Inhibition of macrophage inflammatory protein-1β improves endothelial progenitor cell function and ischemia-induced angiogenesis in diabetes

Ting Ting Chang, Liang Yu Lin, Jaw Wen Chen

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)

Abstract

Systemic inflammation might contribute to the impairment of neovasculogenesis and endothelial progenitor cell (EPC) function in clinical diabetes mellitus (DM). Macrophage inflammatory protein-1β (MIP-1β) is an inflammatory chemokine that may be up-regulated in clinical DM. Its role in diabetic vasculopathy was not clarified. This study aimed to investigate the role of MIP-1β in human EPCs and in neovasculogenesis in different diabetic animal models with hindlimb ischemia. EPCs chamber assay and in vitro tube formation assay were used to estimate the degree of EPC migration and tube formation abilities. Lepr db /JNarl mice, C57BL/6 mice fed a high-fat diet, and streptozotocin-induced diabetic mice were used as different diabetic animal models. Laser Doppler imaging and flow cytometry were used to evaluate the degree of neovasculogenesis and the circulating levels of EPCs, respectively. MIP-1β impaired human EPC function for angiogenesis in vitro. Plasma MIP-1β levels were up-regulated in type 2 DM patients. MIP-1β inhibition enhanced the function and the C-X-C chemokine receptor type 4 expression of EPCs from type 2 diabetic patients, and improved EPC homing for ischemia-induced neovasculogenesis in different types of diabetic animals. MIP-1β directly impaired human EPC function. Inhibition of MIP-1β improved in vitro EPC function, and enhanced in vivo EPC homing and ischemia-induced neovasculogenesis, suggesting the critical role of MIP-1β for vasculopathy in the presence of DM.

Original languageEnglish
Pages (from-to)53-65
Number of pages13
JournalAngiogenesis
Volume22
Issue number1
DOIs
Publication statusPublished - Feb 15 2019
Externally publishedYes

Keywords

  • Angiogenesis
  • Diabetes mellitus
  • Endothelial progenitor cell
  • Inflammation
  • Ischemia
  • Macrophage inflammatory protein-1β

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cancer Research

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