared with the young animals, the correlation between Vmax and percent type IIb MHC was relatively low (r = 0.50; P = 0.05). These data support the hypothesis that an age-related increase in diaphragmatic Vmax occurs; however, factors in addition to type IIb MHC are involved in regulating diaphragmatic Vmax. Interestingly, although aging resulted in a decrease in diaphragmatic maximal specific force production, power output at all muscle loads was maintained in the old animals due to the increase in diaphragmatic shortening velocity.

scholarly journals Induction of G1 checkpoint in the gastric mucosa of aged rats

1999 ◽  
Vol 277 (5) ◽  
pp. G929-G934 ◽  
Author(s):  
Zhi-Qiang Xiao ◽  
Yingjie Yu ◽  
Ahmed Khan ◽  
Richard Jaszewski ◽  
Murray N. Ehrinpreis ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Proliferative Activity ◽  
Protein A ◽  
S Phase ◽  
Aged Rats ◽  
Fischer 344 Rats ◽  
Protein Levels ◽  
Fischer 344 ◽  
Age Related ◽  
P53 Status

Although in Fischer 344 rats aging is found to be associated with increased gastric mucosal proliferative activity, little is known about specific changes in the regulatory mechanisms of this process. To determine whether changes in cell cycling events could partly contribute to the age-related rise in gastric mucosal proliferative activity, the present investigation examines changes in cyclin-dependent kinase (Cdk2) activity and the regulation of this process in the gastric mucosa of Fischer 344 rats aged 4 (young), 13 (middle aged), and 24 (old) mo. We observed that aging is associated with a progressive rise in activity and protein levels of Cdk2 in the gastric mucosa. This is also found to be accompanied by a concomitant increase in cyclin E but not cyclin D1 levels. On the other hand, the levels of p21Waf1/Cip1 (total as well as the fraction associated with Cdk2), a nuclear protein that is known to inhibit different cyclin-Cdk complexes, are found to decline in the gastric mucosa with advancing age. In contrast, with aging, there was a steady rise in p53 levels in the gastric mucosa. We have also observed that the levels of phosphorylated retinoblastoma protein, a form that participates in regulating progression through the S phase, are markedly elevated in the gastric mucosa of aged rats. In conclusion, our data suggest that, in the gastric mucosa, aging enhances transition of G1 to S phase as well as progression through the S phase of the cell cycle. However, the age-related decline in p21Waf1/Cip1 in the gastric mucosa appears to be independent of p53 status.

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