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Macrophage migration inhibitory factor in hypothalamic paraventricular nucleus neurons decreases blood pressure in

Hongwei Li1, Yongxin Gao, Yanfei Qi

  • 1Dept. of Physiology and Functional Genomics, College of Medicine, 1600 SW Archer Rd., University of Florida, Gainesville, FL 32610-0274, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|June 7, 2008
PubMed

Insights

Reduced macrophage migration inhibitory factor (MIF) in the paraventricular nucleus (PVN) contributes to hypertension in spontaneously hypertensive rats (SHRs). Restoring MIF expression in PVN neurons attenuates hypertension and cardiac hypertrophy.

Area of Science:

  • Neuroendocrinology
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Angiotensin II (Ang II) normally increases paraventricular nucleus (PVN) macrophage migration inhibitory factor (MIF) to regulate blood pressure.
  • Enhanced PVN-mediated Ang II actions contribute to hypertension in spontaneously hypertensive rats (SHRs).

Purpose of the Study:

  • To investigate the MIF regulatory mechanism in the PVN of SHRs.
  • To determine if reduced MIF contributes to hypertension and cardiac hypertrophy in SHRs.

Main Methods:

  • Compared MIF protein and mRNA expression in the PVN of SHRs and normotensive rats.
  • Used Adeno-Associated Virus 2 (AAV2) to modulate MIF expression in PVN neurons of young SHRs.
  • Assessed the impact of MIF restoration on hypertension and cardiac hypertrophy.

Main Results:

  • Ang II failed to increase MIF protein in the PVN of SHRs.
  • MIF was diminished or absent in PVN neurons of SHRs.
  • AAV2-mediated increases in MIF expression attenuated hypertension and cardiac hypertrophy in SHRs.
  • AAV2-mediated transduction of a non-functional MIF mutant ([C60S]-MIF) did not affect hypertension or cardiac hypertrophy.

Conclusions:

  • A lack of MIF expression within PVN neurons contributes to the development of hypertension and cardiac hypertrophy in SHRs.
  • MIF's thiol protein oxidoreductase (TPOR) activity is crucial for its antihypertensive effects in the PVN.

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