Key result
Cigarette smoke extract stimulates rat pulmonary artery smooth muscle cell proliferation via the PKCδ-PDGFB pathway.
Why the study?
The molecular mechanisms underlying cigarette smoke-induced pulmonary vascular remodeling and pulmonary hypertension remained poorly understood.
Does cigarette smoke extract stimulate proliferation of rat pulmonary artery smooth muscle cells via PKC-PDGFB signaling?
Does cigarette smoke extract stimulate proliferation of rat pulmonary artery smooth muscle cells via PKC-PDGFB signaling?
Cigarette smoke extract promotes pulmonary artery smooth muscle cell proliferation through the PKCδ-PDGFB pathway, providing a potential molecular mechanism for smoking-induced pulmonary vascular remodeling.
No immediate clinical implications; hypothesis-generating for smoking-related pulmonary vascular remodeling in humans.
Accumulating evidence suggests a direct role for cigarette smoke in pulmonary vascular remodeling, which contributes to the development of pulmonary hypertension. However, the molecular mechanisms underlying this process remain poorly understood. Platelet-derived growth factor (PDGF) is a potential mitogen and chemoattractant implicated in several biological processes, including cell survival, proliferation, and migration. In this study, we investigated the effect of cigarette smoke extract (CSE) on cell proliferation of rat pulmonary artery smooth muscle cells (rPASMCs). We found that stimulation of rPASMCs with CSE significantly increased cell proliferation and promoted cell cycle progression from G1 phase to the S and G2 phases. CSE treatment also significantly upregulated the mRNA and protein levels of PDGFB and PDGFRβ. Our study also revealed that Rottlerin, an inhibitor of PKCδ signaling, prevented CSE-induced cell proliferation, attenuated the increase of S and G2 phase populations induced by CSE treatment, and downregulated PDGFB and PDGFRβ mRNA and protein levels in rPASMCs exposed to CSE. Collectively, our data demonstrated that CSE-induced cell proliferation of rPASMCs involved upregulation of the PKCδ-PDGFB pathway.
No takes yet. Share an insight, caveat, or question.
Xing et al. (2012) studied Pulmonary hypertension. Cigarette smoke extract (CSE) was evaluated on Cell proliferation and cell cycle progression. Cigarette smoke extract stimulated rat pulmonary artery smooth muscle cell proliferation and cell cycle progression via upregulation of the PKCδ-PDGFB pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: