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High-density lipoprotein regulates angiogenesis by long non-coding RNA HDRACA.

Zhi-Wei Mo1,2,3, Yue-Ming Peng1,2, Yi-Xin Zhang2,4

  • 1Division of Cardiac Surgery, Cardiovascular Diseases Institute, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.

Signal Transduction and Targeted Therapy
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Normal high-density lipoprotein (HDL) promotes blood vessel formation by downregulating HDRACA. Dysfunctional HDL fails to inhibit HDRACA, explaining its reduced ability to induce angiogenesis.

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Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • RNA Biology

Background:

  • Normal high-density lipoprotein (nHDL) promotes angiogenesis, but dysfunctional HDL (dHDL) from coronary artery disease patients loses this ability.
  • The mechanisms underlying HDL's regulation of angiogenesis and the role of dysfunctional HDL remain incompletely understood.

Purpose of the Study:

  • To identify novel molecular regulators involved in HDL-mediated angiogenesis.
  • To elucidate the role of a long non-coding RNA, HDRACA, in the differential effects of nHDL and dHDL on angiogenesis.

Main Methods:

  • Investigated the interaction between HDL, endothelial cells, and HDRACA expression.
  • Utilized molecular biology techniques including RNA sequencing, protein ubiquitination assays, and mRNA-protein binding analysis.
  • Employed a hindlimb ischemia mouse model to assess the in vivo function of HDRACA in angiogenesis.

Main Results:

  • nHDL downregulates HDRACA expression in endothelial cells via S1P receptor 1 and WW domain-containing E3 ubiquitin protein ligase 2, targeting Kruppel-like factor 5.
  • dHDL, with lower sphingosine 1-phosphate (S1P) levels, was less effective in downregulating HDRACA.
  • HDRACA inhibits angiogenesis by interacting with Ras-interacting protein 1 (RAIN), disrupting RAIN-vigilin interaction, and consequently reducing proliferating cell nuclear antigen (PCNA) mRNA binding to vigilin.
  • Overexpression of HDRACA in a mouse model impaired angiogenesis recovery.

Conclusions:

  • HDRACA is a key mediator in HDL's regulation of angiogenesis.
  • nHDL induces angiogenesis by suppressing HDRACA expression, while dHDL's diminished capacity to do so explains its angiogenic dysfunction.
  • HDRACA represents a potential therapeutic target for cardiovascular diseases characterized by impaired angiogenesis.