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Effect of elastin on abnormal proliferation of pulmonary artery smooth muscle cells at an early stage of hypoxic exposure. | LitMetric

AI Article Synopsis

  • - This study reveals that elastin (Eln), an extracellular matrix protein, can promote the proliferation of mouse pulmonary artery smooth muscle cells (mPASMCs) and its expression increases significantly under hypoxic conditions.
  • - When Eln expression was inhibited using siRNA, there was a notable reduction in key proteins involved in cell growth (PCNA, Cyclin A, and Cyclin D), reversing the proliferation driven by hypoxia.
  • - The research also highlights that the effects of hypoxia on Eln and mPASMCs proliferation are linked to the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, suggesting Eln's crucial role in hypoxic

Article Abstract

Elastin (Eln) is an extracellular matrix protein implicated in the proliferation of vascular smooth muscle cells. However, its potential role in hypoxic pulmonary hypertension (HPH) remains uncertain. This study is the first to demonstrate that elastin can promote the proliferation of mouse pulmonary artery smooth muscle cells (mPASMCs) and that hypoxia significantly induces Eln expression in cultured mPASMCs, thereby participating in the cell cycle. Interference with Eln expression siRNA led to the downregulation of PCNA, Cyclin A, and Cyclin D, thus, the hypoxia-induced proliferation of mPASMCs was reversed. Furthermore, our study demonstrated that the hypoxia-induced expression of Eln and the proliferation of mPASMCs are associated with the proliferation-related phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. In conclusion, these data suggest that Eln is a key regulatory factor in mPASMCs proliferation, potentially elucidating the mechanism underlying hypoxia-induced mPASMCs proliferation. This finding may offer valuable insights for the study of hypoxic pulmonary hypertension.

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Source
http://dx.doi.org/10.1080/10799893.2024.2430489DOI Listing

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