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Retinal Angiogenesis in Methamphetamine Self-Administration Rats.

Minsup Lee1, Bo J Wood2,3, Hyeon Hak Jeong4

  • 1Department of Molecular & Cellular Physiology, Louisiana State University Health Shreveport, Shreveport, Louisiana, United States.

Investigative Ophthalmology & Visual Science
|July 2, 2025
PubMed
Summary
This summary is machine-generated.

Methamphetamine (METH) use causes retinal vascular changes and new blood vessel growth (angiogenesis) by activating hypoxia pathways. Trace amine-associated receptor 1 (TAAR-1) is key in this METH-induced angiogenesis.

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Area of Science:

  • Ophthalmology
  • Vascular Biology
  • Neuroscience

Background:

  • Methamphetamine (METH) exposure is linked to retinal vascular abnormalities.
  • Understanding the molecular mechanisms of METH-induced retinal angiogenesis is crucial for preventing vision loss.

Purpose of the Study:

  • To investigate the molecular and cellular mechanisms of METH-induced retinal angiogenesis.
  • To utilize a rat self-administration model and primary rat retinal microvascular endothelial cells (RRMECs).

Main Methods:

  • Rats underwent an 8-week METH long-access self-administration protocol.
  • Retinal tissues were analyzed using flatmount imaging and vascular quantification.
  • Proteomic analysis, immunoblotting, and quantitative RT-PCR assessed molecular changes in retinal tissues and RRMECs.

Main Results:

  • METH self-administration increased retinal vascular density and dopamine levels.
  • Proteomic analysis revealed 148 differentially expressed proteins, highlighting hypoxia and ischemia pathways.
  • Increased hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor a (VEGFa) confirmed hypoxia-driven angiogenesis.
  • Trace amine-associated receptor 1 (TAAR-1) upregulation was observed, and its antagonism reduced METH-induced proliferation and modulated HIF-1α/VEGFa signaling.

Conclusions:

  • METH self-administration induces significant retinal vascular changes and angiogenesis via hypoxia-related pathways.
  • TAAR-1 plays a critical role in METH-induced endothelial cell proliferation through the HIF-1α/VEGFa pathway.
  • These findings suggest a mechanism for METH-related pathological retinal conditions.