Inflammation alters regional mitochondrial Ca~(2+) in human airway smooth muscle cells

摘要

The importance of defining the role of mitochondrial Ca~(2+) buffering in human airway smooth muscle (ASM) lies in understanding the mechanisms by which [Ca~(2+)]_(cyt) is enhanced in airway diseases such as asthma, which contribute to airway hyperresponsiveness. Mitochondrial dysfunction and some ul-trastructural changes in mitochondria (swelling and loss of cristae) have been observed with airway inflammation (1, 39). In human ASM, mitochondria are present in large numbers (79), and, interestingly, mitochondrial biogenesis is enhanced in asthma (28). Whether such changes can contribute to altered Ca~(2+) homeostasis or other features of asthma, such as airway remodeling, is not known.