Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study characterizes single skeletal muscle fiber contractile properties and myosin heavy chain (MHC) isoform compositions from the soleus (SOL) and deep portion of the lateral head of the gastrocnemius (RG) muscles of 12- and 30-month-old Fischer 344 Brown Norway F1 hybrid rats (FBN F1). Thirty months of age is approximately the age of 50% survival for the FBN F1 rat. For type I MHC individual fibers from the SOL of 30-month-old animals, the diameter was 88 +/- 2 microns, peak active force was 4.4 +/- 0.2 x 10(-4) N, peak specific tension (P0) was 76 +/- 5 kN/m2, and maximal unloaded shortening velocity (V0) was 0.98 +/- 0.09 fl/s. The type I MHC fibers from the SOL of 12-month-old animals had similar properties with the exception of P0 which was 92 +/- 4 kN/m2 and V0 which was 1.65 +/- 0.12 fl/s. Contractile properties of the RG MHC type I fibers were not significantly different from MHC type I fibers from the SOL in both age groups. The V0 of the RG type IIa MHC fibers from the 12-month animals (4.05 +/- 0.36 fl/s) and 30-month animals (3.55 +/- 0.41 fl/s) and of fibers co-expressing type I MHC and type IIa MHC from 12-month animals (4.21 +/- 0.55 fl/s) and 30-month animals (2.22 +/- 0.27 fl/s) were significantly faster than that of MHC type I fibers of the respective age group. In conclusion, skeletal fibers from the 12- and 30-month-old FBN F1 rats demonstrate fiber-type specific properties with a close relationship between the MHC isoform composition and the V0.
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PMID:Contractile properties and protein isoforms of single skeletal muscle fibers from 12- and 30-month-old Fischer 344 brown Norway F1 hybrid rats. 1038 71

The effects of aging on cardiovascular function and cardiac structure were determined in a rat model recommended for gerontological studies. A cross-sectional analysis assessed cardiac changes in male Fischer 344 x Brown Norway F1 hybrid rats (FBN) from adulthood to the very aged (n = 6 per 12-, 18-, 21-, 24-, 27-, 30-, 33-, 36-, and 39-mo-old group). Rats underwent echocardiographic and hemodynamic analyses to determine standard values for left ventricular (LV) mass, LV wall thickness, LV chamber diameter, heart rate, LV fractional shortening, mitral inflow velocity, LV relaxation time, and aortic/LV pressures. Histological analyses were used to assess LV fibrotic infiltration and cardiomyocyte volume density over time. Aged rats had an increased LV mass-to-body weight ratio and deteriorated systolic function. LV systolic pressure declined with age. Histological analysis demonstrated a gradual increase in fibrosis and a decrease in cardiomyocyte volume density with age. We conclude that, although significant physiological and morphological changes occurred in heart function and structure between 12 and 39 mo of age, these changes did not likely contribute to mortality. We report reference values for cardiac function and structure in adult FBN male rats through very old age at 3-mo intervals.
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PMID:Age-related changes in cardiac structure and function in Fischer 344 x Brown Norway hybrid rats. 1614 57

One characteristic of ageing skeletal muscle is a decline in mitochondrial function. Activation of AMP-activated protein kinase (AMPK) occurs in response to an increased AMP/ATP ratio, which is one potential result of mitochondrial dysfunction. We have previously observed higher AMPK activity in old (O; 30 months) vs young adult (YA; 8 months) fast-twitch muscle in response to chronic overload. Here we tested the hypothesis that AMPK would also be hyperactivated in O vs YA fast-twitch extensor digitorum longus muscles from Fischer(344) x Brown Norway (FBN) rats (n = 8 per group) in response to high-frequency electrical stimulation of the sciatic nerve (HFES) or injection of AICAR, an activator of AMPK. Muscles were harvested immediately after HFES (10 sets of six 3-s contractions, 10 s rest between contractions, 1 min rest between sets) or 1 h after AICAR injection (1 mg (g body weight)(-1) subcutaneously). The phosphorylations of AMPKalpha and acetyl-CoA carboxylase (ACC2; a downstream AMPK target) were both greatly increased (P <or= 0.05) in response to HFES in O muscles, but were either unresponsive (AMPK alpha) or much less responsive (ACC) in YA muscles. AMPK alpha2 activity was also greatly elevated in response to HFES in O muscles (but not YA muscles) despite a lower total AMPK alpha2 protein content in O vs YA muscles. In contrast, AMPK alpha2 activity was equally responsive to AICAR treatment in both age groups. Since mitochondrial content and/or efficiency could potentially underlie AMPK hyperactivation, we measured levels of mitochondrial proteins as well as citrate synthase (CS) activity. While CS activity was increased by 25% in O vs YA muscles, uncoupling protein-3 (UCP-3) protein level was upregulated with age by 353%. Thus, AMPK hyperactivation in response to contractile activity in aged fast-twitch muscle may be the result of compromised cellular energetics and not necessarily due to an inherent defect in responsiveness of the AMPK molecule per se.
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PMID:AMP-activated protein kinase response to contractions and treatment with the AMPK activator AICAR in young adult and old skeletal muscle. 1927 78