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Studies on mitogen-activated protein kinase signaling pathway in the alveolar macrophages of chronic bronchitis rats

Yan Huang1, Xiao-Ming Meng, Guo-Lin Jiang

  • 1School of Pharmacy, Anhui Medical University, Tunxi West Road, Hefei, 230032, Anhui, China.

Molecular and Cellular Biochemistry
|December 4, 2014
PubMed

Insights

Lipopolysaccharide (LPS) activates mitogen-activated protein kinases (MAPK) in chronic bronchitis (CB) rats. PI3K signaling negatively regulates downstream proteins in LPS-stimulated alveolar macrophages (AMs).

Area of Science:

  • Cell Biology
  • Immunology
  • Respiratory Medicine

Background:

  • Lipopolysaccharide (LPS) triggers inflammatory responses in alveolar macrophages (AMs) via intracellular signaling pathways like mitogen-activated protein kinases (MAPK).
  • Chronic bronchitis (CB) is characterized by persistent airway inflammation, involving complex signaling cascades within AMs.

Purpose of the Study:

  • To investigate the specific mitogen-activated protein kinase (MAPK) signaling pathway activated by LPS in AMs of CB rats.
  • To elucidate the roles of protein tyrosine kinase (PTK), phosphatidylinositol-3 kinase (PI3K), protein kinase C (PKC), and their downstream effectors in this pathway.

Main Methods:

  • Chronic bronchitis (CB) was induced in rats using LPS and Bacillus Calmette Guerin.
  • Specific pathway inhibitors (Genistein, LY294002, Calphostin C) were administered.
  • Protein phosphorylation levels were quantified using Western blot analysis.

Main Results:

  • Genistein inhibited protein kinase C (PKC), PI3K/protein kinase B (Akt) signaling.
  • LY294002 inhibited phospho-PI3K/Akt, p38, and c-Jun NH2-terminal kinases (JNK) phosphorylation.
  • Calphostin C inhibited phospho-PKC and extracellular signal-regulated kinases (ERK) phosphorylation but not p38 or JNK.

Conclusions:

  • The LPS-mediated MAPK pathway in CB rat AMs involves PTK-PI3K-Akt-JNK/p38 or PTK-PI3K-PKC-ERK signaling.
  • Phosphatidylinositol-3 kinase (PI3K) appears to exert negative regulation on the activation of downstream signaling proteins.

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