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Activation of calpain in pulmonary arterial smooth muscle cells (PASMCs)
Author(s) -
Kovacs Laszlo,
Rafikov Ruslan,
Szabo Andras,
Bagi Zsolt,
Black Stephen M.,
Su Yunchao
Publication year - 2013
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.27.1_supplement.1141.5
Subject(s) - calpain , platelet derived growth factor receptor , intracellular , chemistry , calcium in biology , bapta , growth factor , apoptosis , endocrinology , medicine , vascular smooth muscle , microbiology and biotechnology , biology , smooth muscle , biochemistry , enzyme , receptor
Pulmonary arterial hypertension (PAH) is a disease characterized by remodeling of vessel walls. Growth factors, inflammatory cytokines, reactive oxygen species (ROS), and calpain contribute to pulmonary vascular remodeling. In the present study, we studied whether calpain is activated by growth factors, inflammatory cytokines, and ROS. Pulmonary arterial smooth muscle cells (PASMCs) were treated with platelet‐derived growth factor‐BB (PDGF‐BB), serotonin (5‐HT), endothelin‐1 (ET‐1), interleukin‐6 (IL‐6) as well as H 2 O 2 , and calpain activity was measured using specific fluorescent substrates. Treatment with the stimulators mentioned above caused dramatic increases in calpain activity. The elevated calpain activity correlates with the increases in collagen‐I expression in PASMCs. Incubation of PASMCs with BAPTA/AM, a cell‐permeable intracellular calcium chelator, did not affect the increases in calpain activity induced by PDGF‐BB, 5‐HT, ET‐1, IL‐6, and H 2 O 2 . Conclusion PDGF‐BB, 5‐HT, ET‐1, IL‐6, and H 2 O 2 induce the activation of calpain. The mechanism is not due to increase in intracellular calcium. Supported by NIH and FAMRI