Abstract
The term lung disease describes a broad category of disorders that impair lung function. More than 35 million Americans have a preventable chronic lung disease with high mortality rates due to limited treatment efficacy. The recent increase in patients with lung disease highlights the need to increase our understanding of mechanisms driving lung inflammation. Connexins, gap junction proteins, and more specifically connexin 43 (Cx43), are abundantly expressed in the lung and are known to play a role in lung diseases. This review focuses on the role of Cx43 in pathology associated with acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and asthma. Additionally, we discuss the role of Cx43 in preventing disease through the transfer of mitochondria between cells. We aim to highlight the need to better understand what cell types are expressing Cx43 and how this expression influences lung disease.
Highlights
Connexins (Cx) are gap junction proteins involved in cell-to-cell communication
Sarieddine et al found that mice with reduced connexin 43 (Cx43) (+/−) have decreased neutrophils in the bronchial alveolar lavage fluid (BALF) following an intratracheal challenge with Pseudomonas aeruginosa LPS compared to wild-type Cx43 (+/+) mice [38]
Cx43 is known to be important for acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and asthma, as already described, and the mechanism appears to at least be in part due to propagation of calcium, and possibly other signals, between cells via gap junctions, and adenosine triphosphate (ATP) release through hemichannel opening, as the primary function of Cx43 in lung disease
Summary
Connexins (Cx) are gap junction proteins involved in cell-to-cell communication. There are currently at least mouse and human connexin genes The connexins they encode can assemble to form homomeric or heteromeric connexons [7]. More progress has been made in assessing which connexins can interact heterotypically (i.e., between connexons expressed in different cells) [9]. In a normal lung Cx32 is expressed by Type II alveolar cells and does not form heterotypic-connexons with Cx43. In response to lung injury Cx46 expression is increased on Type II alveolar cells, which can form heterotypic-connexons with Cx43, thereby increasing the potential for communication between the alveolar epithelium [10,11]. In RNA-seq data obtained from The Human Protein Atlas available from http://www.proteinatlas.org
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