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Plantaris muscle capillarity is reduced in pulmonary TNFα over‐expressing mice
Author(s) -
Olfert I. Mark,
Audet Gerald,
Malek Moh,
Tang Kechun,
Breen Ellen C.,
Wagner Peter D.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.989.16
Subject(s) - medicine , endocrinology , plantaris muscle , skeletal muscle , microvessel , hindlimb , chemistry , gastrocnemius muscle , tumor necrosis factor alpha , soleus muscle , lung , inflammation , angiogenesis
Chronic lung inflammation may contribute to abnormal skeletal muscle microvessel structure and function. To test the hypothesis that elevated pulmonary, and, as a result, systemic tumor necrosis factor‐α (TNFα) levels could contribute to skeletal muscle capillary rarefaction, transgenic mice that over‐express TNFα under the control of the lung‐specific SP‐C promoter were studied. Hind limb muscle mass and capillarity, body weight and exercise capacity in 4–5 month old SP‐C/TNFα (Tg, n=7) and littermate, control (C, n=7) mice were evaluated. Serum TNFα in Tg mice was increased (Tg 29.6±3.6 vs. C 5.2±2.9 pg/ml, p<0.001). Maximal running speed was reduced by 18% in Tg vs. C mice (31±1 vs 38±1 m/min, respectively, p<0.01). Body weight, and heart, gastrocnemius, plantaris and soleus mass were not different between Tg and C groups. Plantaris muscle capillary‐to‐fiber (C:F) ratio was 10% lower in Tg vs. C mice (1.32±0.06 vs. 1.46±0.01, respectively, p<0.05). C:F was not altered in the gastrocnemius (Tg 1.51±0.04 vs. C 1.50±0.02) or soleus (Tg 1.63±0.06 vs. C 1.73±0.01, p=0.15). These data suggest that chronically elevated circulating TNFα may contribute to skeletal muscle pathology in part by capillary rarefaction in some, but not all, hind limb locomotor muscles.