A potential contribution of dipeptidyl peptidase-4 by the mediation of monocyte differentiation in the development and progression of abdominal aortic aneurysms

J Vasc Surg. 2017 Oct;66(4):1217-1226.e1. doi: 10.1016/j.jvs.2016.05.093. Epub 2016 Nov 23.

Abstract

Objective: Abdominal aortic aneurysms (AAAs) are characterized by the destruction of elastin and collagen in the media and adventitia. Dipeptidyl peptidase-4 (DPP-4, an adipokine known as CD26) influences cell signaling, cell-matrix interactions, and the regulation of the functional activity of incretins in metabolic and inflammatory disorders. Although the role of DPP-4 in AAA evolution has been demonstrated, the underlying mechanisms of DPP-4-regulated AAA development remains unknown.

Methods: Patients with AAA (n = 93) and healthy controls (CTL, n = 20) were recruited. Based on computed tomography image analyses, 93 patients were divided into two groups: those with a small AAA (SAA, aortic diameter <5 cm, n = 16) and those with a large AAA (LAA, aortic diameter ≥5 cm, n = 77). Plasma DPP-4, glucagon-like peptide-1 levels, and expression of CD26 on mononuclear cells were analyzed. In addition, phorbol 12-myristate 13-acetate (PMA)-induced THP-1 cells and angiotensin II-infused apolipoprotein EtmlUnc mice were used to explore the underlying mechanisms.

Results: The levels of DPP-4 (μU/μg) increased while active glucagon-like peptide-1 (pM) decreased in patients with AAA in a diameter-dependent manner [CTL: 2.3 ± 1.5 and 3.7 ± 2.4, respectively; SAA: 10.0 ± 10.9 and 2.1 ± 0.9, respectively; LAA: 32.2 ± 15.0 and 1.8 ± 1.1, respectively]. A significant decline in monocyte CD26 expression in patients with AAAs was observed relative to the CTL group. In vitro studies demonstrated that the inhibition of DPP-4 promoted PMA-induced monocytic cells differentiation, with increased CD68 and p21 expression, regulated by extracellular signal-regulated protein kinase 1/2 activation. Furthermore, inhibition of DPP-4 significantly increased the phosphorylation of PYK2 and paxillin in PMA-induced THP-1 cell differentiation. Finally, the animal study was used to confirm the in vitro results that LAA mice showed marked macrophage infiltration in the adventitia with a decreased expression of DPP-4 as compared with SAA mice.

Conclusions: Increased plasma DPP-4 activity may correlate with aneurysmal development. CD26 on monocytes plays a critical role in cell differentiation, possibly mediated by extracellular signal-regulated protein kinase 1/2-p21 axis signaling pathways and cytoskeletal proteins reassembly. Exploring the role of DPP-4 further may yield potential therapeutic insights.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Animals
  • Aorta, Abdominal / diagnostic imaging
  • Aorta, Abdominal / enzymology*
  • Aorta, Abdominal / pathology
  • Aortic Aneurysm, Abdominal / diagnostic imaging
  • Aortic Aneurysm, Abdominal / enzymology*
  • Aortic Aneurysm, Abdominal / genetics
  • Aortic Aneurysm, Abdominal / pathology
  • Apolipoproteins E / genetics
  • Case-Control Studies
  • Cell Differentiation* / drug effects
  • Cell Line, Tumor
  • Dilatation, Pathologic
  • Dipeptidyl Peptidase 4 / blood
  • Dipeptidyl Peptidase 4 / genetics
  • Dipeptidyl Peptidase 4 / metabolism*
  • Dipeptidyl-Peptidase IV Inhibitors / pharmacology
  • Disease Models, Animal
  • Disease Progression
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Focal Adhesion Kinase 2 / metabolism
  • Glucagon-Like Peptide 1 / blood
  • Humans
  • Macrophages / drug effects
  • Macrophages / enzymology*
  • Macrophages / pathology
  • Male
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Middle Aged
  • Paxillin / metabolism
  • RNA Interference
  • Transfection

Substances

  • Apolipoproteins E
  • Dipeptidyl-Peptidase IV Inhibitors
  • PXN protein, human
  • Paxillin
  • Glucagon-Like Peptide 1
  • Focal Adhesion Kinase 2
  • PTK2B protein, human
  • Extracellular Signal-Regulated MAP Kinases
  • DPP4 protein, human
  • Dipeptidyl Peptidase 4
  • Dpp4 protein, mouse