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Physiological and pathophysiological stimuli alter endothelial cell autophagy (737.4)
Author(s) -
Uzoigwe Emmanuella,
Panneerseelan Leena,
Li YouYou,
Deeter Lance,
Kunz David,
Graham Timothy,
Jionang Dapeu Elisee,
Symons J David
Publication year - 2014
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.28.1_supplement.737.4
Subject(s) - autophagy , medicine , endocrinology , homeostasis , chemistry , pathophysiology , cytosol , basal (medicine) , biochemistry , enzyme , apoptosis , insulin
Autophagy plays a central role in cellular quality control by destroying damaged or excess proteins, lipids, membranes, and organelles that accumulate in response to deviations from homeostasis. The existence and role of autophagy in endothelial cells (ECs) and blood vessels has not been established. We quantified the ratio of the membrane bound conjugate of microtubule‐associated protein light chain 3 (LC3‐II) to the cytosolic non‐lipidated conjugate LC3‐1 (LC3‐II:LC3‐I) or the protein normalizer GAPDH (LC3‐II:GAPDH) in ECs and blood vessels in response to a variety of cellular stressors. LC3‐II:LC3‐I or LC3‐II:GAPDH was elevated (p<0.05) (i) 450±6% (n=4) in ECs incubated for 2 h in amino acid (AA)‐deplete vs. AA‐replete media; (ii) 47±3% (n=3) in arteries from fasted (14 h) vs. fasted / refed (1 h) mice; (iii) 40±2% (n=3) in arteries from mice that completed acute exercise vs. sedentary controls; (iv) 38±1% in arteries from exercise‐trained vs. sedentary mice under basal conditions (n=2 per group); and was decreased (p<0.05) (v) 57±8% (n=4) in arteries from ~30 month‐old (i.e., old) vs. ~6 month‐old (i.e., young) mice. Further, indices of autophagy were elevated (p<0.05) 101±6% in ECs exposed to 3 h x 500 uM palmitate vs. vehicle (n=4), and 50±6% in arteries from obese vs. lean mice (n=4 per group). Thus, autophagy is altered in ECs and blood vessels in response to physiological (e.g., fasting, acute exercise, exercise training, aging) and pathophysiological (acute lipotoxicity, diet‐induced obesity) stimuli.