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Absence of mannose-binding lectin prevents hyperglycemic cardiovascular complications

Vasile I Pavlov1, Laura R La Bonte, William M Baldwin

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

The American Journal of Pathology
|November 15, 2011
PubMed

Insights

Mannose-binding lectin (MBL) and the lectin complement pathway contribute to cardiovascular damage during acute hyperglycemia. MBL-null mice showed reduced cardiomyopathy and vascular dysfunction compared to wild-type mice.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Endocrinology

Background:

  • Hyperglycemia, a condition of elevated blood sugar, is linked to cardiovascular complications.
  • Chronic inflammation is consistently associated with the cardiovascular issues arising from hyperglycemia.
  • The role of mannose-binding lectin (MBL) and the lectin complement pathway in hyperglycemia-induced cardiovascular damage is not fully understood.

Purpose of the Study:

  • To investigate the hypothesis that acute hyperglycemia-induced cardiomyopathy and vasculopathy depend on MBL and lectin complement pathway activation.
  • To elucidate the specific mechanisms by which MBL influences cardiac and vascular dysfunction in hyperglycemia.

Main Methods:

  • Induction of acute hyperglycemia in wild-type (WT) and MBL-null mice using streptozotocin.
  • Echocardiography to assess cardiac function (cardiomyopathy).
  • Mesenteric arteriole relaxation studies to evaluate vascular function (vasculopathy).
  • Myocardial histochemistry and Western blot analysis for cellular and molecular changes.
  • Measurement of serum transforming growth factor-β1 levels.

Main Results:

  • Hyperglycemic WT mice exhibited dilated cardiomyopathy, unlike hyperglycemic MBL-null mice.
  • Significant loss of nitric oxide-mediated relaxation was observed in mesenteric arterioles of hyperglycemic WT mice.
  • Hyperglycemic WT hearts showed increased macrophage influx, altered morphology, and greater elastin/collagen deposition compared to MBL-null hearts.
  • Serum transforming growth factor-β1 levels were lower in hyperglycemic MBL-null mice, indicating reduced profibrotic signaling.

Conclusions:

  • Mannose-binding lectin (MBL) and the lectin complement pathway are critical mediators of vascular dysfunction and cardiomyopathy following acute hyperglycemia.
  • MBL activation exacerbates cardiac and vascular damage in hyperglycemic conditions.
  • Targeting MBL or the lectin complement pathway may offer therapeutic strategies for mitigating hyperglycemia-related cardiovascular complications.

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